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Product Name | Recombinant Mouse CD5L (carrier-free) |
Description | CD5L was initially identified in a mouse macrophage cDNA library. It is a secreted protein and contains three scavenger receptor cysteine-rich domains (SRCR). It was called AIM, for apoptosis inhibitor expressed by macrophages. CD5L is considered the mouse homologue of human Spαand it shares 73% amino acid identity. In CD5L-deficient mice, the thymocytes are diminished and CD4/CD8 double-positive (DP) thymocytes are more susceptible to apoptosis induced by both dexamethasone and irradiation in vivo. Also, CD5L supports the survival of macrophages, T cells, and NKT cells against various apoptosis-inducing stimuli. CD5L displays a broad pathogen recognition spectrum and is involved in early response to microbial aggression. CD5L regulates lipid biosythesis and restrains Th17 cell pathogenicity. CD5L is mainly expressed in non-pathogenic Th17 cells and is down-regulated by IL-23. Loss of CD5L converts non-pathogenic Th17 cells into disease-inducing Th17 cells. CD5L decreases the level of polyunsaturated fatty acyls, affecting Th17-cell lipidome and the binding and activity of Rorγt. CDL5 is present at high level in blood (approximately 5 μg/mL in humans and 2 μg/mL in mice) where it associates with IgM pentamers, which protects CD5L from renal excretion and maintains high levels of circulating CD5L. Constitutive increase in circulating CD5L levels accelerated chronic inflammation, atherosclerosis, and autoantibody production; therefore, a physiological process must regulate blood CD5L levels. Thus, recent studies suggest that IgM-free CD5L is cleaved in blood and preferentially excreted into urine. |
Size | 100 µg |
Concentration | n/a |
Applications | BA |
Other Names | CD5 antigen-like, Apoptosis inhibitor expressed by macrophages (AIM), Apoptosis inhibitory 6 (Api6), SP-alpha, CT-2, Pdp 1/6 |
Gene, Accession, CAS # | Gene ID: 11801 |
Catalog # | 719306 |
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Order / More Info | Recombinant Mouse CD5L (carrier-free) from BIOLEGEND |
Product Specific References | n/a |
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