Evidence map›Paper›PMID 37418003›Full record

ArticleThe Journal of cell biology2023

PTEN is both an activator and a substrate of chaperone-mediated autophagy.

Katherine K Zhang, Calvin M Burns, Mary E Skinner, David B Lombard, Richard A Miller, S Joseph Endicott

Open access · greenAbstract read
In one paragraph

Article in The Journal of cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Dual role of autophagy in bone metastasis: mechanistic insights and therapeutic targeting.American journal of clinical and experimental urology · 2025
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Roles of Stress Response in Autophagy Processes and Aging-Related Diseases.International journal of molecular sciences · 2023
    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

6 authors at 2 institutions in 1 country.

Katherine K ZhangCollege of Literature, Arts, and the Sciences, University of Michigan, Ann Arbor , Ann Arbor, MI, USA.ORCID 0000-0001-9638-7358
Calvin M BurnsDepartment of Pathology, University of Michigan, Ann Arbor, Ann Arbor, MI, USA.ORCID 0000-0002-8314-6544
Mary E SkinnerDepartment of Neurology, University of Michigan, Ann Arbor, Ann Arbor, MI, USA.ORCID 0000-0002-3853-1478
David B LombardDepartment of Pathology and Laboratory Medicine, and Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, Miami, FL, USA.ORCID 0000-0002-4292-0185
Richard A MillerDepartment of Pathology, University of Michigan, Ann Arbor, Ann Arbor, MI, USA.ORCID 0000-0001-9266-9649
S Joseph EndicottDepartment of Pathology, University of Michigan, Ann Arbor, Ann Arbor, MI, USA.ORCID 0000-0002-8237-9784
University of Michigan · USUniversity of Miami · US

Funding

Systems BiologyU19AG023122 · NIA · TRANSLATIONAL GENOMICS RESEARCH INST · PI FRED H GAGE · 2004 to 2026
$102.6M
Research Education CoreP30AG024824 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Neil Alexander · 2004 to 2026
$29.2M
Laboratory for Anti-Geric Testing, Evaluation and ResearchU01AG022303 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RICHARD A MILLER · 2003 to 2026
$25.4M
Integrative Omics to enhance therapeutics development for healthy agingUH3AG064706 · NIA · TRANSLATIONAL GENOMICS RESEARCH INST · PI MILLER, RICHARD A, SCHORK, NICHOLAS JOSEPH · 2021 to 2024
$3.3M
Regulation of one carbon metabolism and epigenetics by SIRT5R01GM101171 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOMBARD, DAVID BENNER · 2012 to 2021
$2.6M
SIRT5 inhibitors and degraders as novel treatments for Ewing sarcomaR01CA253986 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI David Benner Lombard, NOURI NEAMATI · 2022 to 2026
$2.1M
NCI NIH HHS R01 CA253986NIA NIH HHS P30 AG024824NIA NIH HHS U01 AG022303NIA NIH HHS U19 AG023122NIA NIH HHS UH3 AG064706NIGMS NIH HHS R01 GM101171
6 · The paper itself

Abstract

PTEN is a crucial negative regulator of the INS/PI3K/AKT pathway and is one of the most commonly mutated tumor suppressors in cancer. Global overexpression (OE) of PTEN in mice shifts metabolism to favor oxidative phosphorylation over glycolysis, reduces fat mass, and extends the lifespan of both sexes. We demonstrate that PTEN regulates chaperone-mediated autophagy (CMA). Using cultured cells and mouse models, we show that PTEN OE enhances CMA, dependent upon PTEN's lipid phosphatase activity and AKT inactivation. Reciprocally, PTEN knockdown reduces CMA, which can be rescued by inhibiting class I PI3K or AKT. Both PTEN and CMA are negative regulators of glycolysis and lipid droplet formation. We show that suppression of glycolysis and lipid droplet formation downstream of PTEN OE depends on CMA activity. Finally, we show that PTEN protein levels are sensitive to CMA and that PTEN accumulates in lysosomes with elevated CMA. Collectively, these data suggest that CMA is both an effector and a regulator of PTEN.

Indexed as

Chaperone-Mediated AutophagyPTEN PhosphohydrolaseAnimalsCell LineFemaleGlycolysisLysosomesMaleMiceOxidative PhosphorylationPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID37418003
PMCPMC10327811
OpenAlexW4383479724

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.