Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 정희용 | - |
dc.date.accessioned | 2017-09-06T06:29:08Z | - |
dc.date.available | 2017-09-06T06:29:08Z | - |
dc.date.issued | 2015-11 | - |
dc.identifier.citation | PLOS ONE, v. 10, NO 11, Article Number e0141523, Page. 1-2 | en_US |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0141523 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/28948 | - |
dc.description.abstract | Mad2, 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. | en_US |
dc.description.sponsorship | This study was supported by grants from National Research Foundation of Korea (2012M3A9B6055346), and nuclear R&D program of Korea Ministry of Sciences and Technology. | en_US |
dc.language.iso | en | en_US |
dc.publisher | PUBLIC LIBRARY SCIENCE | en_US |
dc.subject | SPINDLE ASSEMBLY CHECKPOINT | en_US |
dc.subject | ANAPHASE-PROMOTING COMPLEX | en_US |
dc.subject | MITOTIC CHECKPOINT | en_US |
dc.subject | CHROMOSOMAL INSTABILITY | en_US |
dc.subject | LUNG-CANCER | en_US |
dc.subject | P53 GENE | en_US |
dc.subject | HEPATOCELLULAR-CARCINOMA | en_US |
dc.subject | GENOMIC INSTABILITY | en_US |
dc.subject | PROTEIN MAD2 | en_US |
dc.subject | EXPRESSION | en_US |
dc.title | p31(comet)-Induced Cell Death Is Mediated by Binding and Inactivation of Mad2 | en_US |
dc.type | Article | en_US |
dc.relation.no | 11 | - |
dc.relation.volume | 10 | - |
dc.identifier.doi | 10.1371/journal.pone.0141523 | - |
dc.relation.page | 1-2 | - |
dc.relation.journal | PLOS ONE | - |
dc.contributor.googleauthor | Shin, Hyun-Jin | - |
dc.contributor.googleauthor | Park, Eun-Ran | - |
dc.contributor.googleauthor | Yun, Sun-Hee | - |
dc.contributor.googleauthor | Kim, Su-Hyeon | - |
dc.contributor.googleauthor | Jung, Won-Hee | - |
dc.contributor.googleauthor | Woo, Seon Rang | - |
dc.contributor.googleauthor | Joo, Hyun-Yoo | - |
dc.contributor.googleauthor | Jang, Su Hwa | - |
dc.contributor.googleauthor | Chung, Hee Yong | - |
dc.contributor.googleauthor | Hong, Sung Hee | - |
dc.relation.code | 2015008685 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | hychung | - |
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