Der Kaninchen Polyklonal anti-CD5L Antikörper (ABIN7227758) detektiert spezifisch CD5L in WB und ELISA.
Dieser Antikörper reagiert spezifisch mit Proben aus Human und Maus.
CD5L
Reaktivität: Human
FACS
Wirt: Human, Kaninchen
Chimeric
DMC441
unconjugated
Fc fragment
Recombinant Antibody
Applikationshinweise
Optimal working dilutions should be determined experimentally by the investigator. Suggested starting dilutions are as follows: WB 1:500-2000,ELISA 1:5000-20000
Beschränkungen
Nur für Forschungszwecke einsetzbar
Format
Liquid
Konzentration
1 mg/mL
Buffer
PBS, 50 % glycerol, 0.05 % Proclin 300, 0.05 %BSA
Konservierungsmittel
ProClin
Vorsichtsmaßnahmen
This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Lagerung
-20 °C
Informationen zur Lagerung
Stable for one year at -20°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquot to avoid repeated freezing and thawing.
Haltbarkeit
12 months
Target
CD5L
(CD5 Molecule-Like (CD5L))
Andere Bezeichnung
CD5L
Hintergrund
CD5 antigen-like, Apoptosis inhibitor expressed by macrophages, hAIM, CT-2, IgM-associated peptide, SP-alphaSecreted 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 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.