|
Post by beammeup on Jun 18, 2011 17:58:49 GMT -5
|
|
|
Post by skyship on Jun 18, 2011 19:55:45 GMT -5
eLambda
Can't tell me MAYO did not know about this...............
bortezomib
Sub Navigation
* Diseases & Treatments * Diseases & Treatments Alphabetically o A B C D E F G H I J K L M N O P Q R S T U V W X Y Z ALL
* Quality * Patient Stories
Overview
Monoclonal gammopathy of undetermined significance (MGUS) is a common precancerous condition affecting people 50 years of age and older. It was first described by Mayo Clinic researchers in 1978 and is characterized by the presence of an abnormal protein in the blood called a (monoclonal) protein or M protein. Monoclonal gammopathy of undetermined significance has a small risk (1 percent each year) of progressing to a blood cancer called multiple myeloma or a related condition. Why choose Mayo Clinic?
* Experience. Mayo Clinic hematologists diagnose and care for hundreds of patients with monoclonal gammopathy of undetermined significance each year. Experienced pathologists are skilled in the testing and identification of the M protein and determining its potential risk of progression to cancer. * Research advances. Numerous Mayo Clinic researchers are studying MGUS to better understand it and to improve treatment options. Mayo Clinic researchers developed a new risk-assessment model that can predict risk of progression of monoclonal gammopathy of undetermined significance to multiple myeloma. * Coordinated care. A specialist in blood diseases (hematologist) will oversee your care and bring in other specialists as needed, including neurologists if nerve damage is suspected, nephrologists to prevent kidney failure and dermatologists if skin lesions occur. Access to specialists, testing and treatment is available in one convenient location and can be accomplished in a few days.
Read more about monoclonal gammopathy of undetermined significance on MayoClinic.com.
Monoclonal gammopathy of undetermined significance (MGUS) is a common precancerous condition affecting people 50 years of age and older. It was first described by Mayo Clinic researchers in 1978 and is characterized by the presence of an abnormal protein in the blood called a (monoclonal) protein or M protein.
Oh yeayh................................................
Those Morgies would never know would they?
MGUS..............
Skyship
|
|
|
Post by skyship on Jun 18, 2011 20:01:53 GMT -5
MGUS Lambda phage Lambda light chain Paraproteinemia From Wikipedia, the free encyclopedia Jump to: navigation, search Paraproteinemia Classification and external resources ICD-9 273.1-273.2 DiseasesDB 9614 MeSH D010265 Paraproteinemia, or monoclonal gammopathy, is the presence of excessive amounts of a single monoclonal gammaglobulin (in this case denominated "paraprotein") in the blood. It denotes an underlying immunoproliferative disorder. It is sometimes considered equivalent to plasma cell dyscrasia.[1] Paraproteinemias may be categorized according to the type of monoclonal protein found in blood: * Light chains only (also known as "AL amyloidosis or "light chain disease"). * Heavy chains only (also known as "heavy chain disease"); * Whole immunoglobulins (albeit often with an abnormal light / heavy chain ratio). The three types of paraproteins may occur alone or in combination in a given individual. Note that while most heavy chains or whole immunoglobulins remain within blood vessels, light chains frequently escape and are excreted by the kidneys into urine, where they take the name of Bence Jones protein. It is also possible for paraproteins (usually whole immunoglobulins) to form polymers by aggregating with each other; this takes the name of macroglobulinemia and may lead to further complications. For example, certain macroglobulins tend to precipitate within blood vessel with cold, a phenomenon known as cryoglobulinemia. Others may make blood too viscous to flow smoothly (usually with IgM macroglobulins), a phenomenon known as Waldenström macroglobulinemia. [edit] Possible causes * Leukemias and lymphomas of various types, but usually B-cell Non-Hodgkin lymphomas with a plasma cell component. o Myeloma o Plasmacytoma o Lymphoplasmacytic lymphoma * Idiopathic (no discernible cause): some of these will be revealed as leukemias or lymphomas over the years. o Monoclonal gammopathy of undetermined significance o Primary AL amyloidosis (light chains only) [edit] Diagnosis These disorders are characterized by the presence of any abnormal protein that is involved in the immune system, which are most often immunoglobulins and are associated with the clonal proliferation of lymphocytes.[2] When a paraproteinemia is present in the blood, there will be a narrow band, or spike, in the serum protein electrophoresis because there will be an excess of production of one protein.[3] There are two large classes of blood proteins: albumin and globulin. They are generally equal in proportion, but albumin is much smaller than globulin, and slightly negatively charged, which leads to an accumulation at the end of the electrophoretic gel. The globulins separate out into three regions on the electrophoretic gel, which are the α band, the β band, and the γ band. * The α band can be separated into two components: α1 and α2. The α1 region consists mostly of α1-antitrypsin and α1-acid glycoprotein. The α2 region is mostly haptoglobin, α2-macroglobulin, α2-antiplasmin and ceruloplasmin. * The β band consists of transferring, low-density lipoproteins, and complement system proteins.[4] * The γ band is where the immunoglobulins appear, which is why they are also known as gammaglobulins.[5] The majority of paraproteins appear in this band.[4] [edit] See also * Monoclonal gammopathy of undetermined significance en.wikipedia.org/wiki/ParaproteinemiaFollowing up behind ya, fella. Skyship
|
|
|
Post by skyship on Jun 18, 2011 20:06:44 GMT -5
|
|
|
Post by skyship on Jun 18, 2011 20:09:30 GMT -5
# POEMS Syndrome # Scleromyxedema * M-protein (85%): λ; IgG * Onset: Middle aged adults * Skin o Disseminated papules, plaques & infiltrative lesions + Symmetric + Distribution: Face; Neck; Arms o Histology + Accumulation of mucopolysaccharides (Mucin): Hyaluronic acid; In upper dermis + Fibroblast proliferation + Inflammation: Occcasional; Perivascular o External link: Erlangen pictures Skin & Pathology * Myopathy (25%) o Weakness + Proximal + Symmetric + Dysphagia (30% to 100%): Upper Esophagus o Serum CK: Mildly elevated (60%) o Aldolase: High o EMG: Irritative myopathy o Pathology + Myopathic: Degeneration & Regeneration + Vacuoles: Rimmed + Inflammation: Scattered; Large PAS-positive perimysial cells o Treatment: ? Prednisone; Methotrexate (IV) * CNS (10%): Encephalopathy * ± Neuropathy * Vascular: Raynaud's; Telangectasia; Ischemia * Other: Weight loss; Interstitial lung disease; Esophageal dysmotility; ? Thyroid * Associated neoplasm: Myeloma in 10% * Course: Variable - spontaneous resolution to progressive disability neuromuscular.wustl.edu/antibody/mprotein.htmskyship
|
|
|
Post by skyship on Jun 18, 2011 20:41:13 GMT -5
M protein ,,,,,,,,,,,, in Influenza ............ MS2 phage.............. www.wellsphere.com/kidney-failure-article/kappa-versus-lambda-light-chains-in-paraproteinemias/1250134M Protein is a membrane protein..................matrix................protein........... Monoclonal from SV40...................... Cytoskeletin restructuring.............. www.wikigenes.org/e/gene/e/851148.htmlGRIM-19 (Gene associated with Retinoid-Interferon-induced Mortality 19) is a novel tumor suppressor regulated by Interferon/retinoid combination. We have recently shown that GRIM-19 inhibits v-Src-induced oncogenic transformation and metastatic behavior of cells. Oncogenic v-Src induces cell motility by cytoskeletal remodeling especially the formation of podosomes and. Here we show that GRIM-19 inhibited the v-Src-induced cell motility by inhibiting cytoskeletal remodeling i.e., podosome formation. We also show that the N-terminus of GRIM-19 played a major role in this process and identified critical residues in this region. More importantly, we show that tumor-associated GRIM-19 mutations disrupted its ability to inhibit v-Src-induced cell motility. These actions appear to occur independently of STAT3, a known target of GRIM-19-mediated inhibition. Lastly, tumor-associated GRIM-19 mutants significantly lost their ability to control v-Src-induced metastases in vivo, indicating the biological and pathological significance of these observations.
|
|
|
Post by skyship on Jun 18, 2011 20:45:06 GMT -5
|
|
|
Post by skyship on Jun 18, 2011 21:54:00 GMT -5
Hang on folks................
Monoclonal M protein: What is it? Mollicutes: Mollicutes), Acidobacteria, Fibrobacteres, Fusobacteria, Dictyoglomi, Gemmatimonadetes, Lentisphaerae, Verrucomicrobia, Chlamydiae, and Planctomycetes fusobacteria, fibro, chlamydiae.. Mollicutes. fusobacteria......fusobacterium................. fusarium bacteria......microbewiki.kenyon.edu/index.php/Fusobacterium_nucleatum============================= The nucleus..........the mollicute.......................................................................................................... Examples of proto-oncogenes include RAS, WNT, MYC, ERK, and TRK. The MYC gene is implicated in Burkitt's Lymphoma, which starts when a chromosomal translocation moves an enhancer sequence within the vicinity of the myc gene. The myc gene codes for widely used transcription factors. When the enhancer sequence is wrongly placed, these transcription factors are produced at much higher rates. Another example of an oncogene is the Bcr-Abl gene found on the Philadelphia Chromosome, a piece of genetic material seen in Chronic Myelogenous Leukemia caused by the translocation of pieces from chromosomes 9 and 22. Bcr-Abl codes for a receptor tyrosine kinase which is constitutively active, leading to uncontrolled cell proliferation.
en.wikipedia.org/wiki/Oncogene
======================
These are cancer producing recombinant genes. So, is related to blood cancer......... RAS, WNT, MYC, ERK, and TRK.
===================================== RAS:Harvey Ras oncogeneImage HRAS.jpg Cancer occurs when the growth and differentiation of cells in a body tissue become uncontrolled and deranged. While no two cancers are genetically identical (even in the same tissue type), there are relatively few ways in which normal cell growth can go wrong. One of these is to make a gene that stimulates cell growth hyperactive; this altered gene is known as an 'oncogene'.Ras is one such oncogene product that is found on chromosome 11. It is found in normal cells, where it helps to relay signals by acting as a switch. When receptors on the cell surface are stimulated (by a hormone, for example), Ras is switched on and transduces signals that tell the cell to grow. If the cell-surface receptor is not stimulated, Ras is not activated and so the pathway that results in cell growth is not initiated. In about 30% of human cancers, Ras is mutated so that it is permanently switched on, telling the cell to grow regardless of whether receptors on the cell surface are activated or not.www.ncbi.nlm.nih.gov/books/NBK22261/==================== WNT * tch 1 Overexpression Inhibits Osteoblastogenesis by Suppressing ... Among the Wnt proteins, Wnt 1, 3, 3a, 7a, and 8 activate the canonical Wnt/β-catenin ... cloned into the retroviral vector pLPCX (Clontech, Palo Alto, CA) for the creation ... www.jbc.org/content/281/10/6203.full * Related Searches for creation of WNT protein o Wnt Protein Hair Krt17 o Cancer Signaling Pathways o Canonical Pathway o Wnt Proteins Promote Bone Reg… o Signaling Pathways o Wnts * Wnt antagonists and their use in the diagnosis and treatment of ... Additionally, while the creation of Fc fusions is generally known as one technique ... A “Wnt protein” is a ligand of the Wnt signaling pathway component which binds to ... ip.com/patapp/US20080299136 * * Access : Creation of genome-wide protein expression libraries ... Creation of genome-wide protein expression libraries using random activation of gene expression ... I want to purchase this article. Price: US$32. In order to purchase this ... nature.com/nbt/journal/v19/n5/full/nbt0501_440.html * advantages of protein - thoughts.com conversation engine various samples of protine on the market, whey protein ... benefit from, because it aids promote the creation of ... It is perfect to folks who are want to lose weight and ... www.thoughts.com/prestonriver717/advantages-of-protein * Kelly Baggett-Creation of a Bodybuilder | Dr. Squat - Dr. Fred ... Here is what Kelly Baggett wrote in his article "creation of a bodybuilder" ... The rest of your diet is open to virtually whatever you want. Protein builds the muscle ... drsquat.com/content/kelly-baggett-creation-bodybuilder * Modular protein nanostructures.html - 2009.igem.org Approach to creation of modular protein nanostructures. Larger natural proteins are with exception of fibrils composed of folded domains. If we want to prepare the material ... 2009.igem.org/Modular_protein_nanostructures.html * Protein therapy speeds bone healing in mice - FierceBiotech Research Researchers used liposomes to deliver pieces of a genetically-enhanced protein called Wnt, successfully triggering the creation of bone-healing cells in mice. www.fiercebiotechresearch.com/story/protein-therapy-speeds-bone-healing-mice/2010-05-03 * Secreted frizzled related protein 1 is a paracrine modulator of ... Creation of an Sfrp1 lacZ knock-in allele that is null for Sfrp1 function ... A secreted frizzled related protein, FrzA, selectively associates with Wnt-1 protein ... www.ncbi.nlm.nih.gov/pmc/articles/PMC2435376=============================================== abnormal plasma cells in the bone marrow and overproduction of monoclonal immunoglobulin (IgG, IgA, IgD, or IgE) or Bence-Jones proteins (monoclonal globulin protein found in the blood)Read more: www.righthealth.com/topic/Monoclonal_Protein#ixzz1PgctHey2Bence Jones proteins...................... immunoglobulin..................The other proto-oncogenes........................ MYC ERK TRK skyship
|
|
|
Post by skyship on Jun 18, 2011 22:09:06 GMT -5
Bence Jones protein From Wikipedia, the free encyclopedia Jump to: navigation, search "Bence-Jones" redirects here. For Mark Bence-Jones the British author, see Mark Bence-Jones. A crystal of Bence Jones protein.
A Bence Jones protein is a monoclonal globulin protein found in the blood or urine, with a molecular weight of 22-24 kDa.[1] Finding this protein is often suggestive of multiple myeloma or Waldenstrom's macroglobulinemia. Bence Jones Proteins are particularly diagnostic of multiple myeloma in the context of end-organ manifestations such as malignant bone marrow cancer, renal failure, lytic bone disease, or anemia, or large numbers of plasma cells in the bone marrow of patients. Bence Jones Proteins are present in 2/3 of multiple myeloma cases.[2] The proteins are immunoglobulin light chains (paraproteins) and are produced by neoplastic plasma cells. They can be kappa (most of the time) or lambda.[2] The light chains can be immunoglobulin fragments or single homogeneous immunoglobulins. They are found in urine due to the kidneys' decreased filtration capabilities due to renal failure, often induced by hypercalcemia from the calcium released as the bones are destroyed.[citation needed] The light chains have traditionally been detected by heating or electrophoresis of concentrated urine. More recently serum free light chain assays have been utilised in a number of published studies which have indicated superiority over the urine tests, particularly for patients producing low levels of monoclonal free light chains, as seen in nonsecretory multiple myeloma[3][4][5] and AL amyloidosis.[5][6][7][8] This is primarily because of the re-absorption of free light chains in the kidneys, creating a "threshold" of light chain production which must be exceeded before measurable quantities overflow into the urine. As such, urinalysis is a fickle witness to changing free light chain production.
There are various rarer conditions that can produce Bence Jones proteins, such as Waldenström's macroglobulinemia and other malignances.
SKIZIT: BENCE JONES PROTEINS ARE THE TAPES>>>>>>>>>>>>>>>> IMAGE: upload.wikimedia.org/wikipedia/commons/2/27/Bence_Jones_Protein_MLE1.jpgThese will be in the urine.............................. Skyship
|
|
|
Post by skyship on Jun 18, 2011 22:58:33 GMT -5
|
|
|
Post by skyship on Jun 18, 2011 23:18:21 GMT -5
ERK TRK ERK: THE SIGNAL Its Role in Growth Factor Signaling and Cancer First printed in R&D Systems' 2004 Catalog. Contents * Upstream from ERK * The Core Module * Downstream from ERK * Conclusions * References Growth factors, through receptor tyrosine kinases, recruit a large network of signaling proteins to execute their cellular programs. The first of these networks to be discovered was the Ras-Raf-ERK signal transduction cascade, defined by extracellular signal-regulated kinase-1 (ERK1) and ERK2.1 One of four mitogen-activated protein kinase (MAPK) signaling pathways, the ERK phosphorylation cascade's importance in intracellular signaling has been compared to the role of the Krebs cycle in energy metabolism.2 The ERK cascade functions in cellular proliferation, differentiation, and survival, and its inappropriate activation is a common occurrence in human cancers. Figure 1. The activated membrane-spanning epidermal growth factor receptor (EGF R) becomes a platform for the assembly of a signaling complex that includes the cytoplasmic growth factor receptor bound protein 2 (Grb2) and son of sevenless (SOS), which activates the membrane-bound GTPase, Ras. Upstream from ERK During growth factor stimulation, the ERK phosphorylation cascade is linked to cell surface receptor tyrosine kinases (RTKs) and other upstream signaling proteins with known oncogenic potential (Figure 1).3 www.rndsystems.com/mini_review_detail_objectname_MR04_ERKSignalTransduction.aspx============= This is the p38: ERK and p38 MAPK-Activated Protein Kinases: a Family of Protein Kinases with Diverse Biological Functions mmbr.asm.org/cgi/content/full/68/2/320=================== TRK: Human trk oncogenes activated by point mutation, in-frame deletion, and duplication of the tyrosine kinase domain. In the cytoplasma: Malignant activation of the human trk proto-oncogene, a member of the tyrosine protein kinase receptor family, has been implicated in the development of certain human cancers, including colon and thyroid papillary carcinomas. trk oncogenes have also been identified in cultured cells transfected with various DNAs. In this study, we report the characterization of three in vitro-generated trk oncogenes, trk2, trk4, and trk5 (R. Oskam, F. Coulier, M. Ernst, D. Martin-Zanca, and M. Barbacid, Proc. Natl. Acad. Sci. USA 85:2964-2968, 1988), in an effort to understand the spectrum of mutational events that can activate the human trk gene. Nucleotide sequence analysis of cDNA clones of trk2 and trk4 revealed that these oncogenes were generated by a head-to-tail arrangement of two trk tyrosine protein kinase domains connected by a purine-rich region. These oncogenes code for cytoplasmic molecules www.ncbi.nlm.nih.gov/pmc/articles/PMC360953/I hope this shows those 5 oncogenes.................... relate to cytoplasma, cell wall. liposome model membrane: images: tinyurl.com/3vlenv3Skyship
|
|
|
Post by katinka on Jul 14, 2011 19:02:48 GMT -5
|
|
|
Post by skyship on Jul 14, 2011 19:21:45 GMT -5
Katinka, Some of us already had 47 with the trisomy, this makes 48. the other paired with the first. makes a quad. Ha ha... Lets say they are usually paired right? so we have 23, 22 with X now we have 24, are they paired? or single strand? mmmmmm that would make 23 1/2, but since two histones were changed, looks like we may have 48? And us with trisomies have 49. Isn't that the same as the monkey? So, to make animals of us, were they? How dare them! Is that what the first SV40 was? then along comes the second construction in the immunoglobins. RH is Rhesus monkey and SV is from Simian Monkey, and then there's the Green Monkey, So are we in the Green Monkey stage now. that would be 3 trisomies, so we are above the monkey, we are not equal, but above he monkey. Hallelujah! that would make 48 and 1/2....... So, if we are talking single strands here. There is the CD47. Would this be it, you think, Katinka? Looks the the Morgie organism. ET come on in. Lets talk! www.rndsystems.com/ihc_molecule_images.aspx?m=1218what is rnd systems? Oh heck, it is a sheep gene. mmmmmm tried to make us sheep, did they? referring to nitric oxygen? Recent research by us and our collaborators has found that CD47 is the critical signaling receptor by which TSP1 limits nitric oxide signaling in all vascular tissues and cells. The figure below indicates points at which CD47 might interdict NO signaling. Some of these are confirmed and others are still under investigation in our lab. biochem.wustl.edu/frazier/CD47.htmlseems to be falling right into place! What is the H2N have seen that at beginning of the amyloid formation form. Oh my gosh, it is called Amidogen. www.chembase.com/mf_H2N.htmOkay then. Just sliding this in again. Thanks Katinka. Skyship
|
|
|
Post by skyship on Jul 14, 2011 19:23:27 GMT -5
|
|
|
Post by katinka on Jul 14, 2011 20:09:56 GMT -5
The guy in the video made that statement about the 47 chromosomes, I basically just repeated what he said. If his info is new or not, I'm not aware of but since the video is dated June 23 2011 I thought it was fairly new. About the psoriasis link. We were wondering too. Maybe if people are looking up info on itchy scalp issues or something because the docs told them they psoriasis....hmmm....sounds familiar doesn't it Kammy? Actually I stumbled upon this all while searching new info on M in German.
|
|
|
Post by skyship on Jul 14, 2011 21:23:56 GMT -5
You know what, they may have another form, that is not recognized in America. And they may have the key. mmmmm
The guy in the video, oh yes, he is getting the word out. I know he is looking at it very closely, on observant level, and that everyone has these. He found many people at that conference he was at that do not have Morgellons but they have the fibers. And some of them have messages on them, as shown by Skizit on her videos, too, the tape ones had letters on them etc, that lead back to labs that may have made them, or were part of the construction of them. Somehow they seemed to put their signatures on them.
Makes you wonder if there is something bigger than all of this? doesn't it?
Sometimes I get an eery feeling that there is massive info we do not even have a clue about, as Kammy said. Like a secret space program, or alien races who want to knock on our doors.
Anyhow, on that video they talk of the forms found in ice. Lets see, that high up in the release of these foreign proteins, or viruses, or body parts, might be in frozen material, meaning it is all over the universe........ or .......is being sprayed from those UN operated planes, that are rearranging the landscape. I read way back where they bought some old I think they were c135's from the airforce. Wonder what they are doing with them?
So, many avenues this Morgellons is going down. I think the ones who have the newer fibers, have no artifacts. We older folks, have the artifacts, and they are replicating because they are more organic, than inorganic, linking to hidden viruses as the mutators. or bacteriophages, when they realized they could use inorganic material for the Epigenetic approach..........er transhuman approach.
Skyship
The amphiphile/bolamphiphile in my studies say that these have less artifacts, however, the light strands are there, they are not what they called irritants, or aggravators, like The first ones were. They are there just for signaling, whereas us older folks, have the baculo/amyloid/cores, part of the actual chromosome system before its alteration.
These parts can be early or late it seems, The later ones are more formed, less harmful, while the others can cause the old diseases, or newer ones because they cannot handle the changes.
It seems we have been monitored for a long time. What do you think contact will be like?
Was it done here, or from out there?
Are we simply on the wrong planet?
haha...... We did talk of that 47 gene once and there was a scientist interested in it, but we did not hear back from him.
So, our PR man the Morgellon man there, is getting the word out.
Kudos to him. I am wondering if some are saying this is psoriasis, and sure does not seem like it, except for the plaque, which to me is more like calcium desposits or amyloid.
Will try to see if Mr. AJ found a connection to the chemtrails.
mmmmmmm this is getting interesting though.
Skyship
So, wonder why some have issues with them and other dont?
|
|
|
Post by skyship on Jul 15, 2011 0:11:09 GMT -5
I wonder if this is the signaling system? CD47-SHPS-1 system, makes me think that immunoglobin light chains are what these fibers are. the light chains are involved with amyloids(monomers) as well, bench jones proteins (tapes?), has a crystal, Image of crystal: journals.iucr.org/f/issues/2006/03/00/pu5117/pu5117fig1thm.gifand the fibers look like the ragged ones we get, deeper level. Here is the system image: www.imcr.gunma-u.ac.jp/lab/biosig/image/fig1.jpgthis is with a mouse, but, is shown on human IgG................... Check out this IgG picture, compared to the SHPS-1(a novel receptor-type transmembrane protein), www.imcr.gunma-u.ac.jp/lab/biosig/image/fig4a1.jpg and on On SHPS-1-Fc www.imcr.gunma-u.ac.jp/lab/biosig/image/fig4a2.jpgnot much different, so what is this SHPS-1 membrane? ? from mouse or from the novel find? This one shows the actual system: involved dendrites, the synapse points between neurons. that cdc42 could be the amyloid form? www.imcr.gunma-u.ac.jp/lab/biosig/image/fig4b.jpgAmyloid can mess up blood cells....... arteriosclerosis, which has the amyloid in it? Oh my, I am writing a paper on this, and I keep finding more connections to what Morgellons is in relation to a followup after the creation of Alzheimers? which was a followup after the creation of AIDS. Involves the heavy and light chains of the immunoglobins. Makes me wonder if Lymes carries the Aids initiator? or before that the SV40 which is involved in both Aids and Polio vaccines. however the 1933 strain was in Influenza A, first strain, one can follow the path backwards. Okay, before 1933, 1918....all in the current Influ strains. Before that was Glanders, and before that, the amyloid?..... late 1800s. Actually that goes back to 1838 and the talk of the amylaceous mater. or matter. or starchy sugar. This is all about discovery, isn't it? with red blood cell: www.imcr.gunma-u.ac.jp/lab/biosig/image/fig2b.jpgEntire article found here under Biosignals. www.imcr.gunma-u.ac.jp/lab/biosig/english.htm============================ So finding out what this strand is would be helpful. The CD47 is phosphorus particle ? The novel membrane is: SHPS-1-Fc seems a lot of dermatology investigators are investigating this. Will concentrate on this "novel membrane" called SHPS-1-Fc. Skyship
|
|
|
Post by skyship on Jul 15, 2011 1:02:43 GMT -5
CD47 is a membrane-associated glycoprotein novel membrane" called SHPS-1-Fc is a src homology 2 domain containing protein tyrosine phosphate substrate 1, a ligand for CD47. the Fc means fusion protein. in LC(Langerhan Cells) ------
RAC activator with cdc42 and cdc42activator with RAC Rac and Cdc42 ActivatorCat. # CN02 Product Uses Include 1. Positive control for Rac and Cdc42 activation studies. 2. Study the effects of Rac and Cdc42 activation on cell motility 3. Study the effects of Rac activation on the rearrangement of the actin cytoskeleton.
4. Investigate the effects of Rac and Cdc42 activation with respect to cross talk to other signal transduction pathways.www.cytoskeleton.com/products/g-prot/cn02.html============ cdc42 is " CDC42 is a small GTPase of the Rho-subfamily, which regulates signaling pathways that control diverse cellular functions including cell morphology, migration, endocytosis and cell cycle progression. It is a binding protein.........must have some adhesive? en.wikipedia.org/wiki/CDC42RAC: welllllllllllllllllll. Rac 3 is made of: Rac3 (Ras-related C3 botulinum toxin substrate 3) is a small (~21 kDa) monomeric GTP-binding protein G protein and is an important component of intracellular signalling pathways en.wikipedia.org/wiki/Rac3Rac 1[/b]also a C3 botulinium toxin. Ras-related C3 botulinum toxin substrate 1 also known as Rac1
en.wikipedia.org/wiki/Rac1
Rac 2and again they are all C3 botulinium toxin. Rac2 (Ras-related C3 botulinum toxin substrate 2) is a small (~21 kDa)
en.wikipedia.org/wiki/Rac2
======================
So, C3 botulinium toxin? Image: have we seen this before?
www.cellmigration.org/resource/discovery/geiger/geiger2009_rnai_image.cgi?uid=854&file=RAC1_HR.jpg&dir=hr&gene=RAC1&gene_id=5879&desc=ras-related%20C3%20botulinum%20toxin%20substrate%201%20%28rho%20family,%20small%20GTP%20binding%20protein%20Rac1%29&lib=MAR
It is a monomer.........This looks like something we have seen, in fact ann posted something that looks similar.
Barf time............ What is interesting is that this is a clostridium botulinium.
========================= CD47: WOW quite a statement, isn't it?
"CD47 is a membrane-associated glycoprotein that suppresses the function of immune cells" Considered the 'kernal"? www.lib.kobe-u.ac.jp/repository/90000418.pdf
l
----------------------------------
Ligand: (from the Latin ligandum, binding) is a substance that forms a complex with a biomolecule to serve a biological purpose. In a narrower sense, it is a signal triggering molecule, binding to a site on a target protein. en.wikipedia.org/wiki/Ligand_%28biochemistry%29 ====================
SHPS-1 Fc:is a ligand, so this is the membrane.......
So, they used toxic genes on us.................holy crap. that is all they are............................................crap makers.
they make monomers, monomers make dimers, oligomers, protofibrils....... etc...........
I bet bolamphiphiles are made of e bola.............
www.morgboard.proboards.com/index.cgi?board=general&action=display&thread=1167
We are up crap creek without a paddle.
Right back around to the bola amphiphiles, G. Nicholson said these were phospholipids, got that much out of his little talk on Stan Monteith.............
And he knows all about those little immunoglobins, now. doesn't he? I do have compassion for those who try to help, for sure, even tho...... well that is another matter...............Credit where credit is due, I say.
Skyship
|
|
|
Post by skyship on Jul 15, 2011 2:40:03 GMT -5
So, it appears the first ones made for use in the cytoskeletal rearrangement, had to do with the C3 botulinium, gee,,,, would that be the Weizman organism? Betcha.
Clostridium botulinium C3 welllllllllllhere it is in the market, must have made a killing of that Clostridium botulinum C3 Toxoid protein Full length C3 Toxoid purified from Clostridium botulinum type C.www.abcam.com/Clostridium-botulinum-C3-Toxoid-protein-ab63835.html================================ They just kept perfecting the process, till they had no more artifacts from the bolaamphiphiles. I knew this man was involved. I think he is from another planet. An inorganic chemist. Materials chemistryMaterials chemistry encompasses colloids, liquid crystals i norganic nanostructures for nanoplasmonics, template-directed synthesis of inorganic carbonate/phosphates and metallic architectures, protein-mediated biomimetic biomineralization and the development of a rational design protocol for engineering the morphology of self-assembling peptide nanofilaments. Professor Stephen Mann and Dr Adam Perriman reported the first example of a liquid protein (Angew. Chem. Int. Ed. 2009 48, 6242). Functionalising the surface of the iron storage protein ferritin with protonated amines provides an electrostatic binding site for negatively charged polymer surfactant, creating proteins that bristle with long hairs. This composite melts at 30°C to a liquid crystal and at 50°C, the liquid appears to act like an ordinary fluid. The “liquid protein” is more highly concentrated than a protein dissolved in water which offers the possibility of being able to administer higher doses of medically useful proteins. Alginate, a seaweed-derived biopolymer controls the growth of Y124 nanoparticles to produce the first ever single crystal high-temperature superconductor nanowires where the biopolymer directs the reaction and subsequent morphology of the superconductor.(Hall and Mann Adv. Mat. 2008, 20, 1782). image: YBa2Cu4O8 (Y124) nanowires templated by an alginate biopolymerwww.bristol.ac.uk/science/images/chemresimg1a.jpg So, if made the correct way, then they may be useful.or not............. ============== biomachine: "Biological chemistry Biological chemistry from the polyketides group (Simpson, Cox, Willis, Crosby, Crump) has established the programming mechanisms in tenellin synthase where a single gene cluster produces a library of compounds. In bacteria, the group have applied detailed physical and analytical methods to the dissociated actinorhodin polyketide synthase to show for the first time how these complex biomachines coordinate biosynthetic reactions (Nature,1999, 401, 502)." Tenellin: www.bristol.ac.uk/science/images/chemresimg4.gifNow, I am wondering if this is a method to reprogram the errors made, first time around. This could be the error> actinorhodin polyketide synthase Skyship
|
|
|
Post by skyship on Jul 15, 2011 18:24:08 GMT -5
The error was this: actinorhodin polyketide synthase Deadly Carcinogen Unraveled: The Molecular Origami of Fungal Polyketides Aflatoxin is an unavoidable food contaminant in grains and nuts produced in developing countries. Chronic ingestion of nuts and grains contaminated with aflatoxin-producing molds such as Aspergillus parasiticus leads to a high rate of liver cancer, and is a large problem in developing countries. Aflatoxins belong to a class of natural products called polyketides, which are biosynthesized in many bacteria and fungi (1,2). Polyketide natural products produced by bacteria and fungi are often characterized by the presence of multiple aromatic rings that are responsible for the activity of polyketides as antibiotic, anticancer, and toxic compounds (2). Polyketide ring formation by fungal PKSs results from regiospecific cyclizations of reactive poly-β-keto intermediates of specific length that is mediated by the product template (PT) domain (Fig. 1). The mechanism for aromatic ring formation, where a linear intermediate is transformed into a multicyclic product with high fidelity, has remained unclear. To reveal the cyclization mechanism, the Tsai lab at the University of California, Irvine, in collaboration with the Townsend lab at The Johns Hopkins University, solved the structure of the isolated PT domain of PksA to 1.8 Å using data from the SSRL beamline 9.1 and ALS beamline 8.2.2. The work was reported in the Oct 22 issue of Nature. ssrl.slac.stanford.edu/research/highlights_archive/fungal_pks.pdf The PksA megasynthase, containing six enzyme domains covalently linked together, catalyzes the iterative reactions that couple one hexanoyl group with 7 malonyl-CoAs to produce a 20-carbon linear poly β-keto intermediate (Fig. 1). At this point, if left unprotected, the highly reactive poly β-keto moieties would undergo random cyclization to produce dead-end products. Instead, the linear intermediate enters PT, where it is stabilized and transformed into a specific bicyclic intermediate with a highly specific cyclization pattern exclusively observed in fungi. How PT accomplishes this amazing feat of origami remains a mystery. Skyship
|
|
|
Post by kritters on Jul 15, 2011 22:45:32 GMT -5
Dear, awesome Sky,
No matter how they want to say it, fungus is the culprit.
What turns yeast into fungus in our bodies? One thing I have found out that is absent in that event is Biotin.
It's just that simple. Well, maybe not THAT simple, but it all boils down to
FUNGUS!
But, what is the role of fungus in the ecosystem? It's the terminator. When disease is present, Mr. Fungus is NATURALLY called into action.
But, what if the evil scientists already know that and use the fungus dna to UNNATURALLY call it into action?
Huh? Huh? yeah. What about that?
With so much respect and humility,
Kritts
|
|
|
Post by kritters on Jul 15, 2011 22:50:53 GMT -5
You know what, they may have another form, that is not recognized in America. And they may have the key. mmmmm The guy in the video, oh yes, he is getting the word out. I know he is looking at it very closely, on observant level, and that everyone has these. He found many people at that conference he was at that do not have Morgellons but they have the fibers. And some of them have messages on them, as shown by Skizit on her videos, too, the tape ones had letters on them etc, that lead back to labs that may have made them, or were part of the construction of them. Somehow they seemed to put their signatures on them. Makes you wonder if there is something bigger than all of this? doesn't it? Sometimes I get an eery feeling that there is massive info we do not even have a clue about, as Kammy said. Like a secret space program, or alien races who want to knock on our doors. Anyhow, on that video they talk of the forms found in ice. Lets see, that high up in the release of these foreign proteins, or viruses, or body parts, might be in frozen material, meaning it is all over the universe........ or .......is being sprayed from those UN operated planes, that are rearranging the landscape. I read way back where they bought some old I think they were c135's from the airforce. Wonder what they are doing with them? So, many avenues this Morgellons is going down. I think the ones who have the newer fibers, have no artifacts. We older folks, have the artifacts, and they are replicating because they are more organic, than inorganic, linking to hidden viruses as the mutators. or bacteriophages, when they realized they could use inorganic material for the Epigenetic approach..........er transhuman approach. Skyship The amphiphile/bolamphiphile in my studies say that these have less artifacts, however, the light strands are there, they are not what they called irritants, or aggravators, like The first ones were. They are there just for signaling, whereas us older folks, have the baculo/amyloid/cores, part of the actual chromosome system before its alteration. These parts can be early or late it seems, The later ones are more formed, less harmful, while the others can cause the old diseases, or newer ones because they cannot handle the changes. It seems we have been monitored for a long time. What do you think contact will be like? Was it done here, or from out there? Are we simply on the wrong planet? haha...... We did talk of that 47 gene once and there was a scientist interested in it, but we did not hear back from him. So, our PR man the Morgellon man there, is getting the word out. Kudos to him. I am wondering if some are saying this is psoriasis, and sure does not seem like it, except for the plaque, which to me is more like calcium desposits or amyloid. Will try to see if Mr. AJ found a connection to the chemtrails. mmmmmmm this is getting interesting though. Skyship So, wonder why some have issues with them and other dont? Sky, What do you think the spaceships brought back on the surface of their vehicle or what they have collected as samples to bring back to earth and as usual the, "uh oh....it was here just a minute ago". Call me agrobacterium, or space creature kantina, but don't call me late for dinner. Kritts
|
|
|
Post by lilsissy on Jul 16, 2011 0:06:40 GMT -5
OH WOW>>>>>>>>>>
It is also possible for paraproteins (usually whole immunoglobulins) to form polymers by aggregating with each other; this takes the name of macroglobulinemia and may lead to further complications. For example, certain macroglobulins tend to precipitate within blood vessel with cold, a phenomenon known as cryoglobulinemia. Others may make blood too viscous to flow smoothly (usually with IgM macroglobulins), a phenomenon known as Waldenström macroglobulinemia. [edit] Possible causes
end cut
cold allegy , like i have...i bet
fibro cold and stress are the enemy
Dad would hacj like hell from the cold ...about to the point of passing out but he had T.B. that went active in the end.
|
|
|
Post by skyship on Jul 16, 2011 4:11:45 GMT -5
Kritters, I keep pulling out membrane like fibers with pods on ends. Looks like fungus to me. A mycelia, which I do have cladosporium, yeast and a non sporulating one. So, that about covers that. I think as you say Krits, the yeast forms into the mycelia or fungal strands. The yeast has the spitzenkorper in it, especially the candida one. that would be the little spark ball. forms the forms of mycelia. so that would be how it goes from yeast to fungus. goes back to Gilberts report on the unclassified fungus/yeast stuff from way back. Oh thanks for compliment. Lil sis, I do wonder about the membrane protein has maybe having been from m. tuberculosis and the m leprae mixture, the para you talk of. Wouldn't put it past them to make us a bunch of lepers? www.ncbi.nlm.nih.gov/pmc/articles/PMC2427483/pdf/bullwho00216-0024.pdfparaproteins involved there. Skyship
|
|
|
Post by skyship on Jul 16, 2011 4:44:45 GMT -5
(1) Sera from lepromatous cases react more frequently, and with higher titres, than sera from tuberculoid or indeterminate cases. (2) Leprous sera show a broad reactivity with mycobacterial antigens, which can be prepared from cultivated acid-fast mycobacteria as well as from Myco. l prae found in leproma. Myco. lepraemurium s also able to react with leprous sera in complement- fixation tests. www.ncbi.nlm.nih.gov/pmc/articles/PMC2427483/pdf/bullwho00216-0024.pdfgee, could this have been around then? 1970. Probably. www.nejm.org/doi/full/10.1056/NEJM197005142822009Most places where Morgellons started as well: quizlet.com/2802357/microbio-week-6-flash-cards/some good info there. Our myco may be m leprae and m tuberculosis...... related to the HIV immunoglobin problem. Was that virus in the monkey m. leprae or m tuberculosis? Or did the labs know when they created aids that the membrane protein used in both HIV and Influenza was from m leprae and m tuberculosis? mmmmmmm Well, fungus and wax, what a combination: "Mycobacterium is a genus of Actinobacteria, given its own family, the Mycobacteriaceae. The genus includes pathogens known to cause serious diseases in mammals, including tuberculosis (Mycobacterium tuberculosis) and leprosy (Mycobacterium leprae).[1] The Latin prefix "myco—" means both fungus and wax; its use here reflects the "waxy" compounds that compose parts of the cell wall." en.wikipedia.org/wiki/MycobacteriumNotice the waxy part is in the cell wall? ?membrane protein, anyone? M protein So myco means both fungus and wax. oh oh.......the pectin .........amylopectin? ?? okay then............. so. leprosy, tb have nothing to do with amyloid? ???well this gets more interesting by the day.................. Skyship
|
|
|
Post by lilsissy on Jul 17, 2011 2:53:12 GMT -5
|
|
|
Post by skyship on Jul 17, 2011 9:04:28 GMT -5
the list is right there isn't it, Lil sis? Taking the first product:
OFD1: Oral facial digital syndrome 1 the x was activated and in manifesting carriers, it explodes. In this case it is : Chromosomal rearrangement:"Oral-facial-digital syndrome 1 protein is a protein that in humans is encoded by the OFD1 gene. Human chromosomal region Xp22.3-p21.3 comprises the area between the pseudoautosomal boundary and the Duchenne muscular dystrophy gene (MIM 300377). This region harbors several disease loci, including OFD1 (MIM 311200), CFNS (MIM 304110), DFN6 (MIM 300066), and SEDT (MIM 313400). It also contains a region of homology with both the short and the long arms of the Y chromosome and undergoes frequent chromosomal rearrangements".............. en.wikipedia.org/wiki/OFD1============================== Orofaciodigital syndrome 1 DiseasesDB 29898 MeSH D009958 Orofaciodigital syndrome 1 (OFD1), also called Papillon-Leage and Psaume syndrome,[1] is an X-linked congenital disorder characterized by malformations of the face, oral cavity, and digits with polycystic kidney disease and variable involvement of the central nervous system.Cause and Genetics Orofaciodigital syndrome type 1 is caused by mutations in the OFD1 gene. OFD1 localizes to both centrosomes and basal bodies within the human genetic cellular structure. This suggests that this syndrome may fall into a broad category of ciliary diseases. The ciliary organelles are present in many cellular types throughout the human body. The cilia defects adversely affect numerous critical developmental signaling pathways essential to cellular development.[2] Recent findings in genetic research have suggested that a large number of genetic disorders, both genetic syndromes and genetic diseases, that were not previously identified in the medical literature as related, may be, in fact, highly related in the genetypical root cause of the widely-varying, phenotypically-observed disorders. Thus, orofaciodigital syndrome is a ciliopathy. en.wikipedia.org/wiki/Orofaciodigital_syndrome_1================================= so, we are different in Morgellons depending on the genetic makeup and that determines which on that list we have. People accepting the products never had issues, is only lit up gammas light chain, they do not already have carrier status of trisomies, or manifesting carrier status of those diseases mentioned.
This is what we mean by variation.=============================== the list ========================== Check out the gene products, look at your health history, and disease, do you carry any diseases, you know of? And the epigenetic immortal gene is involved in Morgellons, either you intergrate it or accumulation or bundles happen. The fiber bundles, are protein bundles. or oligomers polysaccharides (succinate) Each of these products are made of many types of chemical reactions, and of mutations, and of polymers, artificial rna into dna and heavy/light chain kappa.============================= Table 2. Gene products identified by SEREX in MGUS patients Geneproduct/ Gene ID/ Gene chromosomal locus/ Cellular localization/ Molecular function/ Cellular processOFD1 8481 Xp22.2-p22.3 Basal body/centrosome, cytosol Unknown Ciliogenesis ZNF292 23036 6q15 Nucleus DNA binding Transcription regulation DNA-dependent AKAP11 11215 13q14.11 Centrosome, cytosol PKA binding, PP1-binding Protein-kinase cascade GPATCH4 54865 1q22 Intracellular Nucleic acid binding Unknown SON 6651 21q22.1-22.2; 21q22.11 Intracellular, nucleus Nucleic acid binding, protein binding Antiapoptosis FAM50A 9130 Xq28 Nucleus Unknown Spermatogenesis SSSCA1 10534 11q13.1 Unknown Protein binding Cell cycle, cell division, mitosis IFT57/HIPPI 55081 3q13.12 Golgi, cilium IFT particles DNA binding, protein binding Ciliogenesis, proapoptosis, transcription IRF2BP2 359948 1q42.3 Nucleus Corepressor of IRF-2BP2 Transcription regulation DNA-dependent PSMC1 5700 14q32.11 Cytosol, nucleus, proteasome complex ATP binding ATPase activity, nucleotide-protein binding Regulation of ubiquitin-protein ligase activity There are 10 of them, why so many variations in Morgellons, the digital products. Guess this is what we need to know, how they made the products.Notice it says encoded rather than coded, so means was part of the epigenetic process, and this was started way back, they stopped when eugenics was stopped, in its raw form. then started up again with the genome and other things, after 1957. the epigenetics, comes along and does second form, the third will be when they activate the strands. If they do not work, we with the above, will be very ill. Don't you think, lil sis? As some of us are now. It is not a disease for those who are not manifesting carriers of trisomies. The eugenics hit us first. Gave or parents the gene altering strands, We were genetically predisposed to this. MGUS.......strange name for this bunch isn't it? Skyship
|
|
|
Post by skyship on Jul 17, 2011 9:30:22 GMT -5
Lil sis, If Morgellons is only this one, lets look at it, that would be in addition to any other trisomies, some may have.IRF2BP2 359948 1q42.3 Nucleus Corepressor of IRF-2BP2 Transcription regulation DNA-dependentProduct number is: IRF2BP2 nucleus corepressor of IRF-2BP2, Lets look at IRF-2BP2 first, Entrez Gene summary for IRF2BP2: This gene encodes an interferon regulatory factor-2 (IRF2) binding protein that interacts with the C-terminal transcriptional repression domain of IRF2. Alternative splicing results in multiple transcript variants encoding distinct isoforms. (provided by RefSeq) UniProtKB/Swiss-Prot: I2BP2_HUMAN, Q7Z5L9 Function: Acts as a transcriptional repressor. Acts as a transcriptional corepressor in a IRF2-dependent manner. This repression is not mediated at least in part by histone deacetylase activities Regulatory elements: SABiosciences Regulatory transcription factor binding sites in the IRF2BP2 gene promoter: Pax-5 ATF-2 ISGF-3 c-Myb NF-kappaB NF-kappaB1 RelA AP-4 CREB Other transcription factors Search SABiosciences Chromatin IP Primers for IRF2BP2 Epigenetics: QIAGEN PyroMark CpG Assay predesigned Pyrosequencing DNA Methylation assays for IRF2BP2The epigenetic product was the pyrosequencing DNA METHYLATION assay........ CpG assay...... www.genecards.org/cgi-bin/carddisp.pl?gene=IRF2BP2================================ Pax-5 ATF-2 ISGF-3 c-Myb NF-kappaB NF-kappaB1 RelA AP-4 CREB Other transcription factorsBreaking it down: Pax-5? is B cell lineage. issue with pancreas. The PAX5 gene encodes the B-cell lineage specific activator protein (BSAP) that is expressed at early, but not late stages of B-cell differentiation. Its expression has also been detected in developing CNS and testis, therefore, PAX5 gene product may not only play an important role in B-cell differentiation, but also in neural development and spermatogenesis. en.wikipedia.org/wiki/PAX5====================== ATF-2 this is activation of the trisomy....... the mutation previous we only carried, and should not have gotten because of the inactivation status in the so-called junk dna. it should have stayed inactivated, but the heavy/light chain changes, making it triskelien, rather than y, like Y in the immunoglobins, those chains were altered to the triskelion.will get to triskelion. ATF-2: This gene encodes a transcription factor that is a member of the leucine zipper family of DNA binding proteins. This protein binds to the cAMP-responsive element (CRE), an octameric palindrome. The protein forms a homodimer or heterodimer with c-Jun and stimulates CRE-dependent transcription. The protein is also a histone acetyltransferase (HAT) that specifically acetylates histones H2B and H4 in vitro; thus it may represent a class of sequence-specific factors that activate transcription by direct effects on chromatin components. Additional transcript variants have been identified but their biological validity has not been determined. this means it acetylates: The acetyl group contains a methyl group single-bonded to a carbonyl. The carbonyl center of an acyl radical has one nonbonded electron with which it forms a chemical bond to the remainder R of the molecule.wikipedia. It is a chemical mutation. =============================== ISGF-3These are the ADD genes: Proteins of transcription factor ISGF-3: one gene encodes the 91-and 84-kDa ISGF-3 proteins that are activated by interferon alpha.The CMV: www.addgene.org/8704/====================================== cMyB: the proto oncogene, or cancerous gene Transcriptional activator; DNA-binding protein that specifically recognize the sequence 5'-YAAC[GT]G-3'. Plays an important role in the control of proliferation and differentiation of hematopoietic progenitor cells. Blood cell lineage.............. progenitor beginn cell. location is in nucleus of cell. www.uniprot.org/uniprot/P10242================================ NF-kap kappa? Known for 20 years? Recent evidence proving the molecular link between unchecked, chronic inflammation and cancer has implicated the transcription factor NF-kB as a key factor in both inhibiting apoptosis and promoting cell proliferation. Since its initial identification 20 years ago as a simple regulating factor in one small part of the immune response, NF-kB is proving to be the most protean of all transcription factors. It has been shown to function in most cell types as a key regulator of a number of inducible genes. www.amazon.com/Handbook-Transcription-Factor-NF-kappaB-Sankar/dp/0849327946======================== paB: well here is the b. subtilis, the walking dna. I knew it was here somewhere. An Apparent Bacillus subtilis Folic Acid Biosynthetic Operon Containing pab, an Amphibolic trpG Gene, a Third Gene Required for Synthesis of para-Aminobenzoic Acid, and the Dihydropteroate Synthase GeneSix of the seven tryptophan pathway genes in Bacillus subtilis are clustered in the trpEDCFBA operon (1, 5) found at 205 degrees on the B. subtilis map (36). These genes are coordinately regulated (13) by a recently revealed, unusual mechanism (22, 41), and the complete nucleotide sequence of the operon has been determined (12). The seventh trp gene is not linked to this operon; it participates in both folate and tryptophan syntheses and is located near the pab gene at 10 degrees on the map (36). This gene was originally desig- nated trpX (18), but here it will be called trpG to conform to the terminology used for similar amphibolic genes in Acine- tobacter calcoaceticus (40) and Pseudomonas acidovorans (4).TrpG participates in the first step in the synthesis of tryptophan, the conversion of chorismate and glutamine to anthranilate, glutamate, and pyruvate. www.ncbi.nlm.nih.gov/pmc/articles/PMC210846/pdf/jbacter00166-0613.pdf================================ amphibolic genes? ?? of acinetobacter calcoaceticus and Pseudomonas acidovorans............. OMG M. Darrah,,,,,,,,,,,, here is where the succinyl is! The term amphibolic is used to describe a biochemical pathway that involves both catabolism and anabolism. The citric acid cycle (The Krebs Cycle) is a good example. The first reaction of the cycle, in which oxaloacetate (a four carbon compound) condenses with acetate (a two carbon compound) to form citrate (a six carbon compound) is typically anabolic. The next few reactions, which are intramolecular rearrangements, produce isocitrate. The following two reactions are typically catabolic. -COO is lost in each step and succinate (a four carbon compound) is produced.succinate is produces? The second involves catobolism::::::::::::::::produces the succinate. this brings in the polymers, so the succinate produces the polymers polysaccharides.........Polymer sugars? ?? Catabolism (Greek kata = downward + ballein = to throw) is the set of pathways that break down molecules into smaller units and release energy.[1] In catabolism, large molecules such as polysaccharides, lipids, nucleic acids and proteins are broken down into smaller units such as monosaccharides, fatty acids, nucleotides, and amino acids, respectively. As molecules such as polysaccharides, proteins, and nucleic acids are made from long chains of these small monomer units (mono = one + mer = part), the large molecules are called polymers (poly = many).Cells use the monomers released from breaking down polymers to either construct new polymer molecules, or degrade the monomers further to simple waste products, releasing energy. Cellular wastes include lactic acid, acetic acid, carbon dioxide, ammonia, and urea. The creation of these wastes is usually an oxidation process involving a release of chemical free energy,........... en.wikipedia.org/wiki/Catabolism==================== HERE ARE THE MERS...........................think tau, amyloid oligomers which they are finding is causing Alzheimers and other amyloid diseases. Morgellons extension of Amyloid diseases. Light chain, triskelion. will explain the triskelion later...... What is this chemical free energy? ====================================== "...chemical free energy, some of which is lost as heat, but the rest of which is used to drive the synthesis of adenosine triphosphate"....... this adenosine triphosphate! "Bioenergetics refers to the transformation of energy that occurs within living organisms. In order to fuel the chemical mechanisms within cells, organisms require an input of energy. This energy is used to drive chemical reactions and help store and process information, which is essential in propagating life. Energy may be obtained from sunlight, in which the organisms are referred to as phototrophs, or it may be extracted from chemicals, in which the organisms are referred to as chemotrophs. Because energy may not be available at all times to fuel these life processes, organisms have adapted mechanisms to couple chemical reactions so that the endorgernic reaction can be occured to improve efficiency. The chemical reactions that performed by organisms make up its metabolism. Catabolic reactions involve the break down of chemical molecules, while anabolic reactions involve the synthesis of compounds. The Laws of ThermodynamicsThe energy processes in living organisms are defined by the basic laws of thermodynamics. The first law dictates that the total energy present in the universe always remains constant (Note: though the energy total is static, it often changes forms such as when an animal converts the chemical energy of food to mechanical energy as it moves). Meanwhile, the second law asserts that the total entropy present in the universe is ever increasing.".................Gibbs Free Energy Named after Josiah Willard Gibbs who developed the concept in 1878, the Gibbs free energy describes the overall favorability of a reaction to proceed. It is characterized by the following equation: ΔG = ΔH - TΔS where ΔG is the Gibbs free energy change, ΔH is the change in enthalpy (heat), T is temperature (measured in Kelvins), and ΔS is the change in entropy. A reaction, or process, will occur spontaneously if and only if ΔG < 0 for that reaction. If ΔG > 0 then that reaction must be coupled (see Energy Coupling) with a reaction which has ΔG < 0 such that the overall ΔG of the 2 reactions is <0. ATP hydrolysis is a commonly used reaction for such situations (see ATP). As the equation shows, a reaction is more favorable, the more ΔH < 0 (i.e. the more heat is given off by the reaction) and the more ΔS > 0 (i.e. the more disorder is increased) and the effect of entropy gained or lost is magnified by the temperature surrounding the reaction. ..."For instance, the hydrolysis of ATP is an exergonic reaction, meaning it gives off energy in the form of heat.".............. en.wikibooks.org/wiki/Structural_Biochemistry/Bioenergetics==================================== This energy in a strand, or light chain? ======================================= WE have 4 more to go all within the same 1q42......... If you can follow this we can see where the encoded light strands are being inserted: =============================== NF-kappaB1 RelA AP-4 CREB ===== These are the adhesion molecules: to the blood! Carnicom's bumps on the blood cells? ======= The role of NF-kappa B1 (p50/p105) gene expression in activation of human blood T-lymphocytes via CD2 and CD28 adhesion molecules......"t ranscription factor NF-kappa B participates in the regulation of both IL-2 and IL-2R alpha genes, as well as multiple cellular genes involved in T-cell proliferation. To evaluate the role of NF-kappa B in human peripheral blood T-lymphocytes, we previously analyzed the activation of NF-kappa B-related complexes in response to CD2+CD28 costimulation. We demonstrated a long-term induction of p50/p65 heterodimer, a putative p65/c-Rel heterodimer, and a constitutive nuclear expression of KBF1/p50 homodimers."............. cgd.aacrjournals.org/cgi/content/abstract/4/11/947==========================
so heterodimers and homodimers................. ===================== REL A: Avian? makes you think of avian influe? It is in the Influen A virion.............. Aliases & Descriptions v-rel reticuloendotheliosis viral oncogene homolog A (avian)1 2 MGC1317742 Nuclear factor of kappa light polypeptide gene enhancer in B-cells 31 2 3 transcription factor p652 NFKB32 3 5 v-rel avian reticuloendotheliosis viral oncogene homolog A (nuclear factor of kappa light polypeptide gene enhancer in B-cells 3 (p65))2 p651 2 v-rel reticuloendotheliosis viral oncogene homolog A, nuclear factor of kappa light polypeptide gene enhancer in B-cells 3, p652 Nuclear factor NF-kappa-B p65 subunit2 3 THESE DIMERS? Do others have these? I have them! D - Dimer test will tell you. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family www.genecards.org/cgi-bin/carddisp.pl?gene=RELA======================================== AP-4.............from our lovely friends at SCRIPPS AP4 encodes a c-MYC-inducible repressor of p21www.ncbi.nlm.nih.gov/pmc/articles/PMC2553359/switching from "life to death".............. Switching from life to death: the Miz-ing link between Myc and p53. Vousden KH. Source Beatson Institute for Cancer Research, Garscube Estate, Switchback Road, Bearsden, Galsgow G61 1BD, UK. k.vousden@beatson.gla.ac.uk Abstract Cells can respond to the activation of the tumor suppressor protein p53 by undergoing cell cycle arrest or apoptosis, and Myc has now been shown to help switch the response to apoptosis by repressing the expression of p21(CIP1), a cyclin-dependent kinase inhibitor with antiapoptotic activity. www.ncbi.nlm.nih.gov/pubmed/12450789============== MIZ-1: Expression of Myc in primary cells inhibits the accumulation of p15INK4b that is associated with cellular senescence; conversely, deletion of c-myc in an established cell line activates p15INK4b expression. Alleles of c-myc that are unable to bind to Miz-1 fail to inhibit accumulation of p15INK4b messenger RNA in primary cells and are, as a consequence, deficient in immortalization.This means senescence of cells over rides immortalization (live longer). accumulation of p15INK4b mRNAs............ in primary cells. www.ncbi.nlm.nih.gov/pubmed/11283613Either we accept the immortal cells or we have senescence( death of cells)................ Immortal cells integrate the 12 strands, we cannot. I wonder why? why do they choose senes instead of immortalization? accumulation of p15INK4b mRNAs. =========================== Well this might explain the gains and losses? ========== The Molecular Genetics and Tumor Pathogenesis of Meningiomas: Meningioma Progression Meningioma Progression While genetic analysis of losses on chromosome 22 has provided a foundation for understanding meningioma pathogenesis, the previously discussed genetic alterations constitute early events in meningioma development.[59,70,97] Benign meningiomas rarely have chromosomal aberrations beyond chromosome 22 losses. More complex karyotypes are associated with more aggressive meningioma behavior.[59] Malignant progression, thought to follow the theory of clonal evolution, is associated with a stepwise cumulative acquisition of chromosomal gains and losses, leading to more aggressive subclones with greater growth advantage.[63,123,132] Atypical and anaplastic meningiomas exhibit much more complex genetic changes than their benign counterparts, with losses on 1p, 10q, 14q, and less frequent losses on 6q and 18q. Higher grades are also associated with chromosomal gains on 1q, 9q, 12q, 15q, 17q, and 20q.[59,70] In addition to these genetic changes, anaplastic meningiomas exhibit more frequent losses on 6q, 10q, 14q, and 9p, with amplification on 17q23 (Fig. 1).[12,54,86,97,123] Epigenetic alterations, including increased CpG island hypermethylation, have also been associated with malignant meningioma progression.www.medscape.com/viewarticle/742064_3=========================== in the CpG island hypermethylation which is an epigenetic process.pretty much says it here: "Epigenetic alterations, including increased CpG island hypermethylation, have also been associated with malignant meningioma progression." Epigenetic alterations increased CpG island hypermethylation" CpG islands are characterized by CpG dinucleotide content of at least 60% of that which would be statistically expected (~4-6%), whereas the rest of the genome has much lower CpG frequency (~1%), a phenomenon called CG suppression. Unlike CpG sites in the coding region of a gene, in most instances, the CpG sites in the CpG islands of promoters are unmethylated if genes are expressed. This observation led to the speculation that methylation of CpG sites in the promoter of a gene may inhibit the expression of a gene. Methylation is central to imprinting alongside histone modifications.[5]"....... en.wikipedia.org/wiki/CpG_islandThese islands are what wrapped around the pancreas? Lil sis? malignant meningioma progressionTotally and epigenetic encoding process in extra cellular spaces around outside, inside etc, all dependent on signals............ Light chain signals............................... the 12 immortal genes? Is that what the Pleides want? How many have been transported already? We don't get to ascend? Was that the plan? Any way to communicate with those who have ascended? without the damn 12 strands? How do we hear them? Definite discrimination going on here! Skyship
|
|
|
Post by skyship on Jul 17, 2011 11:47:48 GMT -5
We have B cell lineage, our genotypes? or created phenotypes? The above post, explains the core to the 1q42............... Morgellons........... Please read through, and you can see what has happened. If you don't understand, lets talk! Lets review it all. that table tells the story in link Lil sis put up. If you have any trisomies from any of the other gene locations or mutations, you will have other symptoms, because of their activations in the junk dna, that is where these 12 light encoded strands are. It is in junk dna, where the signals, the extra secondary system was put in to monitor your very genes. Like a quantum computer in your extracellular spaces of your body. Keeping track of the Expression of your dna. A parallel system of light encoded genes, those added to take you to higher frequencies. Many cannot accept them, we have too many things in junk dna that were to help us and those have been substituted with these 12 strands in the junk dna, because that is where the dna can be read, reversed RNA, artificial rna is integrated in. Those are the acetylations, adding other genes, 21, 22, 23 aminos acids which are selenocysteine, pyrrolasine, and the unnatural benzoyl phenylalanine. methylation in the histones, all Epigenetics, selection, adaptation and extinction of certain lineages, especially the B lineages. May the power of the light that surpasses all evil darkness, shine brighter than any of these 12 strands, and those who become immortal, may the goodness of life that is left, leave something to desire, and may restlessness, and the pain we have felt be yours. We know what you have done! But, it is not our right to condemn you or the judge you, but, to lay this at your feet. The Higher power will take care of that. We wish you no hate, only pity. For that is the best we can do. kappa light polypeptide gene enhancer in B-cells p652 The signaling pathway: According to this there are now 14. kugi.kribb.re.kr/KUGI/Pathways/BioCarta/h_cd40Pathway/Skyship
|
|
|
Post by skyship on Jul 17, 2011 12:04:29 GMT -5
CD40 and CD40L Functions of CD40 and its ligand, gp39 (CD40L).
Division of Immunological and Infectious Diseases, TNO Prevention and Health (TNO-PG), Leiden, The Netherlands. . Defective expression of CD40L in humans leads to an inability to produce isotypes other than IgM (hyper IgM syndrome), and to an absence of germinal centers. More recent evidence indicates an expansion of the role of the CD40-CD40L axis in cellular interactions beyond antibody formation. Induced expression of CD40 on monocytes can lead to CD40L-activated monocyte effector mechanisms. In addition, CD40-CD40L interactions are crucially involved in development of autoimmune disease in a number of animal models. CD40-CD40L interactions also impact on growth regulation of certain carcinomas. Manipulation of CD40L has also been used to develop novel strategies for long-term antigen-specific tolerization of peripheral T cells. Finally, the CD40-CD40L axis is involved in thymic selection. Following is a comprehensive overview of CD40L-CD40 interactions in physiological and pathogenic cellular responses and a discussion of the therapeutic ramifications of these interactions. www.ncbi.nlm.nih.gov/pubmed/8809473================================ They knew, because this leads to arteriosclerosis as well......a lot of it there, plus amyloids.------------------ In X chromosome:::::::::::::::::: Defective expression of CD40 ligand on T cells causes "X-linked immunodeficiency with hyper-IgM (HIGM1)".Kroczek RA, Graf D, Brugnoni D, Giliani S, Korthüer U, Ugazio A, Senger G, Mages HW, Villa A, Notarangelo LD. Source Molecular Immunology, Robert Koch-Institute, Berlin, Germany. Abstract X-linked immunodeficiency with hyper-IgM (HIGM1) is a rare disorder, characterized by recurrent infections associated with very low or absent IgG and IgA, and normal to increased IgM serum levels. The disease has been earlier mapped to the q26-27 region of the X-chromosome. We have identified a novel molecule expressed on the surface of activated T cells, which was designated TRAP (Tumor necrosis factor Related Activation Protein), and could demonstrate that TRAP is a ligand for the CD40 receptor expressed on B cells. Our mapping of the TRAP gene to the Xq26.3-27.1 region suggested a causal relationship to HIGM1. Further work revealed that various mutations of the TRAP/CD40 ligand (CD40L) gene may lead to a defective expression of the TRAP/CD40L molecule on the T-cell surface in HIGM1 patients. A combination of structural and functional analyses finally demonstrated that the failure of TRAP/CD40L on T cells to interact with CD40 on B cells is responsible for the inefficient T-cell help for B cells observed in HIGM1. The observations made in HIGM1 allowed us to conclude that TRAP/CD40L is not required for IgM synthesis. In contrast, functional expression of TRAP is a prerequisite for effective immunoglobulin isotype switching and subsequent production of IgG, IgA and IgE by B cells in vivo. The interaction of TRAP/CD40L with CD40 thus provides a very critical link between the cellular and the humoral part of the immune system. The knowledge of TRAP/CD40L cDNA sequence, the availability of various reagents for the testing of expression and function of TRAP/CD40L, and our recent elucidation of the exon-intron structure of the TRAP/CD40L gene now provide all necessary tools for early diagnosis of affected patients and the detection of female carriers of HIGM1. The available information will also provide a basis for future attempts at gene therapy in this disease. www.ncbi.nlm.nih.gov/pubmed/7915248========================= HIGM1?Using this criteria, we found physicians in the following specialties who are likely to address 'higm1 syndrome' (Type 1 Hyper-IgM Immunodeficiency Syndrome) * Gasteroenterology * Allergy and Immunology * Hematology * Medical Genetics * Pediatric Gasteroenterology * Pediatric Hematology and Oncology * Pulmonary Medicine * Oncology * Pediatric Infectious Disease * Pediatric Nephrology * Pediatric Pulmonology * or Generalist Physicians search.apexmd.com/search2.aspx?q=higm1%20syndrome=================================== ================================ X-linked Hyper IgM (HIGM1) in an African kindred: the first report from South AfricaThe CD40L gene comprises 5 exons, 4 introns, and spans 12 kilobases. It encodes a type II transmembrane glycoprotein of 261 amino acids, which has a molecular mass of 39 kDa and is a member of the TNF superfamily. Domains of the protein include a short cytoplasmic tail, a transmembrane section and an extracellular region that shares homology with TNF-α. CD40L is mainly expressed by activated CD4+ T-cells [4,11,12] and is functional as a homotrimer. Other cells expressing CD40L include B cells, macrophages, monocytes, dendritic cells and endothelial cells. The interaction of CD40L on activated CD4 cells with CD40 on B-cells induces B-cell proliferation, immunoglobulin isotype switching, germinal centre formation and somatic hypermutation. Dysfunctional CD40 ligation thus prevents isotype switching from IgM, and results in the typical immunodeficiency [12,13]. Failure to isotype switch, as well as failure to activate Kuppfer cells and pulmonary macrophages increases the risk for Pneumocystis carinii and Cryptosporidial infection [7]. Autosomal forms of hyper-IgM syndrome are due to defects of B-cells, rather than T-cells [14]. The European CD40L defect database contains mutations scattered throughout the length of the gene. However, mutations are more common in the extracellularly located TNF-homology domain [15]. A variety of missense, nonsense, splice-site, deletion and insertion mutations have been reported [15,16]. In the present report we describe the characterisation of a novel deletion mutation in the first South African kindred with HIGM1. www.biomedcentral.com/1471-2431/3/12This was done with missense, nonsense, splice-site, deletion and insertion mutations............this makes Morgellons now a disease.................for those who cannot adapt to the mutations.
Those who intergrate the strands with no immune system issues, will intergrate these strands, these mutations of artificial, synthetic light strands. Skyship
|
|