Mechanisms of p53 Functional De-Regulation: Role of the IκB-α/p53 Complex

TP53 is one of the most frequently-mutated and deleted tumor suppressors in cancer, with a dramatic correlation with dismal prognoses. In addition to genetic inactivation, the p53 protein can be functionally inactivated in cancer, through post-transductional modifications, changes in cellular compar...

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Main Authors: Giovanna Carrà, Sabrina Crivellaro, Riccardo Taulli, Angelo Guerrasio, Giuseppe Saglio, Alessandro Morotti
Format: Article
Language:English
Published: MDPI AG 2016-11-01
Series:International Journal of Molecular Sciences
Subjects:
p53
Online Access:http://www.mdpi.com/1422-0067/17/12/1997
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spelling doaj-e83741b22c524c5e8568953555a0306a2020-11-25T01:47:05ZengMDPI AGInternational Journal of Molecular Sciences1422-00672016-11-011712199710.3390/ijms17121997ijms17121997Mechanisms of p53 Functional De-Regulation: Role of the IκB-α/p53 ComplexGiovanna Carrà0Sabrina Crivellaro1Riccardo Taulli2Angelo Guerrasio3Giuseppe Saglio4Alessandro Morotti5Department of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, 10043 Turin, ItalyDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, 10043 Turin, ItalyDepartment of Oncology, University of Turin, Regione Gonzole 10, 10043 Turin, ItalyDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, 10043 Turin, ItalyDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, 10043 Turin, ItalyDepartment of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, 10043 Turin, ItalyTP53 is one of the most frequently-mutated and deleted tumor suppressors in cancer, with a dramatic correlation with dismal prognoses. In addition to genetic inactivation, the p53 protein can be functionally inactivated in cancer, through post-transductional modifications, changes in cellular compartmentalization, and interactions with other proteins. Here, we review the mechanisms of p53 functional inactivation, with a particular emphasis on the interaction between p53 and IκB-α, the NFKBIA gene product.http://www.mdpi.com/1422-0067/17/12/1997p53IκB-αtumor suppressorsfunctional inactivation
collection DOAJ
language English
format Article
sources DOAJ
author Giovanna Carrà
Sabrina Crivellaro
Riccardo Taulli
Angelo Guerrasio
Giuseppe Saglio
Alessandro Morotti
spellingShingle Giovanna Carrà
Sabrina Crivellaro
Riccardo Taulli
Angelo Guerrasio
Giuseppe Saglio
Alessandro Morotti
Mechanisms of p53 Functional De-Regulation: Role of the IκB-α/p53 Complex
International Journal of Molecular Sciences
p53
IκB-α
tumor suppressors
functional inactivation
author_facet Giovanna Carrà
Sabrina Crivellaro
Riccardo Taulli
Angelo Guerrasio
Giuseppe Saglio
Alessandro Morotti
author_sort Giovanna Carrà
title Mechanisms of p53 Functional De-Regulation: Role of the IκB-α/p53 Complex
title_short Mechanisms of p53 Functional De-Regulation: Role of the IκB-α/p53 Complex
title_full Mechanisms of p53 Functional De-Regulation: Role of the IκB-α/p53 Complex
title_fullStr Mechanisms of p53 Functional De-Regulation: Role of the IκB-α/p53 Complex
title_full_unstemmed Mechanisms of p53 Functional De-Regulation: Role of the IκB-α/p53 Complex
title_sort mechanisms of p53 functional de-regulation: role of the iκb-α/p53 complex
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1422-0067
publishDate 2016-11-01
description TP53 is one of the most frequently-mutated and deleted tumor suppressors in cancer, with a dramatic correlation with dismal prognoses. In addition to genetic inactivation, the p53 protein can be functionally inactivated in cancer, through post-transductional modifications, changes in cellular compartmentalization, and interactions with other proteins. Here, we review the mechanisms of p53 functional inactivation, with a particular emphasis on the interaction between p53 and IκB-α, the NFKBIA gene product.
topic p53
IκB-α
tumor suppressors
functional inactivation
url http://www.mdpi.com/1422-0067/17/12/1997
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