ArticleAnimal cells and systems2011
Mutation of a putative S-nitrosylation site of TRPV4 protein facilitates the channel activates.
Article in Animal cells and systems, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Flipping Off and On the Redox Switch in the Microcirculation.Annual review of physiology · 2023Review
- FAT10 Induces cancer cell migration by stabilizing phosphorylated ABI3/NESH.Animal cells and systems · 2023Article
- TRPV4-A Missing Link Between Mechanosensation and Immunity.Frontiers in immunology · 2020Review
- Dual contribution of TRPV4 antagonism in the regulatory effect of vasoinhibins on blood-retinal barrier permeability: diabetic milieu makes a difference.Scientific reports · 2017Article
- Redox regulation of transient receptor potential channels in the endothelium.Microcirculation (New York, N.Y. : 1994) · 2017Review
- Control of the neurovascular coupling by nitric oxide-dependent regulation of astrocytic Ca(2+) signaling.Frontiers in cellular neuroscience · 2015Review
- Human skeletal dysplasia caused by a constitutive activated transient receptor potential vanilloid 4 (TRPV4) cation channel mutation.Experimental & molecular medicine · 2012Review
- The nuclear localization of glycogen synthase kinase 3β is required its putative PY-nuclear localization sequences.Molecules and cells · 2012Article
- Endoplasmic Reticulum (ER) Stress Enhances Tip60 (A Histone Acetyltransferase) Binding to the Concanavalin A.The open biochemistry journal · 2012Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transient receptor potential vanilloid 4 (TRPV4) cation channel, a member of the TRP vanilloid subfamily, is expressed in a broad range of tissues. Nitric oxide (NO) as a gaseous signal mediator shows a variety of important biological effects. In many instances, NO has been shown to exhibit its activities via a protein S-nitrosylation mechanism in order to regulate its protein functions. With functional assays via site-directed mutagenesis, we demonstrate herein that NO induces the S-nitrosylation of TRPV4 Ca(2+) channel on the Cys(853) residue, and the S-nitrosylation of Cys(853) reduced its channel sensitivity to 4-α phorbol 12,13-didecanoate and the interaction between TRPV4 and calmodulin. A patch clamp experiment and Ca(2+) image analysis show that the S-nitrosylation of Cys(853) modulates the TRPV4 channel as an inhibitor. Thus, our data suggest a novel regulatory mechanism of TRPV4 via NO-mediated S-nitrosylation on its Cys(853) residue.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.