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- Publisher Website: 10.1006/bbrc.2001.5164
- Scopus: eid_2-s2.0-0034741278
- PMID: 11444839
- WOS: WOS:000170020900020
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Article: PKCδ-dependent deubiquitination and stabilization of Gadd45 in A431 cells overexposed to EGF
Title | PKCδ-dependent deubiquitination and stabilization of Gadd45 in A431 cells overexposed to EGF |
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Authors | |
Keywords | A431 Cell Epidermal Growth Factor Gadd45 Protein Kinase C Ubiquitination |
Issue Date | 2001 |
Publisher | Academic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description |
Citation | Biochemical And Biophysical Research Communications, 2001, v. 285 n. 2, p. 283-288 How to Cite? |
Abstract | Epidermal growth factor (EGF) receptor-overexpressing p53-deficient A431 cells response to toxic dose of EGF by G1 arrest and apoptosis was studied. We previously reported an increased expression of growth arrest and DNA-damage-inducible gene, Gadd45, in EGF-overexposed A431 cells. The mechanism for this induction was increased half-lives of mRNA and protein. In this study, using phorbol ester (a PKC activator) and specific inhibitors of PKC isoforms, we showed that protein kinase C-δ (PKCδ) was involved in the increase of Gadd45 protein stability. We further demonstrated that Gadd45 is ubiquitinated and is regulated by proteolysis. While EGF induced ubiquitination of total cellular proteins, there was a decrease in Gadd45 ubiquitination, which could be inhibited by Rottlerin, a PKCδ-specific inhibitor. These results suggest that an increase in Gadd45 stability may involve PKCδ-dependent ubiquitin - proteasome pathway. © 2001 Academic Press. |
Persistent Identifier | http://hdl.handle.net/10722/167671 |
ISSN | 2023 Impact Factor: 2.5 2023 SCImago Journal Rankings: 0.770 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Leung, CH | en_US |
dc.contributor.author | Lam, W | en_US |
dc.contributor.author | Zhuang, WJ | en_US |
dc.contributor.author | Wang, NS | en_US |
dc.contributor.author | Fong, WF | en_US |
dc.date.accessioned | 2012-10-08T03:09:44Z | - |
dc.date.available | 2012-10-08T03:09:44Z | - |
dc.date.issued | 2001 | en_US |
dc.identifier.citation | Biochemical And Biophysical Research Communications, 2001, v. 285 n. 2, p. 283-288 | en_US |
dc.identifier.issn | 0006-291X | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/167671 | - |
dc.description.abstract | Epidermal growth factor (EGF) receptor-overexpressing p53-deficient A431 cells response to toxic dose of EGF by G1 arrest and apoptosis was studied. We previously reported an increased expression of growth arrest and DNA-damage-inducible gene, Gadd45, in EGF-overexposed A431 cells. The mechanism for this induction was increased half-lives of mRNA and protein. In this study, using phorbol ester (a PKC activator) and specific inhibitors of PKC isoforms, we showed that protein kinase C-δ (PKCδ) was involved in the increase of Gadd45 protein stability. We further demonstrated that Gadd45 is ubiquitinated and is regulated by proteolysis. While EGF induced ubiquitination of total cellular proteins, there was a decrease in Gadd45 ubiquitination, which could be inhibited by Rottlerin, a PKCδ-specific inhibitor. These results suggest that an increase in Gadd45 stability may involve PKCδ-dependent ubiquitin - proteasome pathway. © 2001 Academic Press. | en_US |
dc.language | eng | en_US |
dc.publisher | Academic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description | en_US |
dc.relation.ispartof | Biochemical and Biophysical Research Communications | en_US |
dc.subject | A431 Cell | en_US |
dc.subject | Epidermal Growth Factor | en_US |
dc.subject | Gadd45 | en_US |
dc.subject | Protein Kinase C | en_US |
dc.subject | Ubiquitination | en_US |
dc.title | PKCδ-dependent deubiquitination and stabilization of Gadd45 in A431 cells overexposed to EGF | en_US |
dc.type | Article | en_US |
dc.identifier.email | Leung, CH:duncanl@hkucc.hku.hk | en_US |
dc.identifier.authority | Leung, CH=rp00730 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1006/bbrc.2001.5164 | en_US |
dc.identifier.pmid | 11444839 | - |
dc.identifier.scopus | eid_2-s2.0-0034741278 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0034741278&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 285 | en_US |
dc.identifier.issue | 2 | en_US |
dc.identifier.spage | 283 | en_US |
dc.identifier.epage | 288 | en_US |
dc.identifier.isi | WOS:000170020900020 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Leung, CH=7402612570 | en_US |
dc.identifier.scopusauthorid | Lam, W=7203021943 | en_US |
dc.identifier.scopusauthorid | Zhuang, WJ=7103154978 | en_US |
dc.identifier.scopusauthorid | Wang, NS=36985478700 | en_US |
dc.identifier.scopusauthorid | Fong, WF=7102816013 | en_US |
dc.identifier.issnl | 0006-291X | - |