Evidence map›Paper›PMID 26219591›Full record

ArticleNature communications2015

An MTCH2 pathway repressing mitochondria metabolism regulates haematopoietic stem cell fate.

Maria Maryanovich, Yehudit Zaltsman, Antonella Ruggiero, Andres Goldman, Liat Shachnai, Smadar Levin Zaidman, Ziv Porat, Karin Golan, Tsvee Lapidot, Atan Gross

Open access · goldAbstract read
PubMed Publisher
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed
9.0field-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

152 citing papers in PubMed, 240 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Antioxidants (Basel, Switzerland) · 2026
    Review
  6. MTCH2 promotes BAX and BAK self-assembly and apoptotic pore growth.Nature structural & molecular biology · 2026
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Metabolic Signature ofJournal of personalized medicine · 2025
    Review
  20. Article

92 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 1 institution in 1 country.

Maria MaryanovichDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Yehudit ZaltsmanDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Antonella RuggieroDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Andres GoldmanDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Liat ShachnaiDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Smadar Levin ZaidmanDepartment of Chemical Research Support, Weizmann Institute of Science, Rehovot 76100, Israel.
Ziv PoratDepartment of Biological Services, Weizmann Institute of Science, Rehovot 76100, Israel.
Karin GolanDepartment Immunology, Weizmann Institute of Science, Rehovot 76100, Israel.
Tsvee LapidotDepartment Immunology, Weizmann Institute of Science, Rehovot 76100, Israel.
Atan GrossDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The metabolic state of stem cells is emerging as an important determinant of their fate. In the bone marrow, haematopoietic stem cell (HSC) entry into cycle, triggered by an increase in intracellular reactive oxygen species (ROS), corresponds to a critical metabolic switch from glycolysis to mitochondrial oxidative phosphorylation (OXPHOS). Here we show that loss of mitochondrial carrier homologue 2 (MTCH2) increases mitochondrial OXPHOS, triggering HSC and progenitor entry into cycle. Elevated OXPHOS is accompanied by an increase in mitochondrial size, increase in ATP and ROS levels, and protection from irradiation-induced apoptosis. In contrast, a phosphorylation-deficient mutant of BID, MTCH2's ligand, induces a similar increase in OXPHOS, but with higher ROS and reduced ATP levels, and is associated with hypersensitivity to irradiation. Thus, our results demonstrate that MTCH2 is a negative regulator of mitochondrial OXPHOS downstream of BID, indispensible in maintaining HSC homeostasis.

Indexed as

Oxidative PhosphorylationAdenosine TriphosphateAnimalsApoptosisBH3 Interacting Domain Death Agonist ProteinBlotting, WesternCell CycleCell DifferentiationColony-Forming Units AssayFlow CytometryGlycolysisHematopoiesisHematopoietic Stem CellsMembrane Potential, MitochondrialMiceMicroscopy, Electron, TransmissionAdenosine TriphosphateBH3 Interacting Domain Death Agonist ProteinBid protein, mouseMitochondrial Membrane Transport ProteinsMtch2 protein, mouseReactive Oxygen Species

Identifiers

PMID26219591
OpenAlexW2266362809

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.