AIM (CD5L) (NM_005894) Human Recombinant Protein

Specifications

Product Data
Species	Human
Expression cDNA Clone or AA Sequence	Protein Sequence (showhide) Ser20-Gly347
Tag	C-His
Predicted MW	37.1 kDa
Concentration	lot specific
Purity	>95% as determined by SDS-PAGE and Coomassie blue staining
Buffer	Lyophilized from a 0.2 um filtered solution of 20mM PB, 150mM NaCl, pH 7.2.
Storage	Lyophilized protein should be stored at < -20°C, though stable at room temperature for 3 weeks. Reconstituted protein solution can be stored at 4-7°C for 2-7 days. Aliquots of reconstituted samples are stable at < -20°C for 3 months.
Stability	Stable for at least 6 months from date of receipt under proper storage and handling conditions.
Endotoxin	< 0.1 EU per µg protein as determined by LAL test
Reference Data
RefSeq
Locus ID	922
UniProt ID	O43866
Cytogenetics	1q23.1
Synonyms	AIM; API6; CT-2; hAIM; PRO229; SP-ALPHA; Spalpha
Summary	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).[UniProtKB/Swiss-Prot Function]
Protein Families	Druggable Genome, Secreted Protein

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