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  1. Academic Journal articles
  2. Meitinger Unit

53BP1-mediated activation of the tumor suppressor p53

https://oist.repo.nii.ac.jp/records/2000766
https://oist.repo.nii.ac.jp/records/2000766
0f0beb36-ea3a-4e11-a257-33e3027e2ed2
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1-s2.0-S0955067424001030-main.pdf 1-s2.0-S0955067424001030-main.pdf (1.3 MB)
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Item type 学術雑誌論文 / Journal Article(1)
PubDate 2025-01-21
Title
Title 53BP1-mediated activation of the tumor suppressor p53
Language en
Language
Language eng
Resource Type
Resource Type Identifier http://purl.org/coar/resource_type/c_6501
Resource Type journal article
Access Right
Access Rights open access
Access Rights URI http://purl.org/coar/access_right/c_abf2
Author Belal, Hazrat

× Belal, Hazrat

en Belal, Hazrat

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Ying Ng, Esther Feng

× Ying Ng, Esther Feng

en Ying Ng, Esther Feng

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Meitinger, Franz

× Meitinger, Franz

en Meitinger, Franz

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Bibliographic Information en : Current Opinion in Cell Biology

Volume Number 91, p. 102424, Issue Date 2024-09-07
Abstract
Description Type Abstract
Description In recent years, the role of 53BP1 as a cell cycle regulator has come into the spotlight. 53BP1 is best understood for its role in controlling DNA double-strand break repair. However, 53BP1 was initially discovered as an interaction partner of the tumor suppressor p53, which proved to be independent of DNA repair. The importance of this interaction is becoming increasingly clear. 53BP1 responds to mitotic stress, which prolongs mitosis, or to DNA damage and triggers the stabilization of p53 by the deubiquitinase USP28 to stop the proliferation of potentially damaged cells. The ability of 53BP1 to respond to mitotic stress or DNA damage is controlled by cell cycle-specific post-translational modifications and is therefore restricted to specific cell cycle phases. 53BP1-mediated p53 activation is likely involved in tumor suppression and is associated with genetic diseases such as primary microcephaly. This review emphasizes the importance of these mechanisms for the development and maintenance of healthy tissues.
Language en
Publisher
Publisher Elsevier Ltd.
ISSN
Source Identifier Type PISSN
Source Identifier 0955-0674
ISSN
Source Identifier Type EISSN
Source Identifier 1879-0410
PubMedNo.
Relation Type isIdenticalTo
Identifier Type PMID
Related Identifier 39244835
DOI
Relation Type isIdenticalTo
Identifier Type DOI
Related Identifier 10.1016/j.ceb.2024.102424
Rights
Rights © 2024 The Author(s).
Rights
Rights Resource Creative Commons Attribution 4.0 International
Rights https://creativecommons.org/licenses/by/4.0/
Related site
Relation Type isIdenticalTo
Identifier Type URI
Related Identifier https://www.sciencedirect.com/science/article/pii/S0955067424001030
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Version Type VoR
Version Type Resource http://purl.org/coar/version/c_970fb48d4fbd8a85
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