Evidence map›Paper›PMID 23893410›Full record

ArticleThe Journal of biological chemistry2013

Trypanosome Letm1 protein is essential for mitochondrial potassium homeostasis.

Hassan Hashimi, Lindsay McDonald, Eva Stríbrná, Julius Lukeš

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. 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
3.9field-weighted citation impact, top 6% 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. Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026
    Review
  2. Article
  3. Article
  4. TMBIM5 is the CaEMBO reports · 2022
    Article
  5. Article
  6. Mitochondrial CaAntioxidants & redox signaling · 2022
    Review
  7. Review
  8. Article
  9. Trypanosoma cruzi Letm1 is involved in mitochondrial CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  10. Article
  11. Mitochondrial Calcium Signaling in Pancreatic β-Cell.International journal of molecular sciences · 2021
    Review
  12. Review
  13. Review
  14. Mitochondrial CaInternational review of cell and molecular biology · 2021
    Review
  15. Article
  16. Article
  17. Review
  18. Mitochondrial CaPharmacology & therapeutics · 2018
    Review
  19. 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

4 authors at 1 institution in 2 countries.

Hassan HashimiFrom the Institute of Parasitology, Biology Centre, Czech Academy of Sciences and.
Lindsay McDonald
Eva Stríbrná
Julius Lukeš
Czech Academy of Sciences · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Letm1 is a conserved protein in eukaryotes bearing energized mitochondria. Hemizygous deletion of its gene has been implicated in symptoms of the human disease Wolf-Hirschhorn syndrome. Studies almost exclusively performed in opisthokonts have attributed several roles to Letm1, including maintaining mitochondrial morphology, mediating either calcium or potassium/proton antiport, and facilitating mitochondrial translation. We address the ancestral function of Letm1 in the highly diverged protist and significant pathogen, Trypanosoma brucei. We demonstrate that Letm1 is involved in maintaining mitochondrial volume via potassium/proton exchange across the inner membrane. This role is essential in the vector-dwelling procyclic and mammal-infecting bloodstream stages as well as in Trypanosoma brucei evansi, a form of the latter stage lacking an organellar genome. In the pathogenic bloodstream stage, the mitochondrion consumes ATP to maintain an energized state, whereas that of T. brucei evansi also lacks a conventional proton-driven membrane potential. Thus, Letm1 performs its function in different physiological states, suggesting that ion homeostasis is among the few characterized essential pathways of the mitochondrion at this T. brucei life stage. Interestingly, Letm1 depletion in the procyclic stage can be complemented by exogenous expression of its human counterpart, highlighting the conservation of protein function between highly divergent species. Furthermore, although mitochondrial translation is affected upon Letm1 ablation, it is an indirect consequence of K(+) accumulation in the matrix.

Indexed as

Anti-Bacterial AgentsCationsFlow CytometryGene SilencingGenetic Complementation TestHomeostasisHumansMembrane Potential, MitochondrialMitochondriaMitochondrial ProteinsPhenotypePotassiumProtein BiosynthesisProtozoan ProteinsRNA InterferenceTrypanosoma brucei bruceiAnti-Bacterial AgentsCationsMitochondrial ProteinsPotassiumProtozoan ProteinsBioenergeticsLetm1MitochondriaPotassium TransportTranslationTrypanosome

Identifiers

PMID23893410
PMCPMC3772241
OpenAlexW2134199207

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.