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Product last modified at: 2025-01-01T09:03:35.135Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

GADS Antibody #48287

Filter:
  • WB
Western Blotting Image 1: GADS Antibody
Western blot analysis of extracts from various human cell lines using GADS Antibody (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower). Negative expression of GADS protein in Ramos cells is consistent with published observations.

To Purchase # 48287

Cat. # Size Qty. Price
48287S 100 µl
$306

Supporting Data

REACTIVITY H M
SENSITIVITY Endogenous
MW (kDa) 40
SOURCE Rabbit
Application Key:
  • WB-Western Blotting 
Species Cross-Reactivity Key:
  • H-Human 
  • M-Mouse 
  • Related Products

Product Information

Product Usage Information

Application Dilution
Western Blotting 1:1000

Storage

Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

Protocol

Specificity / Sensitivity

GADS Antibody recognizes endogenous levels of total GADS protein.

Species Reactivity:

Human, Mouse

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly172 of human GADS protein. Antibodies are purified by peptide affinity chromatography.

Background

GRB2-related adaptor downstream of Shc (GADS) belongs to the GRB2 family of adaptor proteins. It is a hematopoietic cell-specific signaling adaptor protein that harbors amino- and carboxy-terminal SH3 domains, a central SH2 domain, and a unique linker region that is rich in proline and glutamine residues (1). The presence of SH2 and SH3 domains within GADS strongly suggest that it functions in signal transduction cascades by facilitating protein-protein interactions. In the context of T cells, research studies have demonstrated that GADS interacts with LAT and SLP-76 signaling complexes to facilitate NFAT activation downstream of TCR engagement (2-4). Given its role as a fundamental mediator of TCR signaling, GADS is subject to multiple modes of negative regulation to limit TCR signal strength. For example, research studies have demonstrated that HPK1 directly phosphorylates GADS at Thr262 within its linker region, a modification that promotes 14-3-3 binding and dissociation of signaling complexes nucleated by LAT, SLP-76, and GADS (5). The linker region of GADS is also subject to caspase-mediated cleavage, which separates its SH2 and SH3 domains and thus impairs the ability of GADS to bridge LAT and SLP-76 signaling complexes for transduction of faithful TCR signals (6,7).
For Research Use Only. Not For Use In Diagnostic Procedures.
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