期刊
JOURNAL OF CELL BIOLOGY
卷 182, 期 1, 页码 7-9出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200806069
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资金
- Associazione Italiana per la Ricerca sul Cancro Funding Source: Custom
Nucleophosmin (NPM) is frequently mutated in acute myeloid leukemias and is thought to act as both a protooncogene and a tumor suppressor. Although genetic and molecular evidence has shed light on the mechanisms of NPM-mediated tumor suppression, the potential role of NPM mutants as oncogenes remains ill defined. Now, new data provide a straightforward mechanism for this latter function, as NPM is shown to regulate the stability and the function of MYC. Remarkably, the same leitmotif of placing a critical cell regulator in the wrong place at the wrong time appears to underscore all the cancer-promoting activities of mutated NPM.
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