Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

Invitrogen™ GITRL Polyclonal Antibody, Biotin, PeproTech®, Invitrogen™

Rabbit Polyclonal Antibody

Supplier:  Invitrogen™ 500P244BT500UG

Encompass_Preferred

 View more versions of this product

Catalog No. 50-271-8576


Only null left
Add to Cart

Description

Description

AA Sequence of recombinant protein: METAKEPCMA KFGPLPSKWQ MASSEPPCVN KVSDWKLEIL QNGLYLIYGQ VAPNANYNDV APFEVRLYKN KDMIQTLTNK SKIQNVGGTY ELHVGDTIDL IFNSEHQVLK NNTYWGIILL ANPQFIS. Preparation: Produced from sera of rabbits immunized with highly pure Recombinant Human AITRL. Anti-Human AITRL-specific antibody was purified by affinity chromatography and then biotinylated. Sandwich ELISA: To detect hAITRL by sandwich ELISA (using 100 μL/well antibody solution) a concentration of 0.25-1.0 μg/mL of this antibody is required. This biotinylated polyclonal antibody, in conjunction with PeproTech Polyclonal Anti-Human AITRL (500-P244) as a capture antibody, allows the detection of at least 0.2-0.4 ng/well of Recombinant hAITRL. Western Blot: To detect hAITRL by Western Blot analysis this antibody can be used at a concentration of 0.1-0.2 μg/mL. Used in conjunction with compatible secondary reagents the detection limit for Recombinant hAITRL is 1.5-3.0 ng/lane, under either reducing or non-reducing conditions. 500-P244BT-1MG will be provided as 2 x 500 μg

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.
TRUSTED_SUSTAINABILITY
Specifications

Specifications

GITRL
Polyclonal
Biotin
TNFSF18
Activation-inducible TNF-related ligand; AITR ligand; AITRL; GITR ligand; Gitrl; GITRLigand; Glucocorticoid-induced TNF-related ligand; glucocorticoid-induced TNFR-related protein ligand; glucocorticoid-induced-tumor necrosis factor receptor ligand; hGITRL; RP1-15D23.1; TL6; TNF superfamily member 18; Tnfsf18; TNLG2A; 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; tumor necrosis factor superfamily member 18; UNQ149/PRO175
Rabbit
Antigen affinity chromatography
RUO
8995
-20°C
Lyophilized
ELISA, Western Blot
0.1-1.0 mg/mL
PBS with no preservative
Q9UNG2
TNFSF18
E.coli-derived Recombinant Human AITRL.
500 μg
Primary
Human
Antibody
IgG
Product Suggestions

Product Suggestions

Videos
SDS
Documents

Documents

Product Certifications
Promotions

Promotions

Product Content Correction

The Fisher Scientific Encompass Program offers items which are not part of our distribution portfolio. These products typically do not have pictures or detailed descriptions. However, we are committed to improving your shopping experience. Please use the form below to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Your feedback has been submitted: Thank you for helping us improve our website.