Evidence map›Paper›PMID 28052107›Full record

ArticlePloS one2017

Ubiquitin Accumulation on Disease Associated Protein Aggregates Is Correlated with Nuclear Ubiquitin Depletion, Histone De-Ubiquitination and Impaired DNA Damage Response.

Adi Ben Yehuda, Marwa Risheq, Ofra Novoplansky, Kirill Bersuker, Ron R Kopito, Michal Goldberg, Michael Brandeis

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Proteotoxic stress and the ubiquitin proteasome system.Seminars in cell & developmental biology · 2024
    Review
  5. Review
  6. Review
  7. Atypical Ubiquitination and Parkinson's Disease.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Quality control of cytoplasmic proteins inside the nucleus.Computational and structural biotechnology journal · 2022
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Minimotifs dysfunction is pervasive in neurodegenerative disorders.Alzheimer's & dementia (New York, N. Y.) · 2018
    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

7 authors at 2 institutions in 2 countries.

Adi Ben YehudaThe Department of Genetics, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem Safra Campus, Jerusalem, Israel.
Marwa RisheqThe Department of Genetics, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem Safra Campus, Jerusalem, Israel.
Ofra NovoplanskyThe Department of Genetics, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem Safra Campus, Jerusalem, Israel.
Kirill BersukerDepartment of Biology, Stanford University, Stanford, California, United States of America.
Ron R KopitoDepartment of Biology, Stanford University, Stanford, California, United States of America.
Michal GoldbergThe Department of Genetics, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem Safra Campus, Jerusalem, Israel.
Michael BrandeisThe Department of Genetics, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem Safra Campus, Jerusalem, Israel.
Hebrew University of Jerusalem · ILStanford University · US

Funding

INSTITUTIONAL TRAINING GRANT IN GENOME SCIENCET32HG000044 · NHGRI · STANFORD UNIVERSITY · PI MICHAEL P. SNYDER · 1995 to 2026
$32.2M
NHGRI NIH HHS T32 HG000044
6 · The paper itself

Abstract

Deposition of ubiquitin conjugates on inclusion bodies composed of protein aggregates is a definitive cytopathological hallmark of neurodegenerative diseases. We show that accumulation of ubiquitin on polyQ IB, associated with Huntington's disease, is correlated with extensive depletion of nuclear ubiquitin and histone de-ubiquitination. Histone ubiquitination plays major roles in chromatin regulation and DNA repair. Accordingly, we observe that cells expressing IB fail to respond to radiomimetic DNA damage, to induce gamma-H2AX phosphorylation and to recruit 53BP1 to damaged foci. Interestingly ubiquitin depletion, histone de-ubiquitination and impaired DNA damage response are not restricted to PolyQ aggregates and are associated with artificial aggregating luciferase mutants. The longevity of brain neurons depends on their capacity to respond to and repair extensive ongoing DNA damage. Impaired DNA damage response, even modest one, could thus lead to premature neuron aging and mortality.

Indexed as

Cell Line, TumorDNA DamageDNA RepairFlow CytometryFluorescent Antibody Technique, IndirectHistonesHumansPeptidesProtein AggregatesUbiquitinUbiquitinationHistonesPeptidespolyglutamineProtein AggregatesUbiquitin

Identifiers

PMID28052107
PMCPMC5215683
OpenAlexW2570707453

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.