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Human, Allograft Inflammatory Factor-1 (AIF-1), E.coli , Rec. Prot.
/Product Detail : RD172204100 Human, Allograft Inflammatory Factor-1 (AIF-1), E.coli , Rec. Prot.
Product name : Human, Allograft Inflammatory Factor-1 (AIF-1), E.coli , Rec. Prot.
Catalog number : RD172204100
Quantity: 0.1 mg
Supplier name : Biovend
Data sheet : Ask more or other datasheet now !
Allograft inflammatory factor 1 (AIF-1), is a 17kDa cytoplasm, calcium-binding protein that in humans is encoded by the AIF1 gene. This gene is induced by cytokines and interferon. Three transcript variants encoding different isoforms have been found for this gene. The AIF1 gene is conserved in chimpanzee, Rhesus monkey, dog, cow, mouse, and rat. Allograft inflammatory factor 1 plays a important role in vascular inflammation. AIF-1 is thought to be involved in negative regulation of growth of vascular smooth muscle cells, which contributes to the anti-inflammatory response to vessel wall trauma. AIF-1 also plays an important role in immune response and vasculopathy in allografts. AIF-1 was found in both cardiac allografts and hearts with other cardiac cellular diseases. In cardiac allografts, expression levels of AIF-1 in both cardiomyocytes and mononuclear cells directly correlated with the severity of cardiac cellular rejection. Thus, AIF-1 shows promise that it can be a potential biomarker for cardiac allograft rejection. AIF-1 is a protein whose expression in transplanted human hearts correlates with rejection and development of coronary artery vasculopathy (CAV). AIF-1 is crucial for the survival and pro-inflammatory activity of macrophages. Pro-inflammatory cytokines induced p-regulation of AIF-1 in macrophages. AIF-1 promote the activation and proliferation of T-lymphocytes and enhances lymphocyte migration. In human coronary artery vasculopathy, AIF-1 is expressed in T lymphocytes, and expression increases when T cells are activated. Increased numbers of AIF-1 immunoreactive macrophages/microglial cells were observed in focal human brain infarctions and human traumatic brain injury, in inflammatory lesions of a rat model of autoimmune disease and other disorders. Functional studies revealed that AIF-1 is secreted into the blood stream during experimental autoimmune neuritis. The results of several studies suggest that enhanced AIF-1 expression leads to augmented incorporation of degenerated LDL by macrophages and promotes development of atherosclerotic vasculopathy. AIF-1 is also expressed in tissues from patients with systemic sclerosis.
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