The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
p53 Mediates Cellular Dysfunction and Behavioral Abnormalities in Huntington’s Disease
Open accessOverview
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.
Integrity signals
Registry
Cites
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.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“mHtt containing expanded polyglutamine (polyQ) tracts increases p53 levels and transcriptional activity in neuronal cells by binding to p53.251”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [251]
In the citing paper
“Affected brain regions in HD patients, HD animal models, and cells overexpressing mHtt present elevated p53 levels.251,255”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [251]
In the citing paper
“inhibition of p53 activity with a small-molecule antagonist of p53, pifithrin-α, or by genetic ablation effectively diminished many of the symptoms in models of these p53-dependent diseases”
From p53 at a glance (2010) · cites this paper as Bae et al., 2005
In the citing paper
“Furthermore, in several neurological disorders, including Alzheimer's, Parkinson's and Huntington's diseases, p53-mediated neuronal apoptosis also contributes to the associated pathologies (Bae et al., 2005; Bretaud et al., 2007; Culmsee and Mattson, 2005; Duan et al., 2002).”
From p53 at a glance (2010) · cites this paper as Bae et al., 2005
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
MACDONALD, M. (1993) · Cell · doi:10.1016/0092-8674(93)90585-e · Cited by 8,366
Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607 · cited 8×
“Because nuclear p53 regulates many mitochondrial genes and genes for oxidative stress (Sharpless and DePinho, 2002; Vogelstein et al., 2000), we hypothesized that p53 might link the nuclear and mitochondrial pathologies in HD.”
BackgroundInfluentialMice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
Tumor suppressor p53 is a direct transcriptional activator of the human bax gene
Toshiyuki, M., & Reed, J. C. (1995) · Cell · doi:10.1016/0092-8674(95)90412-3 · Cited by 4,063
Direct Activation of Bax by p53 Mediates Mitochondrial Membrane Permeabilization and Apoptosis
Chipuk, J. E., Kuwana, T., Bouchier-Hayes, L., Droin, N. M., Newmeyer, D. D., Schuler, M., & Green, D. R. (2004) · Science · doi:10.1126/science.1092734 · Cited by 2,108 · cited 1×
“The increased p53 occurs selectively in the P1 fractions designated as crude nuclei (Figure 1A) in 1% SDS-soluble, nonaggregate fractions (Figure 1C), implying that the transactivation-independent role for p53 in the mitochondria is unlikely (Chipuk et al., 2004).”
BackgroundDefinition of a consensus binding site for p53
El-Deiry, W. S., Kern, S. E., Pietenpol, J. A., Kinzler, K. W., & Vogelstein, B. (1992) · Nature Genetics · doi:10.1038/ng0492-45 · Cited by 1,985
Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death
Arrasate, M., Mitra, S., Schweitzer, E. S., Segal, M. R., & Finkbeiner, S. (2004) · Nature · doi:10.1038/nature02998 · Cited by 1,979
A Chemical Inhibitor of p53 That Protects Mice from the Side Effects of Cancer Therapy
Komarov, P. G., Komarova, E. A., Kondratov, R. V., Christov-Tselkov, K., Coon, J. S., Chernov, M. V., & Gudkov, A. V. (1999) · Science · doi:10.1126/science.285.5434.1733 · Cited by 1,270
Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines
Panov, A. V., Gutekunst, C.-A., Leavitt, B. R., Hayden, M. R., Burke, J. R., Strittmatter, W. J., & Greenamyre, J. T. (2002) · Nature Neuroscience · doi:10.1038/nn884 · Cited by 1,030
Browne, S. E., Bowling, A. C., Macgarvey, U., Baik, M. J., Berger, S. C., Muquit, M. M. K., Bird, E. D., & Beal, M. F. (1997) · Annals of Neurology · doi:10.1002/ana.410410514 · Cited by 885
Cited by
Mitochondrial Dysfunction and Oxidative Stress in Neurodegenerative Diseases
Lin, M. T., & Beal, M. F. (2006) · Nature · doi:10.1038/nature05292 · Cited by 6,455
Blinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163
Telomere dysfunction induces metabolic and mitochondrial compromise
Sahin, E., Colla, S., Liesa, M., Moslehi, J., Müller, F. L., Guo, M., Cooper, M., Kotton, D., Fabian, A. J., Walkey, C., et al. (2011) · Nature · doi:10.1038/nature09787 · Cited by 1,319
Mitochondria in neuroplasticity and neurological disorders
Mattson, M. P., Gleichmann, M., & Cheng, A. (2008) · Neuron · doi:10.1016/j.neuron.2008.10.010 · Cited by 1,081
Vousden, K. H., & Ryan, K. M. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2715 · Cited by 959
Metadata
- Authors
- Bae, B.-I., Xu, H., Igarashi, S., Fujimuro, M., Agrawal, N., Taya, Y., Hayward, S. D., Moran, T. H., Montell, C., Ross, C. A., Snyder, S. H., & Sawa, A.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2005-07
- Volume
- 47
- Issue
- 1
- Pages
- 29-41
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2061258627
- Cited by
- 485
- References
- 12
- FWCI
- 10.98
- Type
- journal article
- Language
- en
- Open access
- bronze
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: p53 Mediates Cellular Dysfunction and Behavioral Abnormalities in Huntington’s Disease. https://app.cochat.ai/papers/10.1016/j.neuron.2005.06.005
- The paper
- Bae, B.-I., Xu, H., Igarashi, S., Fujimuro, M., Agrawal, N., Taya, Y., Hayward, S. D., Moran, T. H., Montell, C., Ross, C. A., Snyder, S. H., & Sawa, A. (2005). p53 Mediates Cellular Dysfunction and Behavioral Abnormalities in Huntington’s Disease. Neuron. https://doi.org/10.1016/j.neuron.2005.06.005
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.
