Investigation of cell cycle arrest effects of actinomycin D at G1 phase using proteomic methods in B104-1-1 cells

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dc.contributor.authorHyae Kyeong Kim-
dc.contributor.authorMi Young Kong-
dc.contributor.authorMoon Jin Jeong-
dc.contributor.authorDong Cho Han-
dc.contributor.authorJ D Choi-
dc.contributor.authorH Y Kim-
dc.contributor.authorKab Seog Yoon-
dc.contributor.authorJung Min Kim-
dc.contributor.authorKwang Hee Son-
dc.contributor.authorByoung-Mog Kwon-
dc.date.accessioned2017-04-19T09:02:59Z-
dc.date.available2017-04-19T09:02:59Z-
dc.date.issued2005-
dc.identifier.issn13572725-
dc.identifier.uri10.1016/j.biocel.2005.04.015ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7001-
dc.description.abstractActinomycin D was previously reported as an inhibitor of Shc/Grb2 interaction in B104-1-1 cells. Actinomycin D arrested the cell cycle at the G1 phase at 1 nM, which is about 10 times lower than the inhibition of Shc/Grb2 interactions in B104-1-1 cells. To evaluate other mechanisms of actinomycin D affected suppression of tumors and cell growth, except inhibition of Shc/Grb2 interactions, we examined the proteomic expression profile by proteomic technology. We found up-regulation of MEKK3 and down-regulation of Hsp70 expression from proteomic analysis, which is a very interesting observation because MEKK3 is strongly related with G1 arrest of cell cycle and Hsp70 is also involved in cell cycle regulation. These results indicate that the anti-tumor effects of actinomycin D is due to synergic effects of various proteins regulated by the compound including inhibition of the Shc/Grb2 interaction and other signaling pathways in the cytoplasm. Here we provide a mechanism-based explanation for growth inhibition by actinomycin D using proteomic technology. Thus, this approach may be a potentially useful method to reveal new mechanisms of active compounds or drugs with unknown cellular function.-
dc.publisherElsevier-
dc.titleInvestigation of cell cycle arrest effects of actinomycin D at G1 phase using proteomic methods in B104-1-1 cells-
dc.title.alternativeInvestigation of cell cycle arrest effects of actinomycin D at G1 phase using proteomic methods in B104-1-1 cells-
dc.typeArticle-
dc.citation.titleInternational Journal of Biochemistry & Cell Biology-
dc.citation.number9-
dc.citation.endPage1929-
dc.citation.startPage1921-
dc.citation.volume37-
dc.contributor.affiliatedAuthorDong Cho Han-
dc.contributor.affiliatedAuthorKwang Hee Son-
dc.contributor.affiliatedAuthorByoung-Mog Kwon-
dc.contributor.alternativeName김혜경-
dc.contributor.alternativeName공미영-
dc.contributor.alternativeName정문진-
dc.contributor.alternativeName한동초-
dc.contributor.alternativeName최정도-
dc.contributor.alternativeName김학용-
dc.contributor.alternativeName윤갑석-
dc.contributor.alternativeName김정민-
dc.contributor.alternativeName손광희-
dc.contributor.alternativeName권병목-
dc.identifier.bibliographicCitationInternational Journal of Biochemistry & Cell Biology, vol. 37, no. 9, pp. 1921-1929-
dc.identifier.doi10.1016/j.biocel.2005.04.015-
dc.subject.keywordActinomycin-
dc.subject.keywordCell cycle-
dc.subject.keywordHsp70-
dc.subject.keywordMEKK3-
dc.subject.keywordProteomics-
dc.subject.localActinomycin-
dc.subject.localCell cycle-
dc.subject.localHsp70-
dc.subject.localMEKK3-
dc.subject.localProteomics-
dc.subject.localProteomic-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
Division of Biomaterials Research > Industrial Bio-materials Research Center > 1. Journal Articles
Division of Biomedical Research > Genome Editing Research Center > 1. Journal Articles
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