Mitotic Kinases and p53 Signaling
Mitosis is tightly regulated and any errors in this process often lead to aneuploidy, genomic instability, and tumorigenesis. Deregulation of mitotic kinases is significantly associated with improper cell division and aneuploidy. Because of their importance during mitosis and the relevance to ca...
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Format: | Article |
Language: | English |
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Wiley
2012-01-01
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Series: | Biochemistry Research International |
Online Access: | http://dx.doi.org/10.1155/2012/195903 |
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author | Geun-Hyoung Ha Eun-Kyoung Yim Breuer |
author_facet | Geun-Hyoung Ha Eun-Kyoung Yim Breuer |
author_sort | Geun-Hyoung Ha |
collection | DOAJ |
description | Mitosis is tightly regulated and any errors in this process often lead to aneuploidy, genomic instability, and tumorigenesis. Deregulation of mitotic kinases is significantly associated with improper cell division and aneuploidy. Because of their importance during mitosis and the relevance to cancer, mitotic kinase signaling has been extensively studied over the past few decades and, as a result, several mitotic kinase inhibitors have been developed. Despite promising preclinical results, targeting mitotic kinases for cancer therapy faces numerous challenges, including safety and patient selection issues. Therefore, there is an urgent need to better understand the molecular mechanisms underlying mitotic kinase signaling and its interactive network. Increasing evidence suggests that tumor suppressor p53 functions at the center of the mitotic kinase signaling network. In response to mitotic spindle damage, multiple mitotic kinases phosphorylate p53 to either activate or deactivate p53-mediated signaling. p53 can also regulate the expression and function of mitotic kinases, suggesting the existence of a network of mutual regulation, which can be positive or negative, between mitotic kinases and p53 signaling. Therefore, deciphering this regulatory network will provide knowledge to overcome current limitations of targeting mitotic kinases and further improve the results of targeted therapy. |
format | Article |
id | doaj-art-66f235bf67bf47ce8af0425f252f4fc7 |
institution | Kabale University |
issn | 2090-2247 2090-2255 |
language | English |
publishDate | 2012-01-01 |
publisher | Wiley |
record_format | Article |
series | Biochemistry Research International |
spelling | doaj-art-66f235bf67bf47ce8af0425f252f4fc72025-02-03T05:43:52ZengWileyBiochemistry Research International2090-22472090-22552012-01-01201210.1155/2012/195903195903Mitotic Kinases and p53 SignalingGeun-Hyoung Ha0Eun-Kyoung Yim Breuer1Department of Radiation Oncology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USADepartment of Radiation Oncology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USAMitosis is tightly regulated and any errors in this process often lead to aneuploidy, genomic instability, and tumorigenesis. Deregulation of mitotic kinases is significantly associated with improper cell division and aneuploidy. Because of their importance during mitosis and the relevance to cancer, mitotic kinase signaling has been extensively studied over the past few decades and, as a result, several mitotic kinase inhibitors have been developed. Despite promising preclinical results, targeting mitotic kinases for cancer therapy faces numerous challenges, including safety and patient selection issues. Therefore, there is an urgent need to better understand the molecular mechanisms underlying mitotic kinase signaling and its interactive network. Increasing evidence suggests that tumor suppressor p53 functions at the center of the mitotic kinase signaling network. In response to mitotic spindle damage, multiple mitotic kinases phosphorylate p53 to either activate or deactivate p53-mediated signaling. p53 can also regulate the expression and function of mitotic kinases, suggesting the existence of a network of mutual regulation, which can be positive or negative, between mitotic kinases and p53 signaling. Therefore, deciphering this regulatory network will provide knowledge to overcome current limitations of targeting mitotic kinases and further improve the results of targeted therapy.http://dx.doi.org/10.1155/2012/195903 |
spellingShingle | Geun-Hyoung Ha Eun-Kyoung Yim Breuer Mitotic Kinases and p53 Signaling Biochemistry Research International |
title | Mitotic Kinases and p53 Signaling |
title_full | Mitotic Kinases and p53 Signaling |
title_fullStr | Mitotic Kinases and p53 Signaling |
title_full_unstemmed | Mitotic Kinases and p53 Signaling |
title_short | Mitotic Kinases and p53 Signaling |
title_sort | mitotic kinases and p53 signaling |
url | http://dx.doi.org/10.1155/2012/195903 |
work_keys_str_mv | AT geunhyoungha mitotickinasesandp53signaling AT eunkyoungyimbreuer mitotickinasesandp53signaling |