Cytoplasmic localization and ubiquitination of p21Cip1 by reactive oxygen species

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dc.contributor.authorC Y Hwang-
dc.contributor.authorI Y Kim-
dc.contributor.authorKi Sun Kwon-
dc.date.accessioned2017-04-19T09:07:17Z-
dc.date.available2017-04-19T09:07:17Z-
dc.date.issued2007-
dc.identifier.issn0006-291X-
dc.identifier.uri10.1016/j.bbrc.2007.04.120ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7937-
dc.description.abstractReactive oxygen species were previously shown to trigger p21Cip1 protein degradation through a proteasome-dependent pathway, however the detailed mechanism of degradation remains to be elucidated. In this report, we showed that p21Cip1 was degraded at an early phase after low dose H2O2 treatment of a variety of cell types and that preincubation of cells with the antioxidant, N-acetylcysteine, prolonged p21Cip1 half-life. A mutant p21Cip1 in which all six lysines were changed to arginines was protected against H2O2 treatment. Direct interaction between p21Cip1 and Skp2 was elevated in the H2O2-treated cells. Disruption of the two nuclear export signal (NES) sequences in p21Cip1, or treatment with leptomycin B blocked H2O2-induced p21Cip1 degradation. Altogether, these results demonstrate that reactive oxygen species induce p21Cip1 degradation through an NES-, Skp2-, and ubiquitin-dependent pathway.-
dc.publisherElsevier-
dc.titleCytoplasmic localization and ubiquitination of p21Cip1 by reactive oxygen species-
dc.title.alternativeCytoplasmic localization and ubiquitination of p21Cip1 by reactive oxygen species-
dc.typeArticle-
dc.citation.titleBiochemical and Biophysical Research Communications-
dc.citation.number1-
dc.citation.endPage225-
dc.citation.startPage219-
dc.citation.volume358-
dc.contributor.affiliatedAuthorC Y Hwang-
dc.contributor.affiliatedAuthorKi Sun Kwon-
dc.contributor.alternativeName황채영-
dc.contributor.alternativeName김익영-
dc.contributor.alternativeName권기선-
dc.identifier.bibliographicCitationBiochemical and Biophysical Research Communications, vol. 358, no. 1, pp. 219-225-
dc.identifier.doi10.1016/j.bbrc.2007.04.120-
dc.subject.keywordCyclin-dependent kinase inhibitor-
dc.subject.keywordDegradation-
dc.subject.keywordNuclear export-
dc.subject.keywordReactive oxygen species-
dc.subject.keywordUbiquitination-
dc.subject.localCyclin-dependent kinase inhibitor-
dc.subject.localcyclin-dependent kinase inhibitor-
dc.subject.localDegradation-
dc.subject.localdegradation-
dc.subject.localNuclear export-
dc.subject.localReactive oxidative species-
dc.subject.localReactive oxygen species(ROS)-
dc.subject.localReactive oxygen species-
dc.subject.localReactive Oxygen Species (ROS)-
dc.subject.localReactive Oxygen Species-
dc.subject.localROS-
dc.subject.localReactive oxygen species (ROS)-
dc.subject.localreactive oxygen species-
dc.subject.localreactive oxygen species (ROS)-
dc.subject.localUbiquitination-
dc.subject.localubiquitination-
dc.description.journalClassY-
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Aging Convergence Research Center > 1. Journal Articles
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