Render Target: STATIC
Render Timestamp: 2025-01-03T12:02:12.400Z
Commit: 286c369131ceeedcf44c821941824d8d7e009e57
XML generation date: 2024-04-05 20:24:56.240
Product last modified at: 2025-01-01T09:05:39.187Z
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PDP - Template Name: Blocking Peptide
PDP - Template ID: *******6db2f4c

TrkA Blocking Peptide #1435

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Important Ordering Details

Custom Ordering Details: This product is assembled upon order. Please allow two-four weeks for your product to be processed.

    Product Information

    Product Usage Information

    Use as a blocking reagent to evaluate the specificity of antibody reactivity in dot blot protocols.

    Storage

    Supplied in 20 mM potassium phosphate (pH 7.0), 50 mM NaCl, 0.1 mM EDTA, 1 mg/ml BSA and 5% glycerol. 1% DMSO. Store at –20°C.

    Product Description

    This peptide is used to block TrkA (14G6) Rabbit mAb #2508 reactivity in dot blot protocols.

    Quality Control

    The quality of the peptide was evaluated by reversed-phase HPLC and by mass spectrometry. The peptide blocks TrkA (14G6) Rabbit mAb #2508 by dot blot.

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