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MGI contains information about mouse genes, DNA segments, cytogenetic markers and QTLs. Each record may include. STSs, chromosomal. EC number (for enzymes), phenotypic classifications, human. Gene Ontology (GO) terms, MGI accession IDs and supporting references. Users can create graphical displays of genome features on the. Mouse Genome Browser. A variety of types of Genetic Mapping Data are available from marker detail pages, including data from genetic linkage crosses, cytogenetic localization, recombinant inbred and recombinant congenic strains, and radiation hybrid mapping. Complement receptor 1 - Wikipedia. CR1. Identifiers. Aliases. CR1, C3. BR, C4. BR, CD3. 5, KN, complement component 3b/4b receptor 1 (Knops blood group), complement C3b/C4b receptor 1 (Knops blood group)External IDs. OMIM: 1. 20. 62. 0Homolo. Gene: 5. 54. 74. Gene. Xeroderma pigmentosum, complementation group C, also known as XPC, is a protein which in humans is encoded by the XPC gene. XPC is involved in the recognition of. Complete information for DRD4 gene (Protein Coding), Dopamine Receptor D4, including: function, proteins, disorders, pathways, orthologs, and expression. The Saccharomyces Genome Database (SGD) provides comprehensive integrated biological information for the budding yeast Saccharomyces cerevisiae. Cards: CR1. Orthologs. Species. Human. Mouse. Entrez. Ensembl. Uni. Prot. Ref. Seq (m. RNA)Ref. Seq (protein)Location (UCSC)Chr 1: 2. Mbn/a. Pub. Med search. The gene encodes a monomeric single- pass type I membrane glycoprotein found on erythrocytes, leukocytes, glomerular podocytes, hyalocytes, and splenic follicular dendritic cells. The Knops blood group system is a system of antigens located on this protein. The protein mediates cellular binding to particles and immune complexes that have activated complement. Decreases in expression of this protein and/or mutations in its gene have been associated with gallbladder carcinomas, mesangiocapillary glomerulonephritis, systemic lupus erythematosus and sarcoidosis. Mutations in this gene have also been associated with a reduction in Plasmodium falciparum rosetting, conferring protection against severe malaria. Alternate allele- specific splice variants, encoding different isoforms, have been characterized. Additional allele specific isoforms, including a secreted form, have been described but have not been fully characterized. It has been shown that CR1 can act as a negative regulator of the complement cascade, mediate immune adherence and phagocytosis and inhibit both the classic and alternative pathways. The number of CR1 molecules decreases with aging of erythrocytes in normal individuals and is also decreased in pathological conditions such as systemic lupus erythematosus (SLE), HIV infection, some haemolytic anaemia s and other conditions featuring immune complexes. In 5’- 3’ order the genes in this region are: membrane cofactor protein - CR1- complement receptor type 2 - decay- accelerating factor - C4- binding protein. Factor H, another immunoregulatory protein, also maps to this location. Da; CR2, ca. 1. 45 k. Da) via alternative m. RNA splicing. The murine Cr. CR1 and CR2, respectively. A transcript with an open reading frame of 4,2. CR1; this is predicted to be a protein of 1,4. SCR) of ca. 6. 0 amino acids each, plus transmembrane and cytoplasmic regions. Isoform CR2 (1,0. SCR1- 6. CR1 and CR2 on murine B cells form complexes with a co- accessory activation complex containing CD1. CD8. 1, and the fragilis/Ifitm (murine equivalents of LEU1. CR1 can bind to C4b and C3b complexes, whereas CR2 (murine and human) binds to C3dg- bound complexes. CR1, a surface protein produced primarily by follicular dendritic cells, appears to be critical for generation of appropriately activated B cells of the germinal centre and for mature antibody responses to bacterial infection. Large insertions and deletions have given rise to four structurally variant genes and some alleles may extend up to 1. The transcription start site has been mapped to 1. ATG and there is another possible start site 2. The promoter region lacks a distinct TATA box sequence. The gene is expressed principally on erythrocytes, monocytes, neutrophils and B cells but is also present on some T lymphocytes, mast cells and glomerular podocytes. Structure. The leader sequence and 5'- untranslated region are contained in one exon. The large extracellular domain of CR1, which has 2. N- glycosylation sites, can be divided into 3. SCRs) (also known as complement control protein repeats (CCPs) or sushi domains), each having 6. The sequence homology between SCRs ranges between 6. The transmembrane region is encoded by 2 exons and the cytoplasmic domain and the 3'- untranslated regions are coded for by two separate exons. The 3. 0 or so SCRs are further grouped into four longer regions termed long homologous repeats (LHRs) each encoding approximately 4. Da of protein and designated LHR- A, - B, - C, and - D. The first three have seven SCRs while LHR- D has 9 or more. Each LHR is composed of 8 exons and within an LHR, SCR 1, 5, and 7 are each encoded by a single exon, SCR 2 and 6 are each encoded by 2 exons, and a single exon codes for SCR 3 and 4. The LHR seem to have arisen as a result of unequal crossing over and the event that gave rise to LHR- B seems to have occurred within the fourth exon of either LHR- A or –C. To date the atomic structure have been solved for SCRs 1. Alleles. These short CR1 forms, some of which are glycosylphosphatidylinositol (GPI) anchored, are expressed on erythrocytes and the 2. Da CR1 form is expressed on monocytes. The gene including the repeats is highly conserved in primates possibly because of the ability of the repeats to bind complement. LHR- A binds preferentially to the complement component C4b: LHR- B and LHR- C bind to C3b and also, albeit with a lower affinity, to C4b. Curiously the human CR1 gene appears to have an unusual protein conformation but the significance of this finding is not clear. The mean number of complement receptor 1 (CR1) molecules on erythrocytes in normal individuals lies within the range of 1. Two codominantalleles exist - one controlling high and the other low expression. Homozygotes differ by a factor of 1. These two alleles appear to have originated before the divergence of the European and African populations. Rosetting. This 'stickiness', known as rosetting, is believed to be a strategy used by the parasite to remain sequestered in the microvasculature to avoid destruction in the spleen and liver. Erythrocyte rosetting causes obstruction of the blood flow in microcapillaries. There is a direct interaction between Pf. EMP1 and a functional site of complement receptor type 1 on uninfected erythrocytes. Racial differences exist in the frequency of these antigens: 9. American Caucasians and Africans respectively are positive for Mc. C(a). 3. 6% of a Mali population were Kn(a) and 1. Helgeson) phenotype compared with only 1% in the American population. The frequencies of Mc. C (b) and Sl (2) are higher in Africans compared with Europeans and while the frequency of Mc. C (b) was similar between Africans from the United States or Mali, the Sl (b) phenotype is significantly more common in Mali - 3. In Gambia the Sl (2)/Mc. C(b) phenotype appears to have been positively selected - presumably due to malaria. Papua New Guineans have the Helgesonphenotype and case control studies suggest this phenotype has a protective effect against severe malaria. References. 1. 73 (5): 1. PMC 2. 11. 88. 66 . PMID 1. 70. 88. 09. Molecular Immunology. PMID 1. 90. 04. 49. PMID 1. 97. 34. 90. Lay summary – TIME Magazine (2. Advances in experimental medicine and biology. PMID 2. 34. 02. 01. UNITED STATES. 1. PMC 3. 36. 64. 32 . PMID 1. 87. 13. 96. PMC 3. 70. 74. 06 . PMID 2. 37. 33. 87. Further reading. 4. PMID 2. 55. 11. 47. Wong WW, Farrell SA (1. Loss of a C3b binding site may be associated with altered function. PMID 1. 67. 09. 49. Tuveson DA, Ahearn JM, Matsumoto AK, Fearon DT (1. PMC 2. 11. 88. 40 . PMID 1. 70. 88. 08. Moulds JM, Nickells MW, Moulds JJ, Brown MC, Atkinson JP (1. PMC 2. 11. 88. 66 . PMID 1. 70. 88. 09. Rao N, Ferguson DJ, Lee SF, Telen MJ (1. PMID 1. 82. 74. 86. Hourcade D, Miesner DR, Bee C, Zeldes W, Atkinson JP (1. An example of concerted (horizontal) evolution within a gene. PMID 2. 29. 56. 27. Reynes M, Aubert JP, Cohen JH, Audouin J, Tricottet V, Diebold J, Kazatchkine MD (1. PMID 2. 41. 18. 09. Hinglais N, Kazatchkine MD, Mandet C, Appay MD, Bariety J (1. An immunohistochemical study. PMID 2. 47. 87. 58. Fearon DT, Klickstein LB, Wong WW, Wilson JG, Moore FD, Weis JJ, Weis JH, Jack RM, Carter RH, Ahearn JA (1. PMID 2. 53. 14. 19. Wong WW, Cahill JM, Rosen MD, Kennedy CA, Bonaccio ET, Morris MJ, Wilson JG, Klickstein LB, Fearon DT (1. Molecular basis of the structural and quantitative polymorphisms and identification of a new CR1- like allele. PMC 2. 18. 92. 69 . PMID 2. 56. 44. 14. Wong WW, Kennedy CA, Bonaccio ET, Wilson JG, Klickstein LB, Weis JH, Fearon DT (1. ![]() USB flash drive - Wikipedia. For the fictional propulsion system, see Jump drive. For the USB flash drive brand of the same name, see Lexar. USB flash drives are typically removable and rewritable, and physically much smaller than an optical disc. Most weigh less than 3. 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October 2017
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