The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
CDK2-Dependent Phosphorylation of FOXO1 as an Apoptotic Response to DNA Damage
Abstract
The function of cyclin-dependent kinase 2 (CDK2) is often abolished after DNA damage. The inhibition of CDK2 plays a central role in DNA damage–induced cell cycle arrest and DNA repair. However, whether CDK2 also influences the survival of cells under genotoxic stress is unknown. Forkhead box O (FOXO) transcription factors are emerging as key regulators of cell survival. CDK2 specifically phosphorylated FOXO1 at serine-249 (Ser 249 ) in vitro and in vivo. Phosphorylation of Ser 249 resulted in cytoplasmic localization and inhibition of FOXO1. This phosphorylation was abrogated upon DNA damage through the cell cycle checkpoint pathway that is dependent on the protein kinases Chk1 and Chk2. Moreover, silencing of FOXO1 by small interfering RNA diminished DNA damage–induced death in both p53-deficient and p53-proficient cells. This effect was reversed by restored expression of FOXO1 in a manner depending on phosphorylation of Ser 249 . Functional interaction between CDK2 and FOXO1 provides a mechanism that regulates apoptotic cell death after DNA strand breakage.
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.
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.
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
Kastan, M. B., Zhan, Q., El-Deiry, W. S., Carrier, F., Jacks, T., Walsh, W. V., Plunkett, B. S., Vogelstein, B., & Fornace, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90593-2 · Cited by 3,047
Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions
Gorgoulis, V. G., Vassiliou, L.-V. F., Karakaidos, P., Zacharatos, P., Kotsinas, A., Liloglou, T., Venere, M., DiTullio, R. A., Kastrinakis, N. G., Levy, B., et al. (2005) · Nature · doi:10.1038/nature03485 · Cited by 2,009
Forkhead transcription factor FOXO3a protects quiescent cells from oxidative stress
Kops, G. J. P. L., Dansen, T. B., Polderman, P. E., Saarloos, I., Wirtz, K. W. A., Coffer, P. J., Huang, T.-T., Bos, J. L., Medema, R. H., & Burgering, B. M. T. (2002) · Nature · doi:10.1038/nature01036 · Cited by 1,580
The ATM-Chk2-Cdc25A checkpoint pathway guards against radioresistant DNA synthesis
Falck, J., Mailand, N., Syljuåsen, R. G., Bartek, J., & Lukas, J. (2001) · Nature · doi:10.1038/35071124 · Cited by 1,085
Rapid Destruction of Human Cdc25A in Response to DNA Damage
Mailand, N., Falck, J., Lukas, C., Syljuåsen, R. G., Welcker, M., Bartek, J., & Lukas, J. (2000) · Science · doi:10.1126/science.288.5470.1425 · Cited by 787
Checking on DNA damage in S phase
Bartek, J., Lukas, C., & Lukas, J. (2004) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1493 · Cited by 758
Cited by
ATM and ATR Substrate Analysis Reveals Extensive Protein Networks Responsive to DNA Damage
Matsuoka, S., Ballif, B. A., Smogorzewska, A., McDonald, E. R., Hurov, K. E., Luo, J., Bakalarski, C. E., Zhao, Z., Solimini, N., Lerenthal, Y., et al. (2007) · Science · doi:10.1126/science.1140321 · Cited by 3,075
Calnan, D. R., & Brunet, A. (2008) · Oncogene · doi:10.1038/onc.2008.21 · Cited by 1,170
Dynamic FoxO transcription factors
Huang, H., & Tindall, D. J. (2007) · Journal of Cell Science · doi:10.1242/jcs.001222 · Cited by 1,113
Self-citationFOXOs: signalling integrators for homeostasis maintenance
Eijkelenboom, A., & Burgering, B. M. T. (2013) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3507 · Cited by 1,080
The emerging roles of forkhead box (Fox) proteins in cancer
Myatt, S. S., & Lam, E. W. F. (2007) · Nature Reviews Cancer · doi:10.1038/nrc2223 · Cited by 1,070
Metadata
- Authors
- Huang, H., Regan, K. M., Lou, Z., Chen, J., & Tindall, D. J.
- Venue
- Science
- Published
- 2006-10-13
- Volume
- 314
- Issue
- 5797
- Pages
- 294-297
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2056677650
- Cited by
- 336
- References
- 6
- FWCI
- 8.23
- 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: CDK2-Dependent Phosphorylation of FOXO1 as an Apoptotic Response to DNA Damage. https://app.cochat.ai/papers/10.1126/science.1130512
- The paper
- Huang, H., Regan, K. M., Lou, Z., Chen, J., & Tindall, D. J. (2006). CDK2-Dependent Phosphorylation of FOXO1 as an Apoptotic Response to DNA Damage. Science. https://doi.org/10.1126/science.1130512
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.