Thermo Fisher Scientific Human AITRL Recombinant Protein, PeproTech

Applications

Tested Dilution

Publications

Western Blot (WB)

Assay-dependent

-

ELISA (ELISA)

Assay-dependent

-

Functional Assay (Functional)

Assay-dependent

-

Product Specifications

Species

Human

Expression System

E. coli

Amino acid sequence

METAKEPCMA KFGPLPSKWQ MASSEPPCVN KVSDWKLEIL QNGLYLIYGQ VAPNANYNDV APFEVRLYKN KDMIQTLTNK SKIQNVGGTY ELHVGDTIDL IFNSEHQVLK NNTYWGIILL ANPQFIS

Molecular weight

14.3 kDa

Class

Recombinant

Type

Protein

Purity

≥ 98% by SDS-PAGE gel and HPLC analyses.

Endotoxin concentration

<1 EU/µg

Activity

Determined by its ability to stimulate IL-8 production by human PBMC using a concentration range of 1.0-10.0 ng/ml. Please Note: Results may vary with PBMC donors.

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Lyophilized

Purification

purified

Contains

no preservative

Storage conditions

-20°C

Shipping conditions

Ambient

Product Specific Information

Recombinant Human soluble AITRL is a 14.4 kDa protein, containing 127 amino acid residues corresponding to the extracellular domain of AITRL.

This product is shipped at ambient temperature. For storage, handling and reconstitution information, please see the lot-specific Certificate of Analysis

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.