Evidence map›Paper›PMID 24300389›Full record

ReviewEuropean journal of pharmacology2014

Intracellular calcium channels: inositol-1,4,5-trisphosphate receptors.

Olena A Fedorenko, Elena Popugaeva, Masahiro Enomoto, Peter B Stathopulos, Mitsuhiko Ikura, Ilya Bezprozvanny

Open access · greenAbstract readReview
In one paragraph

Review in European journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 46 citations in OpenAlex.

  1. Wound Repair and CaCells · 2024
    Review
  2. Review
  3. Review
  4. CaCancers · 2021
    Review
  5. Calmodulin and Its Binding Proteins in Parkinson's Disease.International journal of molecular sciences · 2021
    Review
  6. Review
  7. Channels that Cooperate with TRPV4 in the Brain.Journal of molecular neuroscience : MN · 2020
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Strontium fails to induce CaHuman reproduction open · 2018
    Article
  15. Review
  16. Review
  17. IPFrontiers in oncology · 2017
    Review
  18. Review
  19. 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

6 authors at 3 institutions in 4 countries.

Olena A FedorenkoDepartment of Brain Physiology, Bogomoletz Institute of Physiology, 01024 Kiev, Ukraine; State Key Laboratory of Molecular and Cellular Biology, 01024 Kiev, Ukraine.
Elena PopugaevaLaboratory of Molecular Neurodegeneration, Department of Medical Physics, St. Petersburg State Polytechnical University, 195251 St. Petersburg, Russia.
Masahiro EnomotoPrincess Margaret Cancer Centre, Department of Medical Biophysics, University of Toronto, M5G1L7 Toronto, Ontario, Canada.
Peter B StathopulosPrincess Margaret Cancer Centre, Department of Medical Biophysics, University of Toronto, M5G1L7 Toronto, Ontario, Canada.
Mitsuhiko IkuraPrincess Margaret Cancer Centre, Department of Medical Biophysics, University of Toronto, M5G1L7 Toronto, Ontario, Canada.
Ilya BezprozvannyLaboratory of Molecular Neurodegeneration, Department of Medical Physics, St. Petersburg State Polytechnical University, 195251 St. Petersburg, Russia; Department of Physiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: ilya.bezprozvanny@utsouthwestern.edu.
Princess Margaret Cancer Centre · CAPeter the Great St. Petersburg Polytechnic University · RUBogomoletz Institute of Physiology · UA

Funding

Deranged calcium signaling and polyglutamine expansion disordersR01NS056224 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI BEZPROZVANNY, ILYA B · 2008 to 2020
$3.5M
Presenilins and neuronal calcium dyshomeostasisR01NS080152 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI BEZPROZVANNY, ILYA B · 2013 to 2017
$2.3M
Calcium channels as novel therapeutic targets for Huntingtons DiseaseR01NS074376 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI BEZPROZVANNY, ILYA B · 2012 to 2015
$1.4M
NINDS NIH HHS R01 NS056224NINDS NIH HHS R01NS056224NINDS NIH HHS R01 NS074376NINDS NIH HHS R01NS074376NINDS NIH HHS R01 NS080152NINDS NIH HHS R01NS080152
6 · The paper itself

Abstract

The inositol-1,4,5-trisphosphate receptors (InsP3Rs) are the major intracellular Ca(2+)-release channels in cells. Activity of InsP3Rs is essential for elementary and global Ca(2+) events in the cell. There are three InsP3Rs isoforms that are present in mammalian cells. In this review we will focus primarily on InsP3R type 1. The InsP3R1 is a predominant isoform in neurons and it is the most extensively studied isoform. Combination of biophysical and structural methods revealed key mechanisms of InsP3R function and modulation. Cell biological and biochemical studies lead to identification of a large number of InsP3R-binding proteins. InsP3Rs are involved in the regulation of numerous physiological processes, including learning and memory, proliferation, differentiation, development and cell death. Malfunction of InsP3R1 play a role in a number of neurodegenerative disorders and other disease states. InsP3Rs represent a potentially valuable drug target for treatment of these disorders and for modulating activity of neurons and other cells. Future studies will provide better understanding of physiological functions of InsP3Rs in health and disease.

Indexed as

AnimalsBiophysical PhenomenaHumansInositol 1,4,5-Trisphosphate ReceptorsIntracellular SpaceNeurodegenerative DiseasesInositol 1,4,5-Trisphosphate ReceptorsCa(2+) signalingCell nucleusInositol 1,4,5-trisphosphate receptorsNeurodegeneration

Identifiers

PMID24300389
PMCPMC4040340
OpenAlexW2009273046

What OpenQuestion holds

Textmetadata
LicenceTDM
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.