Render Target: SSR
Render Timestamp: 2024-11-14T23:08:18.361Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-09-30 01:58:04.426
Product last modified at: 2024-09-30T08:02:21.873Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

TRPV4 (E6W1P) Rabbit mAb #91660

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H Mk
    SENSITIVITY Endogenous
    MW (kDa) 95-102
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • 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, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    TRPV4 (E6W1P) Rabbit mAb recognizes endogenous levels of total TRPV4 protein.

    Species Reactivity:

    Human, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro838 of human TRPV4 protein.

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