Mouse period 2 mRNA circadian oscillation is modulated by PTP-mediated rhythmic mRNA degradation

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dc.contributor.authorK C Woo-
dc.contributor.authorTae-Don Kim-
dc.contributor.authorK H Lee-
dc.contributor.authorD Y Kim-
dc.contributor.authorW Kim-
dc.contributor.authorK Y Lee-
dc.contributor.authorK T Kim-
dc.date.accessioned2017-04-19T09:13:06Z-
dc.date.available2017-04-19T09:13:06Z-
dc.date.issued2009-
dc.identifier.issn0305-1048-
dc.identifier.uri10.1093/nar/gkn893ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/8800-
dc.description.abstractCircadian mRNA oscillations are the main feature of core clock genes. Among them, period 2 is a key component in negative-feedback regulation, showing robust diurnal oscillations. Moreover, period 2 has been found to have a physiological role in the cell cycle or the tumor suppression. The present study reports that 3'-untranslated region (UTR)-dependent mRNA decay is involved in the regulation of circadian oscillation of period 2 mRNA. Within the mper2 3'UTR, both the CU-rich region and polypyrimidine tract-binding protein (PTB) are more responsible for mRNA stability and degradation kinetics than are other factors. Depletion of PTB with RNAi results in mper2 mRNA stabilization. During the circadian oscillations of mper2, cytoplasmic PTB showed a reciprocal expression profile compared with mper2 mRNA and its peak amplitude was increased when PTB was depleted. This report on the regulation of mper2 proposes that post-transcriptional mRNA decay mediated by PTB is a fine-tuned regulatory mechanism that includes dampening-down effects during circadian mRNA oscillations.-
dc.publisherOxford Univ Press-
dc.titleMouse period 2 mRNA circadian oscillation is modulated by PTP-mediated rhythmic mRNA degradation-
dc.title.alternativeMouse period 2 mRNA circadian oscillation is modulated by PTP-mediated rhythmic mRNA degradation-
dc.typeArticle-
dc.citation.titleNucleic Acids Research-
dc.citation.number1-
dc.citation.endPage37-
dc.citation.startPage26-
dc.citation.volume37-
dc.contributor.affiliatedAuthorTae-Don Kim-
dc.contributor.alternativeName우경철-
dc.contributor.alternativeName김태돈-
dc.contributor.alternativeName이경하-
dc.contributor.alternativeName김도연-
dc.contributor.alternativeName김완일-
dc.contributor.alternativeName이경열-
dc.contributor.alternativeName김경태-
dc.identifier.bibliographicCitationNucleic Acids Research, vol. 37, no. 1, pp. 26-37-
dc.identifier.doi10.1093/nar/gkn893-
dc.description.journalClassY-
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Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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