Oncogenic AKTivation by methylation
| dc.contributor.author | Luciano, Amelia K. | |
| dc.contributor.author | Guertin, David A. | |
| dc.date | 2022-08-11T08:10:17.000 | |
| dc.date.accessioned | 2022-08-23T17:03:16Z | |
| dc.date.available | 2022-08-23T17:03:16Z | |
| dc.date.issued | 2019-02-01 | |
| dc.date.submitted | 2019-07-18 | |
| dc.identifier.citation | <p>Nat Cell Biol. 2019 Feb;21(2):114-115. doi: 10.1038/s41556-019-0275-8. <a href="https://doi.org/10.1038/s41556-019-0275-8">Link to article on publisher's site</a></p> | |
| dc.identifier.issn | 1465-7392 (Linking) | |
| dc.identifier.doi | 10.1038/s41556-019-0275-8 | |
| dc.identifier.pmid | 30692624 | |
| dc.identifier.uri | http://hdl.handle.net/20.500.14038/44387 | |
| dc.description.abstract | AKT, also known as protein kinase B, is one of the most frequently dysregulated serine/threonine kinases in cancer, and its hyperactivity drives tumorigenesis and chemotherapy resistance. Two studies now find that AKT methylation by the methyltransferase SETDB1 is an early step in its oncogenic activation. | |
| dc.language.iso | en_US | |
| dc.relation | <p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=30692624&dopt=Abstract">Link to Article in PubMed</a></p> | |
| dc.relation.url | https://doi.org/10.1038/s41556-019-0275-8 | |
| dc.subject | Cancer | |
| dc.subject | Growth factor signalling | |
| dc.subject | Methylation | |
| dc.subject | Ubiquitylation | |
| dc.subject | Cancer Biology | |
| dc.subject | Cell Biology | |
| dc.subject | Cellular and Molecular Physiology | |
| dc.title | Oncogenic AKTivation by methylation | |
| dc.type | Journal Article | |
| dc.source.journaltitle | Nature cell biology | |
| dc.source.volume | 21 | |
| dc.source.issue | 2 | |
| dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/pmm_pp/114 | |
| dc.identifier.contextkey | 14954526 | |
| html.description.abstract | <p>AKT, also known as protein kinase B, is one of the most frequently dysregulated serine/threonine kinases in cancer, and its hyperactivity drives tumorigenesis and chemotherapy resistance. Two studies now find that AKT methylation by the methyltransferase SETDB1 is an early step in its oncogenic activation.</p> | |
| dc.identifier.submissionpath | pmm_pp/114 | |
| dc.contributor.department | Department of Molecular, Cell, and Cancer Biology | |
| dc.contributor.department | Program in Molecular Medicine | |
| dc.source.pages | 114-115 |