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TNFRSF18 antibody (FITC)
TNFRSF18
Reactivity: Mouse
FACS, WB, IHC
Host: Rat
Monoclonal
YGITR 765
FITC
Product Details anti-TNFRSF18 Antibody (FITC)
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Target
See all TNFRSF18 Antibodies
TNFRSF18
(Tumor Necrosis Factor Receptor Superfamily, Member 18 (TNFRSF18))
Reactivity
All reactivities for TNFRSF18 antibodies
Mouse
Host
All hosts for TNFRSF18 antibodies
Rat
Clonality
All clonalities for TNFRSF18 antibodies
Monoclonal
Conjugate
All conjugates for TNFRSF18 antibodies
This TNFRSF18 antibody is conjugated to FITC
Application
All applications for TNFRSF18 antibodies
Flow Cytometry (FACS), Western Blotting (WB), Immunohistochemistry (IHC)
Purification
The antibody was purified by affinity chromatography, and conjugated with FITC under optimal conditions. The solution is free of unconjugated FITC.
Clone
YGITR 765
Isotype
IgG2b kappa
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Alternatives
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Application Details
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Application Notes
Optimal working dilution should be determined by the investigator.
Restrictions
For Research Use only
Handling
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Concentration
0.5 mg/mL
Buffer
Phosphate-buffered solution, pH 7.2, containing 0.09 % sodium azide.
Preservative
Sodium azide
Precaution of Use
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Handling Advice
Protect from prolonged exposure to light. Do not freeze.
Storage
4 °C
Storage Comment
The antibody solution should be stored undiluted between 2°C and 8°C.
Target Details for TNFRSF18
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Target
TNFRSF18
(Tumor Necrosis Factor Receptor Superfamily, Member 18 (TNFRSF18))
Alternative Name
CD357 (TNFRSF18 Products )
Synonyms
GITR antibody, TNFRSF18 antibody, AITR antibody, Gitr antibody, CD357 antibody, GITR-D antibody, TNF receptor superfamily member 18 antibody, tumor necrosis factor receptor superfamily, member 18 antibody, TNFRSF18 antibody, Tnfrsf18 antibody
Background
GITR, Glucocorticoid-induced TNFR-related gene, is a member of the TNF receptor superfamily, also known as TNFRSF18, and AITR (in humans). It is expressed at low levels on resting T lymphocytes and at high levels on CD4+ CD25+ T regulatory (Treg) cells. The expression of GITR on T cells can be upregulated upon activation. Interaction of GITR with its ligand (GITRL) has been demonstrated to augment T cell activation, proliferation, cytokine production, as well as MAPKs and NF-κB activation, and abrogate the inhibitory functions of CD4+CD25+ Treg cells. In vivo activation GITR causes development of autoimmune diseases and restores the suppressed immune responses.
Pathways
Cancer Immune Checkpoints
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