Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 797

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Abnormal Centrosome Amplification in the Absence of p53

Fukasawa, Kenji, Choi, Taesaeng, Kuriyama, Ryoko, Rulong, Shen, Woude, George F. Vande·1996·Science

Abstract

The centrosome plays a vital role in mitotic fidelity, ensuring establishment of bipolar spindles and balanced chromosome segregation. Centrosome duplication occurs only once during the cell cycle and is therefore highly regulated. Here, it is shown that in mouse embryonic fibroblasts (MEFs) lacking the p53 tumor suppressor protein, multiple copies of functionally competent centrosomes are generated during a single cell cycle. In contrast, MEFs prepared from normal mice or mice deficient in the retinoblastoma tumor suppressor gene product do not display these abnormalities. The abnormally amplified centrosomes profoundly affect mitotic fidelity, resulting in unequal segregation of chromosomes. These observations implicate p53 in the regulation of centrosome duplication and suggest one possible mechanism by which the loss of p53 may cause genetic instability.

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 · 10.1126/science.271.5256.1744

Cites

5 of 5 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 5 references

Cited by

See all 797

Metadata

Authors
Fukasawa, K., Choi, T., Kuriyama, R., Rulong, S., & Woude, G. F. V.
Venue
Science
Published
1996-03-22
Volume
271
Issue
5256
Pages
1744-1747
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2040154374
Cited by
797
References
5
FWCI
20.83
Type
journal article
Language
en
Open access
closed

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: Abnormal Centrosome Amplification in the Absence of p53. https://app.cochat.ai/papers/10.1126/science.271.5256.1744
The paper
Fukasawa, K., Choi, T., Kuriyama, R., Rulong, S., & Woude, G. F. V. (1996). Abnormal Centrosome Amplification in the Absence of p53. Science. https://doi.org/10.1126/science.271.5256.1744

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.