The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
Aurora-A Abrogation of p53 DNA Binding and Transactivation Activity by Phosphorylation of Serine 215
Open accessAbstract
The tumor suppressor p53 is important in the decision to either arrest cell cycle progression or induce apoptosis in response to a variety of stimuli. p53 posttranslational modifications and association with other proteins have been implicated in the regulation of its stability and transactivation activity. Here we show that p53 is phosphorylated by the mitotic kinase Aurora-A at serine 215. Unlike most identified phosphorylation sites of p53 that positively associate with p53 function (Brooks, C. L., and Gu, W. (2003) Curr. Opin. Cell Biol. 15, 164-171), the phosphorylation of p53 by Aurora-A at Ser-215 abrogates p53 DNA binding and transactivation activity. Downstream target genes of p53, such as p21Cip/WAF1 and PTEN, were inhibited by Aurora-A in a Ser-215 phosphorylation-dependent manner (i.e. phosphomimic p53-S215D lost and non-phosphorylatable p53-S215A retained normal p53 function). As a result, Aurora-A overrides the apoptosis and cell cycle arrest induced by cisplatin and gamma-irradiation, respectively. However, the effect of Aurora-A on p53 DNA binding and transactivation activity was not affected by phosphorylation of Ser-315, a recently identified Aurora-A phosphorylation site of p53 (Katayama, H., Sasai, K., Kawai, H., Yuan, Z. M., Bondaruk, J., Suzuki, F., Fujii, S., Arlinghaus, R. B., Czerniak, B. A., and Sen, S. (2004) Nat. Genet. 36, 55-62). Our data indicate that phosphorylation of p53 at Ser-215 by Aurora-A is a major mechanism to inactivate p53 and can provide a molecular insight for Aurora-A function.
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3 retracted
Yuan, Z., Feldman, R. I., Sun, M., Olashaw, N., Coppola, D., Sussman, G. E., Shelley, S. A., Nicosia, S. V., & Cheng, J. Q. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m203636200 · Cited by 57
Self-citationRetractedPositive Feedback Regulation between Akt2 and MyoD during Muscle Differentiation
Kaneko, S., Feldman, R. I., Yu, L., Wu, Z., Gritsko, T. M., Shelley, S. A., Nicosia, S. V., Nobori, T., & Cheng, J. Q. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m201733200 · Cited by 55
Self-citationRetractedKaneko, S., Feldman, R. I., Yu, L., Wu, Z., Gritsko, T. M., Shelley, S. A., Nicosia, S. V., Nobori, T., & Cheng, J. Q. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.a116.201733 · Cited by 53
Self-citationRetractedCurrent protocols in molecular biology
Sargent, T. (1988) · Analytical Biochemistry · doi:10.1016/0003-2697(88)90147-9 · Cited by 7,205
Tumour amplified kinase STK15/BTAK induces centrosome amplification, aneuploidy and transformation
Zhou, H., Kuang, J., Zhong, L., Kuo, W.-L., Gray, J., Sahin, A., Brinkley, B., & Sen, S. (1998) · Nature Genetics · doi:10.1038/2496 · Cited by 1,276
A role for ATR in the DNA damage-induced phosphorylation of p53
Tibbetts, R. S., Brumbaugh, K. M., Williams, J. M., Sarkaria, J. N., Cliby, W. A., Shieh, S.-Y., Taya, Y., Prives, C., & Abraham, R. T. (1999) · Genes & Development · doi:10.1101/gad.13.2.152 · Cited by 1,046
Database of p53 gene somatic mutations in human tumors and cell lines.
Hollstein, M. C., Rice, K., Greenblatt, M. S., Soussi, T., Fuchs, R., Sørlie, T., Hovig, E. J., Smith‐Sørensen, B., Montesano, R., & Harris, C. C. (1994) · Europe PMC (PubMed Central) · Cited by 858
Abnormal Centrosome Amplification in the Absence of p53
Fukasawa, K., Choi, T., Kuriyama, R., Rulong, S., & Woude, G. F. V. (1996) · Science · doi:10.1126/science.271.5256.1744 · Cited by 797
Anand, S., Penrhyn-Lowe, S., & Venkitaraman, A. R. (2003) · Cancer Cell · doi:10.1016/s1535-6108(02)00235-0 · Cited by 631
Phosphorylation by aurora kinase A induces Mdm2-mediated destabilization and inhibition of p53
Katayama, H., Sasai, K., Kawai, H., Yuan, Z.-M., Bondaruk, J., Suzuki, F., Fujii, S., Arlinghaus, R. B., Czerniak, B. A., & Sen, S. (2004) · Nature Genetics · doi:10.1038/ng1279 · Cited by 588
Cited by
Regulating the p53 pathway: in vitro hypotheses, in vivo veritas
Toledo, F., & Wahl, G. M. (2006) · Nature reviews. Cancer · doi:10.1038/nrc2012 · Cited by 1,286
Targeting AURKA in Cancer: molecular mechanisms and opportunities for Cancer therapy
Du, R., Huang, C., Liu, K., Li, X., & Dong, Z. (2021) · Molecular Cancer · doi:10.1186/s12943-020-01305-3 · Cited by 586
Aurora A kinase (AURKA) in normal and pathological cell division
Nikonova, A. S., Astsaturov, I., Serebriiskii, I. G., Dunbrack, R. L., & Golemis, E. A. (2013) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-012-1073-7 · Cited by 448
The Aurora kinase family in cell division and cancer
Vader, G., & Lens, S. M. A. (2008) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2008.07.003 · Cited by 417
Aurora kinases: novel therapy targets in cancers
Tang, A., Gao, K., Chu, L., Zhang, R., Yang, J., & Zheng, J. (2017) · Oncotarget · doi:10.18632/oncotarget.14893 · Cited by 382
Metadata
- Authors
- Liu, Q., Kaneko, S., Yang, L., Feldman, R. I., Nicosia, S. V., Chen, J., & Cheng, J. Q.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2004-12
- Volume
- 279
- Issue
- 50
- Pages
- 52175-52182
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2091312754
- Cited by
- 334
- References
- 38
- FWCI
- 7.05
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Liu, Q., Kaneko, S., Yang, L., Feldman, R. I., Nicosia, S. V., Chen, J., & Cheng, J. Q. (2004). Aurora-A Abrogation of p53 DNA Binding and Transactivation Activity by Phosphorylation of Serine 215. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m406802200
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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