M. Scott
Cancer Cell · 2001–2013
A researcher in the Science corpus: 5 papers; trusts 0 researchers and is trusted by 0 researchers here, as inferred from the citation graph.
Whom M. Scott trusts overall
Their strongest outbound trust, strongest first, inferred from their citations.
Papers from M. Scott's perspective
Ordered by how strongly the researchers M. Scott trusts endorse each paper. Same corpus, a different order for every researcher.
- SUZ12 is required for both the histone methyltransferase activity and the silencing function of the EED-EZH2 complex. (Molecules and Cells)
- hDOT1L links histone methylation to leukemogenesis. (Cell)
- High-resolution profiling of histone methylations in the human genome. (Cell)
- Chromatin signatures in multipotent human hematopoietic stem cells indicate the fate of bivalent genes during differentiation (Cell Stem Cell)
- MLL translocations, histone modifications and leukaemia stem-cell development (Nature Reviews. Cancer)
- Methylation of H3-lysine 79 is mediated by a new family of HMTases without a SET domain. (Current Biology)
- MLL translocations specify a distinct gene expression profile that distinguishes a unique leukemia (Nature Genetics)
- Classification, subtype discovery, and prediction of outcome in pediatric acute lymphoblastic leukemia by gene expression profiling.
- The SET-domain protein superfamily: protein lysine methyltransferases (Genome Biology)
- EZH1 mediates methylation on histone H3 lysine 27 and complements EZH2 in maintaining stem cell identity and executing pluripotency. (Molecules and Cells)
Their papers
- Selective Killing of Mixed Lineage Leukemia Cells by a Potent Small-Molecule DOT1L Inhibitor (2011) — 928 citations
- A selective inhibitor of EZH2 blocks H3K27 methylation and kills mutant lymphoma cells. (2012) — 770 citations
- Coordinated activities of wild-type plus mutant EZH2 drive tumor-associated hypertrimethylation of lysine 27 on histone H3 (H3K27) in human B-cell lymphomas (2010) — 682 citations
- Progesterone receptor contains a proline-rich motif that directly interacts with SH3 domains and activates c-Src family tyrosine kinases. (2001) — 602 citations
- Potent inhibition of DOT1L as treatment of MLL-fusion leukemia. (2013) — 684 citations