Evidence map›Paper›PMID 38822085›Full record

ArticleScientific reports2024

Regulation of TSC2 lysosome translocation and mitochondrial turnover by TSC2 acetylation status.

Patricia Marqués, Jesús Burillo, Carlos González-Blanco, Beatriz Jiménez, Gema García, Ana García-Aguilar, Sarai Iglesias-Fortes, Ángela Lockwood, Carlos Guillén

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. TSC2 is a stress granule suppressor.bioRxiv : the preprint server for biology · 2026
    Article
  2. Review
  3. Sirtuins in mitophagy: key gatekeepers of mitochondrial quality.Molecular and cellular biochemistry · 2025
    Review
  4. Review
  5. Review
  6. Article
  7. 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.

Patricia MarquésDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University of Madrid, Madrid, Spain.
Jesús BurilloCIBER of Diabetes and Associated Metabolic Disorders, Instituto de Salud Carlos III, Madrid, Spain.
Carlos González-BlancoDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University of Madrid, Madrid, Spain.
Beatriz JiménezDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University of Madrid, Madrid, Spain.
Gema GarcíaCIBER of Diabetes and Associated Metabolic Disorders, Instituto de Salud Carlos III, Madrid, Spain.
Ana García-AguilarCIBER of Diabetes and Associated Metabolic Disorders, Instituto de Salud Carlos III, Madrid, Spain.
Sarai Iglesias-FortesDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University of Madrid, Madrid, Spain.
Ángela LockwoodDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University of Madrid, Madrid, Spain.
Carlos GuillénDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University of Madrid, Madrid, Spain. cguillen@ucm.es.

Funding

Ministerio de Ciencia e Innovación PID2020-113361RB-I00
6 · The paper itself

Abstract

Sirtuin1 (SIRT1) activity decreases the tuberous sclerosis complex 2 (TSC2) lysine acetylation status, inhibiting the mechanistic target of rapamycin complex 1 (mTORC1) signalling and concomitantly, activating autophagy. This study analyzes the role of TSC2 acetylation levels in its translocation to the lysosome and the mitochondrial turnover in both mouse embryonic fibroblast (MEF) and in mouse insulinoma cells (MIN6) as a model of pancreatic β cells. Resveratrol (RESV), an activator of SIRT1 activity, promotes TSC2 deacetylation and its translocation to the lysosome, inhibiting mTORC1 activity. An improvement in mitochondrial turnover was also observed in cells treated with RESV, associated with an increase in the fissioned mitochondria, positive autophagic and mitophagic fluxes and an enhancement of mitochondrial biogenesis. This study proves that TSC2 in its deacetylated form is essential for regulating mTORC1 signalling and the maintenance of the mitochondrial quality control, which is involved in the homeostasis of pancreatic beta cells and prevents from several metabolic disorders such as Type 2 Diabetes Mellitus.

Indexed as

LysosomesMitochondriaTuberous Sclerosis Complex 2 ProteinAcetylationAnimalsAutophagyCell Line, TumorFibroblastsInsulin-Secreting CellsMechanistic Target of Rapamycin Complex 1MiceProtein TransportResveratrolSignal TransductionSirtuin 1Mechanistic Target of Rapamycin Complex 1ResveratrolSirtuin 1Tsc2 protein, mouseTuberous Sclerosis Complex 2 ProteinAcetylationLysosomeMitophagymTORC1Pancreatic β cellsTSC2

Identifiers

PMID38822085
PMCPMC11143182

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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.