KAISO, a critical regulator of p53-mediated transcription of CDKN1A and apoptotic genes. Koh, D., Han, D., Ryu, H., Choi, W., Jeon, B., Kim, M., Kim, Y., Kim, J. Y., Parry, L., Clarke, A. R., Reynolds, A. B., & Hur, M. Proceedings of the National Academy of Sciences, 111(42):15078–15083, October, 2014. Publisher: National Academy of Sciences Section: Biological Sciences![KAISO, a critical regulator of p53-mediated transcription of CDKN1A and apoptotic genes [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex An unresolved issue in genotoxic stress response is identification of induced regulatory proteins and how these activate tumor suppressor p53 to determine appropriate cell responses. Transcription factor KAISO was previously described to repress transcription following binding to methylated DNA. In this study, we show that KAISO is induced by DNA damage in p53-expressing cells and then interacts with the p53–p300 complex to increase acetylation of p53 K320 and K382 residues, although decreasing K381 acetylation. Moreover, the p53 with this particular acetylation pattern shows increased DNA binding and potently induces cell cycle arrest and apoptosis by activating transcription of CDKN1A (cyclin-dependent kinase inhibitor 1) and various apoptotic genes. Analogously, in Kaiso KO mouse embryonic fibroblast cells, p53-to-promoter binding and up-regulation of p21 and apoptosis gene expression is significantly compromised. KAISO may therefore be a critical regulator of p53-mediated cell cycle arrest and apoptosis in response to various genotoxic stresses in mammalian cells.
@article{koh_kaiso_2014,
title = {{KAISO}, a critical regulator of p53-mediated transcription of {CDKN1A} and apoptotic genes},
volume = {111},
issn = {0027-8424, 1091-6490},
url = {https://www.pnas.org/content/111/42/15078},
doi = {10.1073/pnas.1318780111},
abstract = {An unresolved issue in genotoxic stress response is identification of induced regulatory proteins and how these activate tumor suppressor p53 to determine appropriate cell responses. Transcription factor KAISO was previously described to repress transcription following binding to methylated DNA. In this study, we show that KAISO is induced by DNA damage in p53-expressing cells and then interacts with the p53–p300 complex to increase acetylation of p53 K320 and K382 residues, although decreasing K381 acetylation. Moreover, the p53 with this particular acetylation pattern shows increased DNA binding and potently induces cell cycle arrest and apoptosis by activating transcription of CDKN1A (cyclin-dependent kinase inhibitor 1) and various apoptotic genes. Analogously, in Kaiso KO mouse embryonic fibroblast cells, p53-to-promoter binding and up-regulation of p21 and apoptosis gene expression is significantly compromised. KAISO may therefore be a critical regulator of p53-mediated cell cycle arrest and apoptosis in response to various genotoxic stresses in mammalian cells.},
language = {en},
number = {42},
urldate = {2021-04-04},
journal = {Proceedings of the National Academy of Sciences},
author = {Koh, Dong-In and Han, Dohyun and Ryu, Hoon and Choi, Won-Il and Jeon, Bu-Nam and Kim, Min-Kyeong and Kim, Youngsoo and Kim, Jin Young and Parry, Lee and Clarke, Alan R. and Reynolds, Albert B. and Hur, Man-Wook},
month = oct,
year = {2014},
pmid = {25288747},
note = {Publisher: National Academy of Sciences
Section: Biological Sciences},
keywords = {KAISO, apoptosis, cell cycle arrest, p300, p53},
pages = {15078--15083},
}
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