NewEast Biosciences pioneered the research and development of the antibodies for GTPases and mutated Oncogene ten years ago. GTPases involve (1) signal transduction in response to activation of cell surface receptors, including transmembrane receptors such as those mediating taste, smell and vision, (2) protein biosynthesis at the ribosome, (3) regulation of cell differentiation, proliferation, division and movement, (4) translocation of proteins through membranes, (5) transport of vesicles within the cell, and vesicle-mediated secretion and uptake, through GTPase control of vesicle coat assembly. An oncogene is a gene that has the potential to cause cancer.
We offer three unique categories of antibodies, which (1) recognize only the active configuration of GTPase (not the inactive one), (2) mutated Oncogene (not mild type) and (3) have super affinity for cAMP and cGMP (no acetylation required). We have over one thousand peer reviewed articles cited our products.
$445.00
Cat.#: 28229 |
Product Name: Anti-CD5L(DMC441) IgG1 Chimeric Monoclonal Antibody |
Synonyms: AIM; API6; CT-2; hAIM; PRO229; SP-ALPHA; Spalpha |
Description: Anti-CD5L antibody(DMC441) IgG1 Chimeric Monoclonal Antibody |
Background: 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). |
Applications: Flow Cyt |
Recommended Dilutions: Flow Cyt 1:100 |
Host Species: Rabbit |
Isotype: Rabbit:Human Fc chimeric IgG1 |
Purification: Purified from cell culture supernatant by affinity chromatography |
Species Reactivity: Human CD5L |
Constituents: Lyophilized from sterile PBS, pH 7.4. 5 % – 8% trehalose is added as protectants before lyophilization. |
Storage & Shipping: Store at -20°C to -80°C for 12 months in lyophilized form. After reconstitution, if not intended for use within a month, aliquot and store at -80°C (Avoid repeated freezing and thawing). |
Figure 1. Flow cytometry analysis with Anti-CD5L (DMC441) on Expi293 cells transfected with human CD5L (Blue histogram) or Expi293 transfected with irrelevant protein (Red histogram). |