Literature DB >> 11825686

p53, p63 and p73--solos, alliances and feuds among family members.

U M Moll1, S Erster, A Zaika.   

Abstract

p53 controls crucial stress responses that play a major role in preventing malignant transformation. Hence, inactivation of p53 is the single most common genetic defect in human cancer. With the recent discovery of two close structural homologs, p63 en p73, we are getting a broader view of a fascinating gene family that links developmental biology with tumor biology. While unique roles are apparent for each of these genes, intimate biochemical cross-talk among family members suggests a functional network that might influence many different aspects of individual gene action. The most interesting part of this family network derives from the fact that the p63 and p73 genes are based on the "two-genes-in-one" idea, encoding both agonist and antagonist in the same open reading frame. In this review, we attempt to present an overview of the current status of this fast moving field.

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Year:  2001        PMID: 11825686     DOI: 10.1016/s0304-419x(01)00036-1

Source DB:  PubMed          Journal:  Biochim Biophys Acta        ISSN: 0006-3002


  34 in total

1.  Thyroid transcription factor 1 (TTF-1) and p63 expression in two primary thyroid papillary carcinomas of branchial cleft cysts.

Authors:  S Lanzafame; R Caltabiano; L Puzzo; A Cappellani
Journal:  Virchows Arch       Date:  2006-04-21       Impact factor: 4.064

2.  DNA damage induces transcriptional activation of p73 by removing C-EBPalpha repression on E2F1.

Authors:  Mirko Marabese; Faina Vikhanskaya; Cristina Rainelli; Toshiyuki Sakai; Massimo Broggini
Journal:  Nucleic Acids Res       Date:  2003-11-15       Impact factor: 16.971

3.  DeltaNp73beta is active in transactivation and growth suppression.

Authors:  Gang Liu; Susan Nozell; Hui Xiao; Xinbin Chen
Journal:  Mol Cell Biol       Date:  2004-01       Impact factor: 4.272

4.  Association of a p73 exon 2 GC/AT polymorphism with colorectal cancer risk and survival in Tunisian patients.

Authors:  Amira Toumi Arfaoui; Lilia Ben Mahmoud Kriaa; Olfa El Amine El Hadj; Majid A Ben Hmida; Myriam Khiari; T Khalfallah; Lasaad Gharbi; Sabeh Mzabi; Sadaa Bouraoui
Journal:  Virchows Arch       Date:  2010-07-20       Impact factor: 4.064

5.  Control of p53-dependent transcription and enhancer activity by the p53 family member p63.

Authors:  Gizem Karsli Uzunbas; Faraz Ahmed; Morgan A Sammons
Journal:  J Biol Chem       Date:  2019-05-21       Impact factor: 5.157

6.  Expression and regulation of the ΔN and TAp63 isoforms in salivary gland tumorigenesis clinical and experimental findings.

Authors:  Yoshitsugu Mitani; Jie Li; Randal S Weber; Scott L Lippman; Elsa R Flores; Carlos Caulin; Adel K El-Naggar
Journal:  Am J Pathol       Date:  2011-05-07       Impact factor: 4.307

7.  Association of p73 G4C14-to-A4T14 polymorphism with lung cancer risk.

Authors:  Hua Liu; Yuli Liang; Hua Liao; Lanying Li; Hongyun Wang
Journal:  Tumour Biol       Date:  2014-06-19

8.  Identification of DeltaN isoform and polyadenylation site choice variants in molluscan p63/p73-like homologues.

Authors:  Annette F Muttray; Rachel L Cox; Carol L Reinisch; Susan A Baldwin
Journal:  Mar Biotechnol (NY)       Date:  2007-01-22       Impact factor: 3.619

9.  Biochemical and functional evidence of p53 homology is inconsistent with molecular phylogenetics for distant sequences.

Authors:  Andrew D Fernandes; William R Atchley
Journal:  J Mol Evol       Date:  2008-06-17       Impact factor: 2.395

Review 10.  The biological properties of E6 and E7 oncoproteins from human papillomaviruses.

Authors:  Raffaella Ghittoni; Rosita Accardi; Uzma Hasan; Tarik Gheit; Bakary Sylla; Massimo Tommasino
Journal:  Virus Genes       Date:  2009-10-17       Impact factor: 2.332

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