Recombinant Human CD5L/CT-2 protein
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Recombinant Human CD5L/CT-2 protein is a Human Full Length protein, in the 20 to 347 aa range, expressed in Escherichia coli, with >95%, < 1 EU/µg endotoxin level, suitable for SDS-PAGE, WB, Mass Spec.
View Alternative Names
API6, UNQ203/PRO229, CD5L, CD5 antigen-like, Apoptosis inhibitor expressed by macrophages, CT-2, IgM-associated peptide, SP-alpha, hAIM
- SDS-PAGE
Supplier Data
SDS-PAGE - Recombinant Human CD5L/CT-2 protein (AB184604)
14% SDS-PAGE analysis of ab184604.
Lane 1 : Reduced and boiled CD5L/CT-2, 2.5 μg/lane
Lane 2 : Non-reduced and non-boiled CD5L/CT-2, 2.5 μg/lane
Reactivity data
Product details
Sequence info
Properties and storage information
Shipped at conditions
Appropriate short-term storage conditions
Appropriate long-term storage conditions
Storage information
Supplementary information
This supplementary information is collated from multiple sources and compiled automatically.
Biological function summary
CD5L influences several immune processes modulating macrophage function and lipid metabolism. It plays a role within a complex system transforming macrophages into an anti-inflammatory phenotype. This helps the clearance of apoptotic cells and prevents tissue damage during inflammation. CD5L also impacts cholesterol homeostasis contributing to lipid clearance and influencing foam cell formation which serves a significant role in atherosclerosis development.
Pathways
This protein integrates into the lipid metabolism pathway and the immune regulation pathway. Within the lipid metabolism pathway interaction with proteins such as apolipoprotein AI demonstrates its role in controlling cholesterol and triglyceride levels. In the immune regulation pathway CD5L collaborates with other immune-related proteins including CD36 and TLR2 to regulate immune response and inflammation affecting macrophage activation and phagocytosis.
Specifications
Form
Lyophilized
General info
Function
Secreted protein that acts as a key regulator of lipid synthesis : mainly expressed by macrophages in lymphoid and inflamed tissues and regulates mechanisms in inflammatory responses, such as infection or atherosclerosis. Able to inhibit lipid droplet size in adipocytes. Following incorporation into mature adipocytes via CD36-mediated endocytosis, associates with cytosolic FASN, inhibiting fatty acid synthase activity and leading to lipolysis, the degradation of triacylglycerols into glycerol and free fatty acids (FFA). CD5L-induced lipolysis occurs with progression of obesity : participates in obesity-associated inflammation following recruitment of inflammatory macrophages into adipose tissues, a cause of insulin resistance and obesity-related metabolic disease. Regulation of intracellular lipids mediated by CD5L has a direct effect on transcription regulation mediated by nuclear receptors ROR-gamma (RORC). Acts as a key regulator of metabolic switch in T-helper Th17 cells. Regulates the expression of pro-inflammatory genes in Th17 cells by altering the lipid content and limiting synthesis of cholesterol ligand of RORC, the master transcription factor of Th17-cell differentiation. CD5L is mainly present in non-pathogenic Th17 cells, where it decreases the content of polyunsaturated fatty acyls (PUFA), affecting two metabolic proteins MSMO1 and CYP51A1, which synthesize ligands of RORC, limiting RORC activity and expression of pro-inflammatory genes. Participates in obesity-associated autoimmunity via its association with IgM, interfering with the binding of IgM to Fcalpha/mu receptor and enhancing the development of long-lived plasma cells that produce high-affinity IgG autoantibodies (By similarity). Also acts as an inhibitor of apoptosis in macrophages : promotes macrophage survival from the apoptotic effects of oxidized lipids in case of atherosclerosis (PubMed : 24295828). Involved in early response to microbial infection against various pathogens by acting as a pattern recognition receptor and by promoting autophagy (PubMed : 16030018, PubMed : 24223991, PubMed : 24583716, PubMed : 25713983).
Post-translational modifications
Not N-glycosylated (PubMed:23236605). Probably not O-glycosylated (PubMed:23236605).
Target data
Complementary Products
Product promise
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