ELISA/assay

Human CD5L/CT-2 PicoKine® Quick ELISA Kit

FEK1413

96 wells/kit, with removable strips.

Human CD5L/CT-2 PicoKine® Quick ELISA Kit

96 wells/kit, with removable strips.

Human CD5L / CT 2 PicoKine® Quick ELISA Kit (90 minutes, 96 Tests). Quantitate Human CD5L in cell culture supernatants, cell lysates, serum and plasma (heparin, EDTA). Sensitivity: 10pg/ml.

Human

ELISA

CD5L

O43866

Expression system for standard: NS0; Immunogen sequence: S20-G347

There is no detectable cross-reactivity with other relevant proteins.

156 pg/ml - 10,000 pg/ml

<10 pg/ml

cell culture supernatants, cell lysates, serum and plasma (heparin, EDTA)

polyclonal antibody from goat, polyclonal antibody from goat

Store at 4°C for 6 months, at -20°C for 12 months. Avoid multiple freeze-thaw cycles (Ships with gel ice, can store for up to 3 days in room temperature. Freeze upon receiving.)

CD5 antigen-like

CD5 antigen-like;Apoptosis inhibitor expressed by macrophages ;hAIM ;CT-2 ;IgM-associated peptide ;SP-alpha ;CD5L;API6;UNQ203/PRO229 ;

CD5 antigen-like

38088 MW

Secreted protein that acts as a key regulator of lipid synthesis: mainly expressed by macrophages in lymphoid and inflammed 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 to 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).

Secreted . Cytoplasm . Secreted by macrophages and circulates in the blood (PubMed:24223991, PubMed:24804991). Transported in the cytoplasm via CD36-mediated endocytosis (By similarity).

Expressed in spleen, lymph node, thymus, bone marrow, and fetal liver, but not in non-lymphoid tissues.

Contains 3 SRCR domains.

CD5 antigen-like, also known as Sp alpha and AIM, is a protein that in humans is encoded by the CD5L gene. It is mapped to 1q21-q23 by fluorescence in situ hybridization. It is found that Aim expression is induced in mouse macrophages in response to loading with highly oxidized low density lipoprotein (oxLDL), and that Aim is expressed in foam cells within atherosclerotic lesions. Both the expression of Aim in lesions and its induction by oxLDL require Lxr /Rxr heterodimers. Aim-null macrophages are highly susceptible to oxLDL-induced apoptosis in vitro and undergo accelerated apoptosis in atherosclerotic lesions in vivo. Double knockout of Aim and Ldlr reduce atherosclerotic lesions. Therefore, it is concluded that AIM expression protects macrophages from apoptosis within atherosclerotic lesions, promoting early lesion development.