Evidence map›Paper›PMID 11248050›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2001

Activation of Trp3 by inositol 1,4,5-trisphosphate receptors through displacement of inhibitory calmodulin from a common binding domain.

Z Zhang, J Tang, S Tikunova, J D Johnson, Z Chen, N Qin, A Dietrich, E Stefani, L Birnbaumer, M X Zhu

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

89 citing papers in PubMed, 224 citations in OpenAlex.

  1. Review
  2. Review
  3. The role of IPPflugers Archiv : European journal of physiology · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Calcium and Neural Stem Cell Proliferation.International journal of molecular sciences · 2024
    Review
  8. Article
  9. The odyssey of the TR(i)P journey to the cellular membrane.Frontiers in cell and developmental biology · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. TRPC3 shapes the ER-mitochondria CaNature communications · 2022
    Article
  15. Role of Store-Operated CaBiomolecules · 2021
    Review
  16. Article
  17. CaCells · 2021
    Review
  18. Article
  19. Review
  20. Article

29 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Z ZhangNeurobiotechnology Center and Departments of Neuroscience and Molecular and Cellular Biochemistry, Ohio State University, Columbus, OH 43210, USA.
J Tang
S Tikunova
J D Johnson
Z Chen
N Qin
A Dietrich
E Stefani
L Birnbaumer
M X Zhu
University of Kentucky · USUniversity of California, Los Angeles · US

Funding

MECHANISM OF CONFORMATIONAL COUPLINGR01NS042183 · NINDS · OHIO STATE UNIVERSITY · PI ZHU, MICHAEL X · 2001 to 2004
$1.1M
MODULATION OF CALMODULIN AND THE CALCIUM SIGNALR01DK033727 · NIDDK · OHIO STATE UNIVERSITY · PI ALTSCHULD, RUTH A · 1986 to 2003
$641k
RECEPTOR COUPLING MECHANISMSR01HL045198 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BIRNBAUMER, MARIEL · 1990 to 2001
$557k
HUMAN TRP GENES IN RELATION TO CALCIUM ENTRY CHANNELSR01GM054235 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ZHU, MICHAEL X · 1997 to 2001
$291k
NHLBI NIH HHS HL45198NIDDK NIH HHS DK33727NIGMS NIH HHS GM54235NINDS NIH HHS R01 NS042183
6 · The paper itself

Abstract

Mammalian homologues of Drosophila Trp form plasma membrane channels that mediate Ca(2+) influx in response to activation of phospholipase C and internal Ca(2+) store depletion. Previous studies showed that human Trp3 is activated by inositol 1,4,5-trisphosphate (IP(3)) receptors (IP(3)Rs) and identified interacting domains, one on Trp and two on IP(3)R. We now find that Trp3 binds Ca(2+)-calmodulin (Ca(2+)/CaM) at a site that overlaps with the IP(3)R binding domain. Using patch-clamp recordings from inside-out patches, we further show that Trp3 has a high intrinsic activity that is suppressed by Ca(2+)/CaM under resting conditions, and that Trp3 is activated by the following: a Trp-binding peptide from IP(3)R that displaces CaM from Trp3, a myosin light chain kinase Ca(2+)/CaM binding peptide that prevents CaM from binding to Trp3, and calmidazolium, an inactivator of Ca(2+)/CaM. We conclude that inhibition of the inhibitory action of CaM is a key step of Trp3 channel activation by IP(3)Rs.

Indexed as

Amino Acid SequenceBinding, CompetitiveBinding SitesCalciumCalcium ChannelsCalmodulinCations, DivalentCell LineHumansInositol 1,4,5-Trisphosphate ReceptorsMolecular Sequence DataPeptidesReceptors, Cytoplasmic and NuclearTRPC Cation ChannelsCalciumCalcium ChannelsCalmodulinCations, DivalentInositol 1,4,5-Trisphosphate ReceptorsITPR1 protein, humanPeptidesReceptors, Cytoplasmic and NuclearTRPC3 cation channelTRPC Cation Channels

Identifiers

PMID11248050
PMCPMC30625
OpenAlexW2002613167

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.