Evidence map›Paper›PMID 16301334›Full record

ArticleThe Journal of cell biology2005

Dissecting independent channel and scaffolding roles of the Drosophila transient receptor potential channel.

Tao Wang, Yuchen Jiao, Craig Montell

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. eLife · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. Rapid Release of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  9. Article
  10. Article
  11. Structure of the mammalian TRPM7, a magnesium channel required during embryonic development.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. Article
  13. A Single Residue Mutation in the GαG3 (Bethesda, Md.) · 2018
    Article
  14. Article
  15. The Phosphorylation State of theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

3 authors at 2 institutions in 1 country.

Tao WangDepartment of Biological Chemistry, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Yuchen Jiao
Craig Montell
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Unconventional roles for opsinsR01EY008117 · NEI · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI MONTELL, CRAIG · 1989 to 2022
$8.2M
TRP CHANNEL SIGNALING COMPLEX AND ITS ROLE IN VISIONR01EY010852 · NEI · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI MONTELL, CRAIG · 1995 to 2021
$7.9M
NEI NIH HHS EY08117NEI NIH HHS EY10852NEI NIH HHS R01 EY008117NEI NIH HHS R01 EY010852
6 · The paper itself

Abstract

Drosophila transient receptor potential (TRP) serves dual roles as a cation channel and as a molecular anchor for the PDZ protein, INAD (inactivation no afterpotential D). Null mutations in trp cause impairment of visual transduction, mislocalization of INAD, and retinal degeneration. However, the impact of specifically altering TRP channel function is not known because existing loss-of-function alleles greatly reduce protein expression. In the current study we describe the isolation of a set of new trp alleles, including trp(14) with an amino acid substitution juxtaposed to the TRP domain. The trp(14) flies stably express TRP and display normal molecular anchoring, but defective channel function. Elimination of the anchoring function alone in trp(Delta)(1272), had minor effects on retinal morphology whereas disruption of channel function caused profound light-induced cell death. This retinal degeneration was greatly suppressed by elimination of the Na(+)/Ca(2+) exchanger, CalX, indicating that the cell death was due primarily to deficient Ca(2+) entry rather than disruption of the TRP-anchoring function.

Indexed as

AllelesAmino Acid SequenceAnimalsAnimals, Genetically ModifiedAntiportersArrestinsBlotting, WesternCalciumCationsDrosophila melanogasterDrosophila ProteinsElectroretinographyGene Expression RegulationGenes, InsectImmunoprecipitationLightAntiportersArr2 protein, DrosophilaArrestinsCalciumCalx protein, DrosophilaCationsDrosophila ProteinsSodium-Calcium ExchangerTransient Receptor Potential Channelstrp protein, Drosophila

Identifiers

PMID16301334
PMCPMC2171549
OpenAlexW2144822393

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.