Evidence map›Paper›PMID 38263327›Full record

ArticleEMBO reports2024

Mitochondrial translocation of TFEB regulates complex I and inflammation.

Chiara Calabrese, Hendrik Nolte, Melissa R Pitman, Raja Ganesan, Philipp Lampe, Raymond Laboy, Roberto Ripa, Julia Fischer, Ruhi Polara, Sameer Kumar Panda and 6 more

Open access · diamondAbstract read
In one paragraph

Article in EMBO reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. TFEB Deficiency Impairs Male Fertility Through Mitochondrial Dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. TFEB controls sensitivity to chemotherapy and immuno-killing in non-small cell lung cancer.Journal of experimental & clinical cancer research : CR · 2024
    Article
  9. 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

16 authors at 5 institutions in 3 countries.

Chiara CalabreseCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Hendrik NolteCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Melissa R PitmanCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, Australia.ORCID http://orcid.org/0000-0002-9587-3837
Raja GanesanCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, Australia.ORCID http://orcid.org/0000-0002-5408-0478
Philipp LampeCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Raymond LaboyCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0002-0375-1550
Roberto RipaMax Planck Institute for Biology of Ageing, Cologne, Germany.
Julia FischerCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0001-6138-7454
Ruhi PolaraCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, Australia.ORCID http://orcid.org/0009-0006-1787-1744
Sameer Kumar PandaCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, Australia.ORCID http://orcid.org/0000-0001-5058-5906
Sandhya ChipurupalliCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, Australia.
Saray GutierrezCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Daniel ThomasAdelaide Medical School, University of Adelaide, Adelaide, Australia.ORCID http://orcid.org/0000-0002-0837-1231
Stuart M PitsonCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, Australia.ORCID http://orcid.org/0000-0002-9527-2740
Adam AntebiCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany. aantebi@age.mpg.de.ORCID http://orcid.org/0000-0002-7241-3029
Nirmal RobinsonCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany. Nirmal.Robinson@unisa.edu.au.ORCID http://orcid.org/0000-0002-7361-9491
South Australia Pathology · AUUniversity of Cologne · DECologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEMax Planck Institute for Biology of Ageing · DESouth Australian Health and Medical Research Institute · AU

Funding

Deutsche Forschungsgemeinschaft (DFG) CECADDeutsche Forschungsgemeinschaft (DFG) SFB 670 N31
6 · The paper itself

Abstract

TFEB is a master regulator of autophagy, lysosome biogenesis, mitochondrial metabolism, and immunity that works primarily through transcription controlled by cytosol-to-nuclear translocation. Emerging data indicate additional regulatory interactions at the surface of organelles such as lysosomes. Here we show that TFEB has a non-transcriptional role in mitochondria, regulating the electron transport chain complex I to down-modulate inflammation. Proteomics analysis reveals extensive TFEB co-immunoprecipitation with several mitochondrial proteins, whose interactions are disrupted upon infection with S. Typhimurium. High resolution confocal microscopy and biochemistry confirms TFEB localization in the mitochondrial matrix. TFEB translocation depends on a conserved N-terminal TOMM20-binding motif and is enhanced by mTOR inhibition. Within the mitochondria, TFEB and protease LONP1 antagonistically co-regulate complex I, reactive oxygen species and the inflammatory response. Consequently, during infection, lack of TFEB specifically in the mitochondria exacerbates the expression of pro-inflammatory cytokines, contributing to innate immune pathogenesis.

Indexed as

AutophagyInflammationActive Transport, Cell NucleusATP-Dependent ProteasesBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCytosolHumansLysosomesMitochondrial ProteinsATP-Dependent ProteasesBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsLONP1 protein, humanMitochondrial ProteinsTFEB protein, humanLONP1MetabolismMitochondriaSalmonellaTFEB

Identifiers

PMID38263327
PMCPMC10897448
OpenAlexW4391132098

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.