Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 윤채옥 | - |
dc.date.accessioned | 2018-03-26T05:31:36Z | - |
dc.date.available | 2018-03-26T05:31:36Z | - |
dc.date.issued | 2014-09 | - |
dc.identifier.citation | The Journal of biological chemistry, v.289 no.36[2014년], pp. 24832-24844 | en_US |
dc.identifier.issn | 0021-9258 | - |
dc.identifier.issn | 1083-351x | - |
dc.identifier.uri | http://www.jbc.org/content/289/36/24832.abstract | - |
dc.identifier.uri | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4155653/ | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/52369 | - |
dc.description.abstract | The Hsp70 family protein mortalin is an essential chaperone that is frequently enriched in cancer cells and exists in various subcellular sites, including the mitochondrion, plasma membrane, endoplasmic reticulum, and cytosol. Although the molecular mechanisms underlying its multiple subcellular localizations are not yet clear, their functional significance has been revealed by several studies. In this study, we examined the nuclear fractions of human cells and found that the malignantly transformed cells have more mortalin than the normal cells. We then generated a mortalin mutant that lacked a mitochondrial targeting signal peptide. It was largely localized in the nucleus, and, hence, is called nuclear mortalin (mot-N). Functional characterization of mot-N revealed that it efficiently protects cancer cells against endogenous and exogenous oxidative stress. Furthermore, compared with the full-length mortalin overexpressing cancer cells, mot-N derivatives showed increased malignant properties, including higher proliferation rate, colony forming efficacy, motility, and tumor forming capacity both in in vitro and in vivo assays. We demonstrate that mot-N promotes carcinogenesis and cancer cell metastasis by inactivation of tumor suppressor protein p53 functions and by interaction and functional activation of telomerase and heterogeneous ribonucleoprotein K (hnRNP-K) proteins. | en_US |
dc.description.sponsorship | This work was supported by grants-in-aid for scientific research (Kakenhi) from the Japanese Society for the Promotion of Science, Japan (to S. C. K.); by Ministry of Knowledge Economy Grant 10030051 (to C.-O. Y.); and by Korea Science Engineering Foundation Grants 2010-0029220, 2013K1A1A2A02050188, and 2013M3A9D3045879 (to C.-O. Y.). | en_US |
dc.language.iso | en | en_US |
dc.publisher | American Society of Biological Chemists. | en_US |
dc.subject | Cancer Biology | en_US |
dc.subject | Heat Shock Protein (HSP) | en_US |
dc.subject | p53 | en_US |
dc.subject | Telomerase | en_US |
dc.subject | Tumor Promoter | en_US |
dc.subject | hnRNP-K | en_US |
dc.subject | Mortalin | en_US |
dc.subject | Nuclear Localization | en_US |
dc.subject | p53 Inactivation | en_US |
dc.subject | Telomerase Activation | en_US |
dc.title | Identification and Functional Characterization of Nuclear Mortalin in Human Carcinogenesis | en_US |
dc.type | Article | en_US |
dc.relation.volume | 289 | - |
dc.identifier.doi | 10.1074/jbc.M114.565929 | - |
dc.relation.page | 24832-24844 | - |
dc.relation.journal | JOURNAL OF BIOLOGICAL CHEMISTRY | - |
dc.contributor.googleauthor | Ryu, Jihoon | - |
dc.contributor.googleauthor | Kaul, Zeenia | - |
dc.contributor.googleauthor | Yoon, A-Rum | - |
dc.contributor.googleauthor | Liu, Ye | - |
dc.contributor.googleauthor | Yaguchi, Tomoko | - |
dc.contributor.googleauthor | Na, Youjin | - |
dc.contributor.googleauthor | Ahn, Hyo Min | - |
dc.contributor.googleauthor | Gao, Ran | - |
dc.contributor.googleauthor | Choi, Il-Kyu | - |
dc.contributor.googleauthor | Yun, Chae-Ok | - |
dc.contributor.googleauthor | 윤채옥 | - |
dc.relation.code | 2014032501 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF ENGINEERING[S] | - |
dc.sector.department | DEPARTMENT OF BIOENGINEERING | - |
dc.identifier.pid | chaeok | - |
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