Evidence map›Paper›PMID 16141322›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Increased susceptibility of cytoplasmic over nuclear polyglutamine aggregates to autophagic degradation.

Atsushi Iwata, John C Christianson, Mirella Bucci, Lisa M Ellerby, Nobuyuki Nukina, Lysia S Forno, Ron R Kopito

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. 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
–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

150 citing papers in PubMed.

  1. Article
  2. GFP-free live neuron quantitative imaging reveals compartmentalization and growth dynamics of polyQ aggregates.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Regulation ofMolecular biology of the cell · 2022
    Article
  15. Review
  16. Review
  17. Cell Autophagy in NASH and NASH-Related Hepatocellular Carcinoma.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Intercellular Propagation and Aggregate Seeding of Mutant Ataxin-1.Journal of molecular neuroscience : MN · 2022
    Article
  20. Review

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

7 authors.

Atsushi IwataDepartment of Biological Sciences, BIO-X Program, Stanford University, Stanford, CA 94305-5430.
John C Christianson
Mirella Bucci
Lisa M Ellerby
Nobuyuki Nukina
Lysia S Forno
Ron R Kopito

Funding

Protein Aggregation and Inclusion Body FormationR01NS042842 · NINDS · STANFORD UNIVERSITY · PI KOPITO, RON R · 2002 to 2016
$6.1M
TRIPLET REPEAT DISEASE: REQUIREMENT FOR CASPASE CLEAVAGER01NS040251 · NINDS · BUCK INSTITUTE FOR RESEARCH ON AGING · PI ELLERBY, LISA M. · 1999 to 2007
$3.1M
Protein Aggregation and Inclusion Body FormationR56NS042842 · NINDS · STANFORD UNIVERSITY · PI KOPITO, RON R · 2007 to 2019
$1.1M
NINDS NIH HHS NS042842NINDS NIH HHS NS40251NINDS NIH HHS R01 NS040251NINDS NIH HHS R01 NS042842NINDS NIH HHS R56 NS042842
6 · The paper itself

Abstract

CNS neurons are endowed with the ability to recover from cytotoxic insults associated with the accumulation of proteinaceous aggregates in mouse models of polyglutamine disease, but the cellular mechanism underlying this phenomenon is unknown. Here, we show that autophagy is essential for the elimination of aggregated forms of mutant huntingtin and ataxin-1 from the cytoplasmic but not nuclear compartments. Human orthologs of yeast autophagy genes, molecular determinants of autophagic vacuole formation, are recruited to cytoplasmic but not nuclear inclusion bodies in vitro and in vivo. These data indicate that autophagy is a critical component of the cellular clearance of toxic protein aggregates and may help to explain why protein aggregates are more toxic when directed to the nucleus.

Indexed as

AutophagyAtaxin-1AtaxinsAutophagy-Related Protein 12Autophagy-Related Protein 5Cell LineCell NucleusCytoplasmHumansHuntingtin ProteinHuntington DiseaseMicrotubule-Associated ProteinsModels, BiologicalNerve Tissue ProteinsNuclear ProteinsPeptidesAtaxin-1AtaxinsATG12 protein, humanATG5 protein, humanATXN1 protein, humanAtxn1 protein, mouseAutophagy-Related Protein 12Autophagy-Related Protein 5HTT protein, humanHuntingtin ProteinMicrotubule-Associated ProteinsNerve Tissue ProteinsNuclear ProteinsPeptidespolyglutamineProteinsSmall Ubiquitin-Related Modifier Proteins

Identifiers

PMID16141322
PMCPMC1201602

What OpenQuestion holds

Textmetadata
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.