Mouse CD5L protein (Recombinant) (C-His) (STJP013772)

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STJP013772-100
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Short Description :Recombinant-Mouse CD5L-C-His protein was developed from mammalian cells and has a target region of C-His. For use in research applications.
Applications:ELISA/WB
Host:Mammalian Cells
Note:STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Conjugation:Unconjugated
Dilution Range:Reconstitute in sterile water for a stock solution.
Formulation:Lyophilized from a 0.22 Mu m filtered solution in PBS, pH 7.4.
Storage Instruction:Use a manual defrost freezer and avoid repeated freeze thaw cycles. Store at 2 to 8°C for one week. Store at-20 to-80°C for twelve months from the date of receipt.
Endotoxin:< 1 EU/µg as determined by LAL test.
Gene Symbol:Cd5l
Gene ID:11801
Uniprot ID:CD5L_MOUSE
Immunogen:Mus musculus (Mouse)
Immunogen Region:Glu22-VaL352
Post Translational Modifications N-glycosylated. N-glycan at Asn-99 possesses only alpha2,6-sialylated terminals, while Asn-229 possesses both alpha2,6-sialylated and non-sialylated terminals. N-glycosylation increases secretion.
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. Also acts as an inhibitor of apoptosis in macrophages: promotes macrophage survival from the apoptotic effects of oxidized lipids in case of atherosclerosis. Involved in early response to microbial infection against various pathogens by acting as a pattern recognition receptor and by promoting autophagy.
Protein Name Cd5 Antigen-Like
Apoptosis Inhibitor Expressed By Macrophages
Maim
Apoptosis Inhibitory 6
Sp-Alpha
Database Links
Cellular Localisation Secreted
Cytoplasm
Secreted By Macrophages And Circulates In The Blood
Transported In The Cytoplasm Via Cd36-Mediated Endocytosis
Alternative Protein Names Cd5 Antigen-Like protein
Apoptosis Inhibitor Expressed By Macrophages protein
Maim protein
Apoptosis Inhibitory 6 protein
Sp-Alpha protein
Cd5l protein
Aim protein
Api6 protein

Information sourced from Uniprot.org