Evidence map›Paper›PMID 21220420›Full record

ArticleThe Journal of biological chemistry2011

Mitofusin 2 regulates STIM1 migration from the Ca2+ store to the plasma membrane in cells with depolarized mitochondria.

Karthika Singaravelu, Charmaine Nelson, Daniel Bakowski, Olga Martins de Brito, Siaw-Wei Ng, Joseph Di Capite, Trevor Powell, Luca Scorrano, Anant B Parekh

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.0field-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

52 citing papers in PubMed, 95 citations in OpenAlex.

  1. Role of STIM1 in the Regulation of Cardiac Energy Substrate Preference.International journal of molecular sciences · 2023
    Review
  2. Review
  3. The Role of Mitochondrial Dynamin in Stroke.Oxidative medicine and cellular longevity · 2022
    Review
  4. Review
  5. The interplay between mitochondria and store-operated CaJournal of cellular and molecular medicine · 2021
    Review
  6. Review
  7. Review
  8. The whole-cell CaThe Journal of physiology · 2020
    Article
  9. The cell biology of mitochondrial membrane dynamics.Nature reviews. Molecular cell biology · 2020
    Review
  10. Fluoride exposure alters CaScience signaling · 2020
    Article
  11. Article
  12. Article
  13. Review
  14. Target Molecules of STIM Proteins in the Central Nervous System.Frontiers in molecular neuroscience · 2020
    Review
  15. Article
  16. Review
  17. Mitochondrial Morphofunction in Mammalian Cells.Antioxidants & redox signaling · 2019
    Review
  18. Article
  19. T Cell Calcium Signaling Regulation by the Co-Receptor CD5.International journal of molecular sciences · 2018
    Review
  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

9 authors at 2 institutions in 3 countries.

Karthika SingaraveluDepartment of Physiology, Anatomy, and Genetics, University of Oxford, Sherrington Building, Parks Road, Oxford OX1 3PT, United Kingdom.
Charmaine Nelson
Daniel Bakowski
Olga Martins de Brito
Siaw-Wei Ng
Joseph Di Capite
Trevor Powell
Luca Scorrano
Anant B Parekh
University of Oxford · GBDulbecco Telethon Institute · IT

Funding

British Heart FoundationMedical Research Council G1000813
6 · The paper itself

Abstract

Store-operated Ca2+ channels in the plasma membrane (PM) are activated by the depletion of Ca2+ from the endoplasmic reticulum (ER) and constitute a widespread and highly conserved Ca2+ influx pathway. After store emptying, the ER Ca2+ sensor STIM1 forms multimers, which then migrate to ER-PM junctions where they activate the Ca2+ release-activated Ca2+ channel Orai1. Movement of an intracellular protein to such specialized sites where it gates an ion channel is without precedence, but the fundamental question of how STIM1 migrates remains unresolved. Here, we show that trafficking of STIM1 to ER-PM junctions and subsequent Ca2+ release-activated Ca2+ channel activity is impaired following mitochondrial depolarization. We identify the dynamin-related mitochondrial protein mitofusin 2, mutations of which causes the inherited neurodegenerative disease Charcot-Marie-Tooth IIa in humans, as an important component of this mechanism. Our results reveal a molecular mechanism whereby a mitochondrial fusion protein regulates protein trafficking across the endoplasmic reticulum and reveals a homeostatic mechanism whereby mitochondrial depolarization can inhibit store-operated Ca2+ entry, thereby reducing cellular Ca2+ overload.

Indexed as

AnimalsBiological TransportCalciumCell LineCell Line, TumorCell MembraneEndoplasmic ReticulumGTP PhosphohydrolasesHumansMembrane GlycoproteinsMembrane ProteinsMicroscopy, ConfocalMicroscopy, ElectronMitochondriaMitochondrial ProteinsNeoplasm ProteinsCalciumGTP PhosphohydrolasesMembrane GlycoproteinsMembrane ProteinsMFN2 protein, humanMfn2 protein, ratMitochondrial ProteinsNeoplasm ProteinsSTIM1 protein, humanStim1 protein, ratStromal Interaction Molecule 1

Identifiers

PMID21220420
PMCPMC3069423
OpenAlexW2122198700

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.