Evidence map›Paper›PMID 17706768›Full record

ArticleCell calcium2008

The TRPV3 mutation associated with the hairless phenotype in rodents is constitutively active.

Rui Xiao, Jinbin Tian, Jisen Tang, Michael X Zhu

Abstract read
In one paragraph

Article in Cell calcium, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.3field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
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  12. Review
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  15. Article
  16. Article
  17. Article
  18. TRP Channels as Drug Targets to Relieve Itch.Pharmaceuticals (Basel, Switzerland) · 2018
    Review
  19. Article
  20. TRP Channels in Skin Biology and Pathophysiology.Pharmaceuticals (Basel, Switzerland) · 2016
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Rui XiaoDepartment of Neuroscience and Center for Molecular Neurobiology, The Ohio State University, Columbus, OH 43210, USA.
Jinbin Tian
Jisen Tang
Michael X Zhu
The Ohio State University · US

Funding

Ohio State Neuroscience Centr CoreP30NS045758 · NINDS · OHIO STATE UNIVERSITY · PI OBRIETAN, KARL H · 2004 to 2015
$7.7M
MECHANISM OF CONFORMATIONAL COUPLINGR01NS042183 · NINDS · OHIO STATE UNIVERSITY · PI ZHU, MICHAEL X · 2001 to 2004
$1.1M
High throughput screening of ligands of TRP channelsR21NS056942 · NINDS · OHIO STATE UNIVERSITY · PI ZHU, MICHAEL X · 2006 to 2008
$261k
NINDS NIH HHS NS 042183NINDS NIH HHS NS 045758NINDS NIH HHS NS 056942NINDS NIH HHS P30 NS045758NINDS NIH HHS R01 NS042183NINDS NIH HHS R21 NS056942
6 · The paper itself

Abstract

TRPV3 is a non-selective cation channel activated by warm to hot temperatures. In rodents, TRPV3 is highly expressed in basal keratinocytes of skin and oral/nasal epithelia. TRPV3 knockout mice showed impaired responses to innocuous and noxious heat but otherwise normal appearance and reactions to many sensory modalities. However, point mutations of TRPV3 at Gly573 to Ser and Cys have recently been linked to autosomal dominant hairless phenotypes and spontaneous dermatitis in mice and rats, implicating an important role for TRPV3 in alopecia and skin diseases. Exactly, how the mutations affect TRPV3 function was unexplained. Here, we show that both G573S and G573C mutations of murine TRPV3 are constitutively active in heterologous systems. In HEK 293 cells, expression of the TRPV3 mutants causes cell death. In Xenopus oocytes, the constitutively active mutant channel is irresponsive to thermal and chemical stimuli but it reduces the temperature threshold and enhances the responses to heat and TRPV3 agonists of the wild type channel when they are co-expressed. We conclude that the G573S and G573C substitutions render the TRPV3 channel spontaneously active under normal physiological conditions, which in turn alters ion homeostasis and membrane potentials of skin keratinocytes, leading to hair loss and dermatitis-like skin diseases.

Indexed as

AlopeciaHairMutationTRPV Cation ChannelsAnimalsCell LineHot TemperatureHumansKeratinocytesMiceOocytesPatch-Clamp TechniquesPhenotypeRatsSkin DiseasesXenopus laevisTrpv3 protein, mouseTRPV Cation Channels

Identifiers

PMID17706768
PMCPMC2287378
OpenAlexW2091153416

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.