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p31(comet)-induced cell death is mediated by binding and inactivation of Mad2

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dc.contributor.authorShin, Hyun-Jin-
dc.contributor.authorPark, Eun-Ran-
dc.contributor.authorYun, Sun-Hee-
dc.contributor.authorKim, Su-Hyeon-
dc.contributor.authorJung, Won-Hee-
dc.contributor.authorWoo, Seon Rang-
dc.contributor.authorJoo, Hyun-Yoo-
dc.contributor.authorJang, Su Hwa-
dc.contributor.authorChung, Hee Yong-
dc.contributor.authorHong, Sung Hee-
dc.contributor.authorCho, Myung-Haing-
dc.contributor.authorPark, Joong-Jean-
dc.contributor.authorYun, Miyong-
dc.contributor.authorLee, Kee-Ho-
dc.date.accessioned2021-01-31T08:49:43Z-
dc.date.available2021-01-31T08:49:43Z-
dc.date.issued2015-11-
dc.identifier.citationPLoS ONE, Vol.10 No.11, p. e0141523-
dc.identifier.issn1932-6203-
dc.identifier.other62090-
dc.identifier.urihttps://hdl.handle.net/10371/172502-
dc.description.abstractMad2, a key component of the spindle checkpoint, is closely associated with chromosomal instability and poor prognosis in cancer. p31(comet) is a Mad2-interacting protein that serves as a spindle checkpoint silencer at mitosis. In this study, we showed that p31(comet)-induced apoptosis and senescence occur via counteraction of Mad2 activity. Upon retroviral transduction of p31(comet), the majority of human cancer cell lines tested lost the ability to form colonies in a low-density seeding assay. Cancer cells with p31(comet) overexpression underwent distinct apoptosis and/or senescence, irrespective of p53 status, confirming the cytotoxicity of p31(comet). Interestingly, both cytotoxic and Mad2 binding activities were eliminated upon deletion of the C-terminal 30 amino acids of p31(comet). Point mutation or deletion of the region affecting Mad2 binding additionally abolished cytotoxic activity. Consistently, wildtype Mad2 interacting with p31(comet), but not its non-binding mutant, inhibited cell death, indicating that the mechanism of p31(comet)-induced cell death involves Mad2 inactivation. Our results clearly suggest that the regions of p31(comet) affecting interactions with Mad2, including the C-terminus, are essential for induction of cell death. The finding that p31(comet)-induced cell death is mediated by interactions with Mad2 that lead to its inactivation is potentially applicable in anticancer therapy.-
dc.titlep31(comet)-induced cell death is mediated by binding and inactivation of Mad2-
dc.typeArticle-
dc.contributor.AlternativeAuthor조명행-
dc.identifier.doi10.1371/journal.pone.0141523-
dc.citation.journaltitlePLoS ONE-
dc.identifier.scopusid2-s2.0-84952673830-
dc.citation.number11-
dc.citation.startpagee0141523-
dc.citation.volume10-
dc.identifier.urlhttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0141523-
dc.identifier.rimsid62090-
dc.identifier.sci000364398700030-
dc.contributor.affiliatedAuthorCho, Myung-Haing-
Appears in Collections:
College of Veterinary Medicine (수의과대학)Dept. of Veterinary Medicine (수의학과)Journal Papers (저널논문_수의학과)
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