The integrin αM (ITGAM), is a protein subunit to form a (αMβ2) hetero molecule known as (CR3) macrophage antigen -1 complement receptor 3 or (MAC-1) dimer integrin αMβ2. ITGAM also known cluster differentiation molecule 11B and CR3A as (the CD11b). In the circuit of the second, belongs to the integrin (white blood cells) or sub-β2 integrin Therefore αMβ2 If it is αMβ2β2 integrin subunit common called CD18. αMβ2 is expressed on the surface of leukocytes number involved in the innate immune system, including natural killer cells monocytes, granulocytes, and macrophages. By adjusting the adhesion and migration of leukocytes, which have been implicated, such as activation of cellular mediators of inflammation, immune phagocytosis Such cell-mediated cytotoxicity, and chemotaxis, several processes directly below. Because of it, because of its ability to bind to and inactivate complement components. 3b (and iC3b), and are involved in the complement system. ITGAM of integrin αMβ2 (alpha) subunit is involved in creating the growth and adhesion of cells directly, but will not be able to mediate cell migration β2 (CD18) subunit does not exist. In genome-wide association studies, odds ratio of 1.65 for the T allele of rs9888739 and lupus single nucleotide polymorphism in ITGAM, had a strong association with the most systemic lupus erythematosus.
Between (also called complement receptor type 3 and MAC-1,, and also CD11b) M and integrin gene that ITGAM and disease, encoding clearly by new genetic analysis is probably the strongest group. And additional ligands contains a .17,18 (ICAM-2 and ICAM-1) 2 and intercellular adhesion molecule 1), fibrinogen, platelet 1bα glycoprotein, lipoprotein (but associated with SLE in the most strongly SNP specific ITGAM within its range, studies1, new 2,4 Three different, and genetic variants, the authors of each study, giving a change of amino acids having or both influence, to the binding function It was concluded that can be. Two people will provide support for the strongest association between the non-synonymous SNP in SLE and ITGAM (from SLEGEN by 4 eggplant et al.) Study of these two, to generate a combined maximum odds ratio of 1.65 and P = 2.02 × 10-26 for the association between alleles of T is combined analysis of independent samples of 7380, but 9073 you have tested and others lupus.2 eggplant and rs9888739 to share one-third of samples from control subjects and case subjects. After that, I set as rs1143679 SNP candidate causal ITGAM SLE, in patients who are African and Europe. Change, which can be changed amino acid change from arginine, histidine at position 77, a three-dimensional structure of the α1 domain of the protein, this variant, encoding the area of responsibility of ICAM-1.
Including atherosclerosis premature and wire-loop lesion “onionskinning” spleen artery, retinopathy, livedo reticularis, glomerular capillary – To identify the ITGAM as lupus related genes typical of many of the SLE (The latter is one of the most important causes of mortality associated with lupus and morbidity) which have to reignite interest in research Mechanisms and pathological features and clinical. The gene encoding the DN-ase and vascular disorders of the retina and (TREX1) wolf, provides additional reasons for the study of mechanisms of vascular disease in SLE 3 ‘exonuclease 1 to repair rare mutation studies 21, 22 recently.
This gene encodes a M integrin chain. Integrin is a heterodimer integral membrane protein consisting of one α and β chain from the chain. In order to form, in combination with beta-2 chain (ITGB2), and the I-domain containing integrin alpha Of inactivated-C3b leukocyte-specific integrin receptor of macrophages or -1 (“Mac -1”) 3 (“CR3”) receptor (and iC3b). In the phagocytosis of complement coated particles, Mβ2 integrin alpha is important for adherence to monocytes and neutrophils to endothelial stimulation as well. numerous variants of the code transcripts have been found for this gene different isoforms.
Monocytes, macrophages and granulocytes, and are involved in the interaction of adhesive various mediating the uptake of complement coated particles Alpha-M/beta-2 integrin. It is identical to the CR-3 receptor fragment iC3b and the third component of complement. Recognize RGD peptide probably because C3b. Fibrinogen, factor X, and alpha-M/beta-2 integrin is a receptor for ICAM1. It recognizes a peptide of P1 and P2 of fibrinogen γ chain
Febrile multiple organ failure often chronic feature of connective tissue, recurrent, and inflammatory, mainly involving skin, joints, kidneys, serous membrane: (SLEB6) systemic lupus erythematosus 6. It is considered that this is the cause unknown, and due to the lack of regulatory mechanisms of the immune system. The disease is characterized by elevated sedimentation rate systemic dysfunction, of red blood cells, by a wide range of formation of LE cells in the bone marrow and blood or. = Please note that may be associated with changes that affect the gene present in this post to disease susceptibility.