Full metadata record
DC Field | Value | Language |
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dc.citation.startPage | 10071 | - |
dc.citation.title | NATURE COMMUNICATIONS | - |
dc.citation.volume | 6 | - |
dc.contributor.author | An, Jungeun | - |
dc.contributor.author | Gonzalez-Avalos, E. | - |
dc.contributor.author | Chawla, Ashu | - |
dc.contributor.author | Jeong, Mira | - |
dc.contributor.author | Lopez-Moyado, Isaac F. | - |
dc.contributor.author | Li, Wei | - |
dc.contributor.author | Goodell, Margaret A. | - |
dc.contributor.author | Chavez, Lukas | - |
dc.contributor.author | Ko, Myunggon | - |
dc.contributor.author | Rao, Anjana | - |
dc.date.accessioned | 2023-12-22T00:37:23Z | - |
dc.date.available | 2023-12-22T00:37:23Z | - |
dc.date.created | 2015-12-08 | - |
dc.date.issued | 2015-11 | - |
dc.description.abstract | TET-family dioxygenases oxidize 5-methylcytosine (5mC) in DNA, and exert tumour suppressor activity in many types of cancers. Even in the absence of TET coding region mutations, TET loss-of-function is strongly associated with cancer. Here we show that acute elimination of TET function induces the rapid development of an aggressive, fully-penetrant and cell-autonomous myeloid leukaemia in mice, pointing to a causative role for TET loss-of-function in this myeloid malignancy. Phenotypic and transcriptional profiling shows aberrant differentiation of haematopoietic stem/progenitor cells, impaired erythroid and lymphoid differentiation and strong skewing to the myeloid lineage, with only a mild relation to changes in DNA modification. We also observe progressive accumulation of phospho-H2AX and strong impairment of DNA damage repair pathways, suggesting a key role for TET proteins in maintaining genome integrity | - |
dc.identifier.bibliographicCitation | NATURE COMMUNICATIONS, v.6, pp.10071 | - |
dc.identifier.doi | 10.1038/ncomms10071 | - |
dc.identifier.issn | 2041-1723 | - |
dc.identifier.scopusid | 2-s2.0-84948446391 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/17940 | - |
dc.identifier.url | http://www.nature.com/ncomms/2015/151126/ncomms10071/full/ncomms10071.html | - |
dc.identifier.wosid | 000366377600001 | - |
dc.language | 영어 | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.title | Acute loss of TET function results in aggressive myeloid cancer in mice | - |
dc.type | Article | - |
dc.description.isOpenAccess | TRUE | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordPlus | HEMATOPOIETIC STEM-CELLS | - |
dc.subject.keywordPlus | METHYLCYTOSINE OXIDASES TET1 | - |
dc.subject.keywordPlus | TUMOR-SUPPRESSOR | - |
dc.subject.keywordPlus | SELF-RENEWAL | - |
dc.subject.keywordPlus | DNA METHYLATION | - |
dc.subject.keywordPlus | DYNAMIC CHANGES | - |
dc.subject.keywordPlus | PROTEINS | - |
dc.subject.keywordPlus | 5-METHYLCYTOSINE | - |
dc.subject.keywordPlus | DIFFERENTIATION | - |
dc.subject.keywordPlus | MUTATIONS | - |
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