Render Target: STATIC
Render Timestamp: 2024-11-21T13:45:56.058Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-30 01:58:04.426
Product last modified at: 2024-11-20T17:00:10.011Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
  1. Products /
  2. Primary Antibodies /
  3. TRPV4 (E6W1P) Rabbit mAb
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).

    Database Links

    UniProt ID: Q9HBA0


    Entrez-Gene Id: 59341


    Limited Uses

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