Literature DB >> 12881708

The proline-rich region of mouse p53 influences transactivation and apoptosis but is largely dispensable for these functions.

Sara J Edwards1, Lynne Hananeia, Michael R Eccles, You Fang Zhang, Antony W Braithwaite.   

Abstract

The N-terminal proline-rich domain of human p53 has been shown to be important for the induction of apoptosis. However, the corresponding region in mouse and other species is not highly conserved and has been less well studied. In this paper, we have characterized mutants with deletions in this region of mouse p53. Our results demonstrate that deletions in the proline-rich domain have varying effects on function ranging from no effect to severe impairment of cell death activity, depending on precisely which residues are deleted. We also show that the mutants differ in their ability to transactivate different p53 target promoters. Although we have been able to obtain mutants selectively impaired for apoptosis, our data are not generally consistent with this region being a functional domain. The data are more consistent with the interpretation that the region influences function by altering local protein structure which may affect promoter discrimination.

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Year:  2003        PMID: 12881708     DOI: 10.1038/sj.onc.1206726

Source DB:  PubMed          Journal:  Oncogene        ISSN: 0950-9232            Impact factor:   9.867


  11 in total

1.  The Trp53 delta proline (Trp53ΔP) mouse exhibits increased genome instability and susceptibility to radiation-induced, but not spontaneous, tumor development.

Authors:  Cassandra J Adams; Jennifer S Yu; Jian-Hua Mao; Kuang-Yu Jen; Sylvain V Costes; Mark Wade; Jocelyn Shoemake; Olulanu H Aina; Reyno Del Rosario; Phuong Thuy Menchavez; Robert D Cardiff; Geoffrey M Wahl; Allan Balmain
Journal:  Mol Carcinog       Date:  2015-08-27       Impact factor: 4.784

2.  Mutations in proline 82 of p53 impair its activation by Pin1 and Chk2 in response to DNA damage.

Authors:  Michael Berger; Nathalie Stahl; Giannino Del Sal; Ygal Haupt
Journal:  Mol Cell Biol       Date:  2005-07       Impact factor: 4.272

3.  The proline-rich domain in p63 is necessary for the transcriptional and apoptosis-inducing activities of TAp63.

Authors:  E S Helton; J Zhang; X Chen
Journal:  Oncogene       Date:  2007-11-26       Impact factor: 9.867

Review 4.  Targeting the p53 pathway.

Authors:  Vita M Golubovskaya; William G Cance
Journal:  Surg Oncol Clin N Am       Date:  2013-07-30       Impact factor: 3.495

5.  Interaction between p53 N terminus and core domain regulates specific and nonspecific DNA binding.

Authors:  Fan He; Wade Borcherds; Tanjing Song; Xi Wei; Mousumi Das; Lihong Chen; Gary W Daughdrill; Jiandong Chen
Journal:  Proc Natl Acad Sci U S A       Date:  2019-04-15       Impact factor: 11.205

6.  The proline rich domain of p53 is dispensable for MGMT-dependent DNA repair and cell survival following alkylation damage.

Authors:  Katherine Baran; Mao Yang; Christopher P Dillon; Leona L Samson; Douglas R Green
Journal:  Cell Death Differ       Date:  2017-07-28       Impact factor: 15.828

7.  Mouse mutants reveal that putative protein interaction sites in the p53 proline-rich domain are dispensable for tumor suppression.

Authors:  Franck Toledo; Crystal J Lee; Kurt A Krummel; Luo-Wei Rodewald; Chung-Wen Liu; Geoffrey M Wahl
Journal:  Mol Cell Biol       Date:  2006-12-11       Impact factor: 4.272

Review 8.  Regulating the p53 pathway: in vitro hypotheses, in vivo veritas.

Authors:  Franck Toledo; Geoffrey M Wahl
Journal:  Nat Rev Cancer       Date:  2006-12       Impact factor: 60.716

9.  N-terminal proline-rich domain is required for scrambling activity of human phospholipid scramblases.

Authors:  Sarika Rayala; Vincent G Francis; Ulaganathan Sivagnanam; Sathyanarayana N Gummadi
Journal:  J Biol Chem       Date:  2014-03-19       Impact factor: 5.157

10.  Chromatin remodeling protein MORC2 promotes breast cancer invasion and metastasis through a PRD domain-mediated interaction with CTNND1.

Authors:  Xiao-Hong Liao; Ye Zhang; Wen-Jie Dong; Zhi-Min Shao; Da-Qiang Li
Journal:  Oncotarget       Date:  2017-06-16
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