Purified anti-human CXCL10 IP-10 Antibody anti-CXCL10 - J036G3,BioLegend,524402

ELISA Capture: The purified J036G3 antibody is useful as the capture antibody in a sandwich ELISA assay, when used in conjunction with the biotinylated Poly5194 antibody (Cat. No. 519403) as the detecting antibody and recombinant human CXCL10 (IP-10) (Cat. No. 573509) as the standard.Note:For testing human CXCL10 (IP-10) in serum, plasma or supernatant, BioLegend's ELISA LEGEND MAX™ Kits (Cat. No. 439907 & 439908) are specially developed and recommended.

Host

Mouse

Reactivity

Human

Application

ELISA Capture - Quality testedWB - Verified

Platform ID

BAB307064476

BioLegend

Headquarters

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Contact

Tel: 1-858-455-9588
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Product Specifications
Scientific Background

Specifications

NamePurified anti-human CXCL10 IP-10 Antibody anti-CXCL10 - J036G3
Cat. No.524402
HostMouse
RRIDAB_2562398 (BioLegend Cat. No. 524401)AB_2562399 (BioLegend Cat. No. 524402)
IsotypeMouse IgG2a, κ
ReactivityHuman
ApplicationELISA Capture - Quality testedWB - Verified
ClonalityMonoclonal
Clone NumberJ036G3
Concentration0.5 mg/ml
TargetCXCL10
ImmunogenRecombinant human CXCL10
PurityThe antibody was purified by affinity chromatography.
FormulationPhosphate-buffered solution, pH 7.2, containing 0.09% sodium azide.
StorageThe antibody solution should be stored undiluted between 2°C and 8°C.
Regulatory StatusResearch Use Only

Scientific Background

CXCL10 is an ELR-negative chemokine structurally and functionally related to CXCL9 and CXCL11.  CXCL10, CXCL9, and CXCL11 are produced and secreted by monocytes, macrophages, fibroblasts, and epithelial cells upon stimulation with proinflammatory cytokines, especially IFNγ. CXCL10 chemoattracts CD4, CD8, and NK and NKT cells through the binding to its receptor CXCR3, which is shared with CXCL9 and CXCL11. In addition, CXCL10 inhibits neovascularization in tumors and in wound healingin vivo. Also, CXCL10 has anti-proliferative effects on endothelial cellsin vitro, and angiostatic and antitumor effectsin vivo. It has been suggested that the anti-proliferative effect of CXCL10 in endothelial cells is CXCR3-independent and that it is mediated through GAG interaction. CXCL10 also possesses antimicrobial activity againstE. coliandL. monocytogenes, and both the spore and bacillus forms ofB. anthracis. CXCL10 expression is strongly upregulated in many human inflammatory diseases, including rheumatoid arthritis, type I diabetes, multiple sclerosis, atherosclerosis, allograft rejection, and others.

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