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dc.contributor.authorLee, Hong-Won-
dc.contributor.authorChoi, Byoungsan-
dc.contributor.authorKang, Han Na-
dc.contributor.authorKim, Hyunwoo-
dc.contributor.authorMin, Ahrum-
dc.contributor.authorCha, Minkwon-
dc.contributor.authorRyu, Ji Young-
dc.contributor.authorPark, Sangwoo-
dc.contributor.authorSohn, Jinyoung-
dc.contributor.authorShin, Kihyuk-
dc.contributor.authorYun, Mi Ran-
dc.contributor.authorHan, Joo Yeun-
dc.contributor.authorShon, Min Ju-
dc.contributor.authorJeong, Cherlhyun-
dc.contributor.authorChung, Junho-
dc.contributor.authorLee, Seung-Hyo-
dc.contributor.authorIm, Seock-Ah-
dc.contributor.authorCho, Byoung Chul-
dc.contributor.authorYoon, Tae-Young-
dc.date.accessioned2024-01-19T23:02:36Z-
dc.date.available2024-01-19T23:02:36Z-
dc.date.created2021-09-03-
dc.date.issued2018-04-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/121524-
dc.description.abstractThe accumulation of genetic and epigenetic alterations in cancer cells rewires cellular signalling pathways through changes in the patterns of protein-protein interactions (PPIs). Understanding these patterns may facilitate the design of tailored cancer therapies. Here, we show that single-molecule pull-down and co-immunoprecipitation techniques can be used to characterize signalling complexes of the human epidermal growth-factor receptor (HER) family in specific cancers. By analysing cancer-specific signalling phenotypes, including post-translational modifications and PPIs with downstream interactions, we found that activating mutations of the epidermal growth-factor receptor (EGFR) gene led to the formation of large protein complexes surrounding mutant EGFR proteins and to a reduction in the dependency of mutant EGFR signalling on phosphotyrosine residues, and that the strength of HER-family PPIs is correlated with the strength of the dependence of breast and lung adenocarcinoma cells on HER-family signalling pathways. Furthermore, using co-immunoprecipitation profiling to screen for EGFR-dependent cancers, we identified non-small-cell lung cancers that respond to an EGFR-targeted inhibitor. Our approach might help predict responses to targeted cancer therapies, particularly for cancers that lack actionable genomic mutations.-
dc.languageEnglish-
dc.publisherNATURE PUBLISHING GROUP-
dc.titleProfiling of protein-protein interactions via single-molecule techniques predicts the dependence of cancers on growth-factor receptors-
dc.typeArticle-
dc.identifier.doi10.1038/s41551-018-0212-3-
dc.description.journalClass1-
dc.identifier.bibliographicCitationNature Biomedical Engineering, v.2, no.4, pp.239 - 253-
dc.citation.titleNature Biomedical Engineering-
dc.citation.volume2-
dc.citation.number4-
dc.citation.startPage239-
dc.citation.endPage253-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000435466700010-
dc.identifier.scopusid2-s2.0-85044743214-
dc.relation.journalWebOfScienceCategoryEngineering, Biomedical-
dc.relation.journalResearchAreaEngineering-
dc.type.docTypeArticle-
dc.subject.keywordPlusCELL LUNG-CANCER-
dc.subject.keywordPlusBINDING-SITES-
dc.subject.keywordPlusKINASE DOMAIN-
dc.subject.keywordPlusSCALE MAP-
dc.subject.keywordPlusMUTATIONS-
dc.subject.keywordPlusGEFITINIB-
dc.subject.keywordPlusTRASTUZUMAB-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusRESISTANCE-
dc.subject.keywordPlusMECHANISM-
dc.subject.keywordAuthorCancer-
dc.subject.keywordAuthorSingle-molecule biophysics-
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KIST Article > 2018
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