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Rabbit anti-Human CD5L Polyclonal Antibody

The antibody against CD5L was raised in rabbit using the Synthetic peptide of Human CD5L as the immunogen. This antibody exists as a non-conjugated isotype IgG, Antigen affinity purified. This antibody has been validated on ELISA, IHC.

ADC-26938A

The antibody against CD5L was raised in rabbit using the Synthetic peptide of Human CD5L as the immunogen. This antibody exists as a non-conjugated isotype IgG, Antigen affinity purified. This antibody has been validated on ELISA, IHC.

$299.00

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Specifications


Cat.No ADC-26938A ClonalityPolyclonal
Host SpeciesRabbitTarget NameCD5L
FormLiquidSpecies ReactivityHuman, Mouse
IsotypeIgGStorage Buffer0.05% NaN3, 40% Glycerol., pH7.4 PBS
Purification MethodAntigen affinity purifiedConjugateNon-conjugated
ApplicationELISA, IHCStorageUpon receipt

Immunogen Information


Immunogen DescriptionSynthetic peptide of Human CD5LTarget SpeciesHuman
Immunogen SequenceComplete sequences for the immunogen, target protein, and peptides are available upon request.Uniprot IDO43866
Background Information
  • Uniprot Id

    O43866

  • Target Species

    Human

  • Target Name

    CD5L

  • Target Full Name

    CD5 antigen-like

  • Target 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.

  • Target Subcellular Location

    Secreted. Cytoplasm.

  • Target Tissue Specificity

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

  • Target Synonyms

    AAC-11; AIM; API6; APOPTOSIS INHIBITOR 6; APOPTOSIS INHIBITOR OF MACROPHAGES; CD5 antigen like (scavenger receptor cysteine rich family); CD5 antigen-like; Cd5l; CD5L_HUMAN; CT 2; CT-2; Highly similar to ANTIGEN WC1.1 [Bos taurus]; IgM associated peptide; IgM-associated peptide; Pdp; PRO229; SCAVENGER RECEPTOR CYSTEINE-RICH FAMILY; SP ALPHA; SP-alpha; Spalpha

  • Target Background

    Predicted to enable serine-type endopeptidase activity. Predicted to be involved in zymogen activation. Predicted to act upstream of or within positive regulation of complement-dependent cytotoxicity and regulation of complement activation. Located in cell surface.

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