Student or educator? Sign up with your school email and get 6 months of Pro free.
CoChat
Sign Up
Cited by 366

The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.

Regulation and localization of tyrosine216phosphorylation of glycogen synthase kinase-3β in cellular and animal models of neuronal degeneration

Open access
Bhat, Ratan V., Shanley, Jason, Correll, Maryann P., Fieles, William E., Keith, Richard A., Scott, Clay W., Lee, Chi-Ming·2000·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.190297597
Open this paper in CoChat — free account

Abstract

Inactivation of glycogen synthase kinase-3β (GSK3β) by S 9 phosphorylation is implicated in mechanisms of neuronal survival. Phosphorylation of a distinct site, Y 216, on GSK3β is necessary for its activity; however, whether this site can be regulated in cells is unknown. Therefore we examined the regulation of Y 216 phosphorylation on GSK3β in models of neurodegeneration. Nerve growth factor withdrawal from differentiated PC12 cells and staurosporine treatment of SH-SY5Y cells led to increased phosphorylation at Y 216, GSK3β activity, and cell death. Lithium and insulin, agents that lead to inhibition of GSK3β and adenoviral-mediated transduction of dominant negative GSK3β constructs, prevented cell death by the proapoptotic stimuli. Inhibitors induced S 9 phosphorylation and inactivation of GSK3β but did not affect Y 216 phosphorylation, suggesting that S 9 phosphorylation is sufficient to override GSK3β activation by Y 216 phosphorylation. Under the conditions examined, increased Y 216 phosphorylation on GSK3β was not an autophosphorylation response. In resting cells, Y 216 phosphorylation was restricted to GSK3β present at focal adhesion sites. However, after staurosporine, a dramatic alteration in the immunolocalization pattern was observed, and Y 216-phosphorylated GSK3β selectively increased within the nucleus. In rats, Y 216 phosphorylation was increased in degenerating cortical neurons induced by ischemia. Taken together, these results suggest that Y 216 phosphorylation of GSK3β represents an important mechanism by which cellular insults can lead to neuronal death.

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 · 10.1073/pnas.190297597

Cites

31 of 31 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 31 references

Cited by

See all 366

Metadata

Authors
Bhat, R. V., Shanley, J., Correll, M. P., Fieles, W. E., Keith, R. A., Scott, C. W., & Lee, C.-M.
Venue
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Published
2000-09-19
Volume
97
Issue
20
Pages
11074-11079
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.190297597
OpenAlex
W2055116915
Cited by
366
References
31
FWCI
5.86
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: Regulation and localization of tyrosine216phosphorylation of glycogen synthase kinase-3β in cellular and animal models of neuronal degeneration. https://app.cochat.ai/papers/10.1073/pnas.190297597
The paper
Bhat, R. V., Shanley, J., Correll, M. P., Fieles, W. E., Keith, R. A., Scott, C. W., & Lee, C.-M. (2000). Regulation and localization of tyrosine216phosphorylation of glycogen synthase kinase-3β in cellular and animal models of neuronal degeneration. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.190297597

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.