Render Target: STATIC
Render Timestamp: 2025-03-14T11:05:43.754Z
Commit: a619ae74f66dae0f27639e88da12bcf600e46428
XML generation date: 2025-03-07 13:14:46.930
Product last modified at: 2025-03-06T12:45:20.660Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464
  1. Products /
  2. Primary Antibodies /
  3. TRPV4 Antibody

TRPV4 Antibody #65893

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M Mk
    SENSITIVITY Endogenous
    MW (kDa) 95-102
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    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

    TRPV4 Antibody recognizes endogenous levels of total TRPV4 protein. The antibody is predicted to detect all isoforms of TRPV4 reported in Uniprot, with the exception of TRPV4-SV (Isoform 3).

    Species Reactivity:

    Human, Mouse, Monkey

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human TRPV4 protein. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    TRPV4 is a member of the transient receptor potential vanilloid (TRPV) family of ion channels, and functions as a Ca2+-permeant non-selective cation channel. TRPV4 channels are expressed in many cell types, with particular abundance in sensory and spinal neurons (1). TRPV4 channels play a role in maintaining cellular homeostasis, by facilitating transmembrane Ca2+ transport in response to various stimuli, including thermal stress, fatty acid metabolites, and hypotonicity (2). Mutations in the TRPV4 gene have consequently been attributed to a variety of pathological conditions. For example, constitutively active TRPV4 mutants can lead to excess Ca2+ influx, resulting in toxicity and degeneration of peripheral nerves (3). TRPV4-dependent Ca2+ influx was also shown to mediate strain-induced and TGFβ1-induced epithelial-mesenchymal transition (EMT), suggesting a mechanistic role for TRPV4-mediated Ca2+ transport in fibrosis and oncogenesis (4). Consistent with this, studies in capillary endothelial cells showed that mechanical strain-induced Ca2+ influx through TRPV4 promote focal adhesion and stress fiber remodeling, mediated specifically through integrins, PI3K, and downstream kinases including Rho and ROCK (5).

    Database Links

    UniProt ID: Q9HBA0


    Entrez-Gene Id: 59341


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