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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

TrkA Antibody #2505

Filter:
  • WB
Western Blotting Image 1: TrkA Antibody
Western blot analysis from various cell lysates and rat brain cell extracts, using TrkA Antibody.

To Purchase # 2505

Cat. # Size Qty. Price
2505S 100 µl
$306

Supporting Data

REACTIVITY H M R
SENSITIVITY Endogenous
MW (kDa) 140
SOURCE Rabbit
Application Key:
  • WB-Western Blotting 
Species Cross-Reactivity Key:
  • H-Human 
  • M-Mouse 
  • R-Rat 
  • 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

TrkA Antibody detects endogenous levels of total TrkA protein.

Species Reactivity:

Human, Mouse, Rat

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to human TrkA. Antibodies are purified by protein A and peptide affinity chromatography.

Background

The family of Trk receptor tyrosine kinases consists of TrkA, TrkB, and TrkC. While the sequence of these family members is highly conserved, they are activated by different neurotrophins: TrkA by NGF, TrkB by BDNF or NT4, and TrkC by NT3 (1). Neurotrophin signaling through these receptors regulates a number of physiological processes, such as cell survival, proliferation, neural development, and axon and dendrite growth and patterning (1). In the adult nervous system, the Trk receptors regulate synaptic strength and plasticity. TrkA regulates proliferation and is important for development and maturation of the nervous system (2). Phosphorylation at Tyr490 is required for Shc association and activation of the Ras-MAP kinase cascade (3,4). Residues Tyr674/675 lie within the catalytic domain, and phosphorylation at these sites reflects TrkA kinase activity (3-6). Point mutations, deletions, and chromosomal rearrangements (chimeras) cause ligand-independent receptor dimerization and activation of TrkA (7-10). TrkA is activated in many malignancies including breast, ovarian, prostate, and thyroid carcinomas (8-13). Research studies suggest that expression of TrkA in neuroblastomas may be a good prognostic marker as TrkA signals growth arrest and differentiation of cells originating from the neural crest (10).

Pathways

Explore pathways related to this product.


For Research Use Only. Not For Use In Diagnostic Procedures.
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