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  • GITRL Antibodies

Invitrogen

GITRL Monoclonal Antibody (109114)

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Datasheet
Protocols
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Datasheet
Protocols
Questions & Answers

Cite GITRL Monoclonal Antibody (109114)

GITRL Monoclonal Antibody (109114)

Product Details

MA5-23852

Applications
Tested Dilution
Publications

Flow Cytometry (Flow)

2.5 µg per million cells
-

ELISA (ELISA)

0.5-2 µg/mL (Detection), 2-8 µg/mL (Capture)
-

Neutralization (Neu)

Assay-Dependent
-
Product Specifications

Species Reactivity

Human

Host/Isotype

Mouse / IgG1

Class

Monoclonal

Type

Antibody

Clone

109114

Immunogen

Sf 21-derived recombinant human GITR Ligand/TNFSF18Glu52-Ser177
View immunogen

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Lyophilized

Concentration

0.5 mg/mL

Purification

Protein A/G

Storage buffer

PBS with 5% trehalose

Contains

No Preservative

Storage conditions

-20°C, Avoid Freeze/Thaw Cycles

Shipping conditions

Ambient (domestic); Wet ice (international)

RRID

AB_2576516

Product Specific Information

In sandwich ELISAs, no cross-reactivity or interference with recombinant human (rh) APRIL, rhLIGHT, rhTNF-alpha, or rhVEGI is observed.

Reconstitute at 0.5 mg/mL in sterile PBS.

Endoxin level is <0.10 EU per 1 µg of the antibody by the LAL method.

Target Information

The tumor necrosis factor (TNF) and TNF receptor (TNFR) gene superfamilies regulate numerous biological functions including cell proliferation, differentiation, and survival through regulating the activation of the transcription factor NF-kappa-B and various mitogen-activated protein kinases. The glucocorticoid-induced tumor necrosis factor receptor (GITR) is an emerging member of this family that is expressed on CD4+ CD25+ regulatory T cells and appears to have crucial immune regulation functions. Its ligand GITRL is expressed in endothelial and antigen-presenting cells and can activate NF-kappa-B, induce both pro- and anti-apoptotic effects, inhibit the suppressive activity of regulatory T cells, and co-stimulate responder T cells through GITR. Dominant negative forms of NIK and TRAF2 expressed in transfected 293 cells substantially inhibited NF-kappa-B activation, suggesting that the GITRL-GITR pathway involves both NIK and TRAF2.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.

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Bioinformatics

Protein Aliases: Activation-inducible TNF-related ligand; AITR ligand; AITRL; GITR ligand; GITRLigand; Glucocorticoid-induced TNF-related ligand; glucocorticoid-induced TNFR-related protein ligand; hGITRL; RP1-15D23.1; TNF superfamily member 18; tumor necrosis factor (ligand) superfamily member 18; tumor necrosis factor (ligand) superfamily, member 18; tumor necrosis factor ligand 2A; Tumor necrosis factor ligand superfamily member 18

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Gene Aliases: AITRL; GITRL; hGITRL; TL6; TNFSF18; TNLG2A; UNQ149/PRO175

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UniProt ID: (Human) Q9UNG2

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Entrez Gene ID: (Human) 8995

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Function(s)
receptor binding cytokine activity tumor necrosis factor receptor superfamily binding
Process(es)
adaptive immune response T cell proliferation involved in immune response positive regulation of leukocyte migration signal transduction cell-cell signaling positive regulation of macrophage chemotaxis tumor necrosis factor-mediated signaling pathway regulation of T cell proliferation positive regulation of tyrosine phosphorylation of Stat1 protein negative regulation of apoptotic process positive regulation of cell adhesion positive regulation of inflammatory response positive regulation of NF-kappaB transcription factor activity positive regulation of monocyte chemotaxis positive regulation of protein homodimerization activity negative regulation of T-helper 17 cell lineage commitment regulation of dendritic cell chemotaxis
It has to be done as per old AB suggested Products section.
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Performance Guarantee

If an Invitrogen™ antibody doesn't perform as described on our website or datasheet,we'll replace the product at no cost to you, or provide you with a credit for a future purchase.*

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