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DC Field | Value | Language |
---|---|---|
dc.citation.endPage | 2090 | - |
dc.citation.number | 12 | - |
dc.citation.startPage | 2076 | - |
dc.citation.title | AUTOPHAGY | - |
dc.citation.volume | 15 | - |
dc.contributor.author | Han, Seung Hun | - |
dc.contributor.author | Korm, Sovannarith | - |
dc.contributor.author | Han, Ye Gi | - |
dc.contributor.author | Choi, Soo-Young | - |
dc.contributor.author | Kim, Soo-Hyun | - |
dc.contributor.author | Chung, Hee Jin | - |
dc.contributor.author | Park, Kibeom | - |
dc.contributor.author | Kim, Jae-Young | - |
dc.contributor.author | Myung, Kyungjae | - |
dc.contributor.author | Lee, Joo-Yong | - |
dc.contributor.author | Kim, Hongtae | - |
dc.contributor.author | Kim, Dong-Wook | - |
dc.date.accessioned | 2023-12-21T18:17:31Z | - |
dc.date.available | 2023-12-21T18:17:31Z | - |
dc.date.created | 2019-05-03 | - |
dc.date.issued | 2019-12 | - |
dc.description.abstract | Imatinib is the first molecularly targeted compound for chronic myeloid leukemia (CML) capable to inhibit BCR-ABL kinase activity. However, recent clinical evidence indicates that a substantial proportion of CML patients exhibit BCR-ABL-dependent or independent resistance to imatinib. Despite the importance of imatinib resistance in CML, the underlying molecular mechanisms of this resistance are largely unknown. Here, we identified GCA (grancalcin) as a critical regulator of imatinib resistance in chronic phase CML via activation of autophagy. Mechanistically, we demonstrated that GCA activates TRAF6 ubiquitin ligase activity to induce Lys63 ubiquitination of ULK1, a crucial regulator of autophagy, resulting in its stabilization and activation. We also highlighted the role of GCA-TRAF6-ULK1 autophagy regulatory axis in imatinib resistance. Our findings represent the basis for novel therapeutic strategies against CML. | - |
dc.identifier.bibliographicCitation | AUTOPHAGY, v.15, no.12, pp.2076 - 2090 | - |
dc.identifier.doi | 10.1080/15548627.2019.1596492 | - |
dc.identifier.issn | 1554-8627 | - |
dc.identifier.scopusid | 2-s2.0-85063671570 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/26647 | - |
dc.identifier.url | https://www.tandfonline.com/doi/full/10.1080/15548627.2019.1596492 | - |
dc.identifier.wosid | 000464622600001 | - |
dc.language | 영어 | - |
dc.publisher | TAYLOR & FRANCIS INC | - |
dc.title | GCA links TRAF6-ULK1-dependent autophagy activation in resistant chronic myeloid leukemia | - |
dc.type | Article | - |
dc.description.isOpenAccess | FALSE | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.type.docType | Article; Early Access | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordAuthor | Autophagy | - |
dc.subject.keywordAuthor | chronic myeloid leukemia (CML) | - |
dc.subject.keywordAuthor | grancalcin (GCA) | - |
dc.subject.keywordAuthor | imatinib resistance | - |
dc.subject.keywordAuthor | TRAF6 | - |
dc.subject.keywordAuthor | ULK1 | - |
dc.subject.keywordPlus | CALCIUM-BINDING PROTEIN | - |
dc.subject.keywordPlus | BCR-ABL | - |
dc.subject.keywordPlus | PHILADELPHIA-CHROMOSOME | - |
dc.subject.keywordPlus | TYROSINE KINASE | - |
dc.subject.keywordPlus | MONITORING AUTOPHAGY | - |
dc.subject.keywordPlus | FOLLOW-UP | - |
dc.subject.keywordPlus | GRANCALCIN | - |
dc.subject.keywordPlus | MTOR | - |
dc.subject.keywordPlus | THERAPY | - |
dc.subject.keywordPlus | PATIENTS RECEIVING IMATINIB | - |
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