The p65 subunit of nuclear factor-κB is a molecular target for radiation sensitization of human squamous carcinoma cells

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dc.contributor.authorK M Kim-
dc.contributor.authorY Zhang-
dc.contributor.authorBo Yeon Kim-
dc.contributor.authorS J Jeong-
dc.contributor.authorS A Lee-
dc.contributor.authorG D Kim-
dc.contributor.authorA Dritschilo-
dc.contributor.authorM Jung-
dc.date.accessioned2017-04-19T09:01:15Z-
dc.date.available2017-04-19T09:01:15Z-
dc.date.issued2004-
dc.identifier.issn1535-7163-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/6552-
dc.description.abstractThe transcription factor nuclear factor-κB (NF-κB) is activated in response to various stimuli including ionizing radiation. Disruption of NF-κB activation by mutant forms of the NF-κB inhibitor IκB-α or by proteasome inhibitors enhances both sensitivity to radiation and radiation-induced apoptosis. Human squamous carcinoma SCC-35 cells stably expressing a fragment (residues 1 to 84) of human p65 have been shown to exhibit down-regulation of both endogenous p65 mRNA and its protein. The mutant protein also inhibited radiation-induced NF-κB activation 6by preventing the proteolysis of IκB-α. This resulted in enhancement of cellular radiosensitivity and radiation-induced apoptosis. The NH2-terminal region of p65 is thus a potential molecular target for disruption of NF-κB activation and sensitization of tumors to radiotherapy.-
dc.publisherAmer Assoc Cancer Research-
dc.titleThe p65 subunit of nuclear factor-κB is a molecular target for radiation sensitization of human squamous carcinoma cells-
dc.title.alternativeThe p65 subunit of nuclear factor-κB is a molecular target for radiation sensitization of human squamous carcinoma cells-
dc.typeArticle-
dc.citation.titleMolecular Cancer Therapeutics-
dc.citation.number6-
dc.citation.endPage698-
dc.citation.startPage693-
dc.citation.volume3-
dc.contributor.affiliatedAuthorBo Yeon Kim-
dc.contributor.alternativeName김경-
dc.contributor.alternativeNameZhang-
dc.contributor.alternativeName김보연-
dc.contributor.alternativeName정숙-
dc.contributor.alternativeName이성-
dc.contributor.alternativeName김건도-
dc.contributor.alternativeNameDritschilo-
dc.contributor.alternativeName정미라-
dc.identifier.bibliographicCitationMolecular Cancer Therapeutics, vol. 3, no. 6, pp. 693-698-
dc.description.journalClassY-
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Ochang Branch Institute > Chemical Biology Research Center > 1. Journal Articles
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