NDLI: TAp63 Is a Transcriptional Target of NF-κB

Content Provider	PubMed Central
Author	Wu, Junfeng Bergholz, Johann Lu, Jinin Sonenshein, Gail E. Xiao, Zhi-xiong Jim
Copyright Year	2010
Abstract	The p53 homologue p63 encodes multiple protein isoforms either with (TA) or without (ΔN) the N-terminal transactivation domain. Accumulating evidence indicates that TAp63 plays an important role in various biological processes, including cell proliferation, differentiation, and apoptosis. However, how TAp63 is regulated remains largely unclear. In this study, we demonstrate that NF-κB induces TAp63 gene expression. The responsible elements for NF-κB-mediated TAp63 induction are located within the region from –784 to –296 bp in the TAp63 promoter, which contains two NF-κB binding sites. Ectopic expression of RelA stimulates TAp63 promoter-driven reporter activity and increases endogenous TAp63 mRNA levels. Inhibition of NF-κB by IκBα super-repressor or with a chemical inhibitor leads to down regulation of TAp63 mRNA expression and activity. In addition, mutations in the critical NF-κB-binding sites significantly abolish the effects of NF-κB on TAp63. Activation of NF-κB by TNFα enhances p50/RelA binding to the NF-κB binding sites. Furthermore, we show that an Sp1 site adjacent to the NF-κB sites plays a role in NF-κB-mediated upregulation of TAp63. Taken together, these data reveal that TAp63 is a transcriptional target of NF-κB, which may play a role in cell proliferation, differentiation and survival upon NF-κB activation by various stimuli.
Related Links	http://dx.doi.org/10.1002/jcb.22449
Page Count	1
Starting Page	702
File Format	PDF
ISSN	07302312
e-ISSN	10974644
Journal	Journal of cellular biochemistry
Issue Number	4
Volume Number	109
Language	English
Publisher Date	2009-01-01
Access Restriction	Open
Subject Keyword	Cell Biology Biochemistry Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

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