渲染靶标:SSR
Render Timestamp: 2025-03-16T12:37:06.747Z
Commit: 9fc0f116116d9da247dc8ddd4e5fe811153412e1
XML generation date: 2024-09-20 06:22:18.765
Product last modified at: 2025-02-27T23:15:08.896Z
1% for the Planet 标识
PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

TRPV4 Antibody #65893

Filter:
  • WB
  • IP
Western Blotting Image 1: TRPV4 Antibody
Western blot analysis of extracts from various cell lines using TRPV4 Antibody (upper) and β-Actin (D6A8) Rabbit mAb #8457 (lower). Expression levels of TRPV4 among cell lines are consistent with expectations based on publicly available bioinformatic databases.

To Purchase # 65893

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 
  • Related Products

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