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% purity, < 1 EU/µg endotoxin level and suitable for SDS-PAGE, WB, MS.
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Application SDS-PAGE | Reactivity Reacts | Dilution info - | Notes - |
Application WB | Reactivity Reacts | Dilution info - | Notes - |
Application MS | Reactivity Reacts | Dilution info - | Notes - |
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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).
API6, UNQ203/PRO229, CD5L, CD5 antigen-like, Apoptosis inhibitor expressed by macrophages, CT-2, IgM-associated peptide, SP-alpha, hAIM
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% purity, < 1 EU/µg endotoxin level and suitable for SDS-PAGE, WB, MS.
Constituents: 0.61% Tris
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).
Not N-glycosylated (PubMed:23236605). Probably not O-glycosylated (PubMed:23236605).
Previously labelled as CD5L.
CD5L also known as CT-2 or CD5 antigen-like is a secreted glycoprotein with a molecular mass of approximately 50 kDa. This protein expresses mainly in liver and to a lesser extent in spleen lymph nodes and other immune-related tissues. The CD5L protein acts as a scavenger receptor cysteine-rich (SRCR) superfamily member which participates in pathogen recognition and clearance. Researchers often measure CD5L levels using CD5L ELISA kits providing quantitative analysis of this biomarker in various biological samples.
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.
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.
CD5L associates with atherosclerosis and systemic lupus erythematosus (SLE). Researchers link elevated CD5L levels with atherosclerosis due to its ability to drive macrophage transformation into foam cells linking it with cardiovascular diseases. In systemic lupus erythematosus CD5L interacts with protein serum amyloid A (SAA) exacerbating the inflammatory processes associated with autoimmune disorders. Understanding CD5L's role may provide insights for developing therapeutic strategies for these conditions.
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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
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