Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 360

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Autophagy-mediated clearance of huntingtin aggregates triggered by the insulin-signaling pathway

Open access
Yamamoto, Ai, Cremona, M. Laura, Rothman, James E.·2006·The Journal of Cell Biology

Abstract

Conditional mouse models of polyglutamine diseases, such as Huntington's disease (HD), have revealed that cells can clear accumulated pathogenic proteins if the continuous production of the mutant transgene is halted. Invariably, the clearance of the protein leads to regression of the disease symptoms in mice. In light of these findings, it is critical to determine the pathway responsible for alleviating this protein accumulation to define targets to fight these diseases. In a functional genetic screen of HD, we found that activation of insulin receptor substrate-2, which mediates the signaling cascades of insulin and insulin-like growth factor 1, leads to a macroautophagy-mediated clearance of the accumulated proteins. The macroautophagy is triggered despite activation of Akt, mammalian target of rapamycin (mTOR), and S6 kinase, but still requires proteins previously implicated in macroautophagy, such as Beclin1 and hVps34. These findings indicate that the accumulation of mutant protein can lead to mTOR-independent macroautophagy and that lysosome-mediated degradation of accumulated protein differs from degradation under conditions of starvation.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1083/jcb.200510065

Cites

11 of 11 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 11 references

Cited by

See all 360

Metadata

Authors
Yamamoto, A., Cremona, M. L., & Rothman, J. E.
Venue
The Journal of Cell Biology
Published
2006-02-27
Volume
172
Issue
5
Pages
719-731
ISSN
  • 0021-9525 (ISSN-L)
  • 1540-8140
OpenAlex
W2154404753
Cited by
360
References
11
FWCI
11.34
Type
journal article
Language
en
Open access
green

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: Autophagy-mediated clearance of huntingtin aggregates triggered by the insulin-signaling pathway. https://app.cochat.ai/papers/10.1083/jcb.200510065
The paper
Yamamoto, A., Cremona, M. L., & Rothman, J. E. (2006). Autophagy-mediated clearance of huntingtin aggregates triggered by the insulin-signaling pathway. The Journal of Cell Biology. https://doi.org/10.1083/jcb.200510065

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.