Evidence map›Paper›PMID 25880015›Full record

ArticleNature communications2015

Regulated degradation of Chk1 by chaperone-mediated autophagy in response to DNA damage.

Caroline Park, Yousin Suh, Ana Maria Cuervo

Open access · goldAbstract read
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 150 papers.

0numbers the graph read from it
0cells of the map it votes in
150citing papers in PubMed
15.3field-weighted citation impact, top 1% 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

150 citing papers in PubMed, 211 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. A C-degron regulates Chk1 kinase by allowing stability of inactive Chk1 and by making it short- lived upon activation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Targeting Lysosomes for Enhanced Anti-Cancer Therapeutics and Immune Response.International journal of biological sciences · 2026
    Review
  15. Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

90 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

3 authors at 1 institution in 1 country.

Caroline Park1] Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA [2] Department of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA [3] Institute for Aging Research, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA.
Yousin Suh1] Department of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA [2] Institute for Aging Research, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA.
Ana Maria Cuervo1] Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA [2] Institute for Aging Research, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA.ORCID 000000020771700X
Albert Einstein College of Medicine · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
THE IMPACT OF CELLULAR DEFENSE ON THE ROLE OF Ku80 IN GENOME MAINTENANCE AND LONGP01AG017242 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI VIJG, JAN · 1999 to 2023
$46.1M
Role of Autophagy in T Cell Function and Immunosenescence (Project 3)P01AG031782 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI MACIAN, FERNANDO · 2009 to 2024
$36.2M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
Special Animal CoreP30DK041296 · NIDDK · YESHIVA UNIVERSITY · PI WOLKOFF, ALLAN W · 1989 to 2018
$22.9M
Einstein's Nathan Shock Center of Excellence in Basic Biology of AgingP30AG038072 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI VIJG, JAN · 2010 to 2024
$10.8M
Control of vesicular trafficking in the hepatocyte.R01DK098408 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CUERVO, ANA MARIA, WOLKOFF, ALLAN W · 2013 to 2022
$5.6M
Decreased Protein Degradation in AgingR37AG021904 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CUERVO, ANA MARIA · 2013 to 2022
$4.4M
DECREASED PROTEIN DEGRADATION IN AGINGR01AG021904 · NIA · YESHIVA UNIVERSITY · PI CUERVO, ANA MARIA · 2003 to 2012
$3.7M
New Methods to Uncover Global Transcriptional Programs for Disease Risk VariantsR01GM104459 · NIGMS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI SUH, YOUSIN · 2013 to 2016
$2.5M
Association Analysis- SNPs in Longevity Assurance GenesR01AG024391 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SUH, YOUSIN · 2004 to 2008
$1.6M
NCI NIH HHS P30 CA013330NIA NIH HHS AG031782NIA NIH HHS AG038072NIA NIH HHS AG17242NIA NIH HHS AG21904NIA NIH HHS P01 AG017242NIA NIH HHS P01 AG031782NIA NIH HHS P30 AG038072NIA NIH HHS R01 AG021904NIA NIH HHS R01 AG024391NIA NIH HHS R37 AG021904NIDDK NIH HHS DK098408NIDDK NIH HHS P30 DK041296NIDDK NIH HHS R01 DK098408NIGMS NIH HHS GM104459NIGMS NIH HHS R01 GM104459NIGMS NIH HHS T32 GM007288NIGMS NIH HHS T32GM007288
6 · The paper itself

Abstract

Chaperone-mediated autophagy (CMA) is activated in response to cellular stressors to prevent cellular proteotoxicity through selective degradation of altered proteins in lysosomes. Reduced CMA activity contributes to the decrease in proteome quality in disease and ageing. Here, we report that CMA is also upregulated in response to genotoxic insults and that declined CMA functionality leads to reduced cell survival and genomic instability. This role of CMA in genome quality control is exerted through regulated degradation of activated checkpoint kinase 1 (Chk1) by this pathway after the genotoxic insult. Nuclear accumulation of Chk1 in CMA-deficient cells compromises cell cycle progression and prolongs the time that DNA damage persists in these cells. Furthermore, blockage of CMA leads to hyperphosphorylation and destabilization of the MRN (Mre11-Rad50-Nbs1) complex, which participates in early steps of particular DNA repair pathways. We propose that CMA contributes to maintain genome stability by assuring nuclear proteostasis.

Indexed as

Acid Anhydride HydrolasesAnimalsATP-Binding Cassette TransportersAutophagyCell CycleCell Cycle ProteinsCell SurvivalCheckpoint Kinase 1Comet AssayDNA-Binding ProteinsDNA DamageDNA Repair EnzymesGenomic InstabilityLysosomesMaleMiceAcid Anhydride HydrolasesATP-Binding Cassette TransportersCell Cycle ProteinsCheckpoint Kinase 1Chek1 protein, mouseChek1 protein, ratDNA-Binding ProteinsDNA Repair EnzymesMRE11 Homologue ProteinMre11 protein, ratNuclear ProteinsProtein KinasesRad50 protein, mouseRNA, Messenger

Identifiers

PMID25880015
PMCPMC4400843
OpenAlexW1983049322

What OpenQuestion holds

Textmetadata
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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.