Regulation of HSF1-responsive gene expression by N-terminal truncated form of p73alpha - PubMed (original) (raw)
Regulation of HSF1-responsive gene expression by N-terminal truncated form of p73alpha
Yasuharu Tanaka et al. Biochem Biophys Res Commun. 2004.
Abstract
DNp73 is a transactivation domain (TAD)-truncated form of p73. The ability of DNp73alpha to regulate gene expression was examined using reporter assays with luciferase gene constructs. Among various promoter-regulated reporter genes tested, heat shock factor (HSF)-responsive gene expression was selectively activated by DNp73alpha, but not by other p73-isoforms with TAD and DNp73beta. Deletion of TAD endowed p73alpha with the ability to activate HSF-responsive gene expression, but deletion of N-terminal proline-rich domain (PRD) rendered both DNp73alpha and the TAD-deleted p73alpha inactive. Considering the inability of DNp73beta, which is the C-terminus-truncated form of DNp73alpha, to function, these results indicate that both the PRD and C-terminus are necessary for DNp73alpha to be able to activate the HSF-dependent gene expression. In addition to the reporter gene expression, both DNp73alpha and TAD-deleted p73alpha activated the expression of an endogenous gene, hsp70, corresponding with an increase in the active form of HSF1. Taken together, these results demonstrate that TAD-truncated p73alpha can activate HSF-dependent gene expression via induction of active HSF1.
Similar articles
- Up-regulation of NFkappaB-responsive gene expression by DeltaNp73alpha in p53 null cells.
Tanaka Y, Ota K, Kameoka M, Itaya A, Yoshihara K. Tanaka Y, et al. Exp Cell Res. 2006 May 1;312(8):1254-64. doi: 10.1016/j.yexcr.2005.12.013. Epub 2006 Jan 23. Exp Cell Res. 2006. PMID: 16430884 - The C terminus of p53 family proteins is a cell fate determinant.
Harms KL, Chen X. Harms KL, et al. Mol Cell Biol. 2005 Mar;25(5):2014-30. doi: 10.1128/MCB.25.5.2014-2030.2005. Mol Cell Biol. 2005. PMID: 15713654 Free PMC article. - Full-length p73alpha represses drug-induced apoptosis in small cell lung carcinoma cells.
Nyman U, Sobczak-Pluta A, Vlachos P, Perlmann T, Zhivotovsky B, Joseph B. Nyman U, et al. J Biol Chem. 2005 Oct 7;280(40):34159-69. doi: 10.1074/jbc.M500394200. Epub 2005 Aug 8. J Biol Chem. 2005. PMID: 16087678 - Mechanism of induction of apoptosis by p73 and its relevance to neuroblastoma biology.
Rossi M, Sayan AE, Terrinoni A, Melino G, Knight RA. Rossi M, et al. Ann N Y Acad Sci. 2004 Dec;1028:143-9. doi: 10.1196/annals.1322.015. Ann N Y Acad Sci. 2004. PMID: 15650240 Review.
Cited by
- Mechanisms of Survival of Cytomegalovirus-Infected Tumor Cells.
Vinogradskaya GR, Ivanov AV, Kushch AA. Vinogradskaya GR, et al. Mol Biol. 2022;56(5):668-683. doi: 10.1134/S0026893322050132. Epub 2022 Oct 5. Mol Biol. 2022. PMID: 36217337 Free PMC article. - Molecular Mechanisms of p63-Mediated Squamous Cancer Pathogenesis.
Moses MA, George AL, Sakakibara N, Mahmood K, Ponnamperuma RM, King KE, Weinberg WC. Moses MA, et al. Int J Mol Sci. 2019 Jul 23;20(14):3590. doi: 10.3390/ijms20143590. Int J Mol Sci. 2019. PMID: 31340447 Free PMC article. Review. - The dominant-negative interplay between p53, p63 and p73: A family affair.
Billant O, Léon A, Le Guellec S, Friocourt G, Blondel M, Voisset C. Billant O, et al. Oncotarget. 2016 Oct 25;7(43):69549-69564. doi: 10.18632/oncotarget.11774. Oncotarget. 2016. PMID: 27589690 Free PMC article. - ∆Np73 is capable of inducing apoptosis by co-ordinately activating several BH3-only proteins.
Sánchez-Carrera D, García-Puga M, Yáñez L, Romón Í, Pipaón C. Sánchez-Carrera D, et al. Biosci Rep. 2015 Apr 28;35(3):e00198. doi: 10.1042/BSR20150039. Biosci Rep. 2015. PMID: 26182360 Free PMC article. - Suppression of acetylpolyamine oxidase by selected AP-1 members regulates DNp73 abundance: mechanistic insights for overcoming DNp73-mediated resistance to chemotherapeutic drugs.
Bunjobpol W, Dulloo I, Igarashi K, Concin N, Matsuo K, Sabapathy K. Bunjobpol W, et al. Cell Death Differ. 2014 Aug;21(8):1240-9. doi: 10.1038/cdd.2014.41. Epub 2014 Apr 11. Cell Death Differ. 2014. PMID: 24722210 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Miscellaneous