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Specificity in Toll-like receptor signalling through distinct effector functions of TRAF3 and TRAF6
Toll-like receptors (TLRs) are activated by pathogen-associated molecular patterns to induce innate immune responses and production of pro-inflammatory cytokines, interferons and anti-inflammatoryExpand
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Quantitative production of macrophages or neutrophils ex vivo using conditional Hoxb8
Differentiation mechanisms and inflammatory functions of neutrophils and macrophages are usually studied by genetic and biochemical approaches that require costly breeding and time-consumingExpand
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NUP98–NSD1 links H3K36 methylation to Hox-A gene activation and leukaemogenesis
Nuclear receptor-binding SET domain protein 1 (NSD1) prototype is a family of mammalian histone methyltransferases (NSD1, NSD2/MMSET/WHSC1, NSD3/WHSC1L1) that are essential in development and areExpand
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Haematopoietic malignancies caused by dysregulation of a chromatin-binding PHD finger
Histone H3 lysine 4 methylation (H3K4me) has been proposed as a critical component in regulating gene expression, epigenetic states, and cellular identities. The biological meaning of H3K4me isExpand
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An orally bioavailable chemical probe of the Lysine Methyltransferases EZH2 and EZH1.
EZH2 or EZH1 is the catalytic subunit of the polycomb repressive complex 2 that catalyzes methylation of histone H3 lysine 27 (H3K27). The trimethylation of H3K27 (H3K27me3) is a transcriptionallyExpand
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Covalent histone modifications — miswritten, misinterpreted and mis-erased in human cancers
Post-translational modification of histones provides an important regulatory platform for processes such as gene transcription and DNA damage repair. It has become increasingly apparent that theExpand
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Chromatin remodeling and cancer, Part II: ATP-dependent chromatin remodeling.
Connections between perturbations that lie outside of our genome, that is, epigenetic alternations, and tumorigenesis have become increasingly apparent. Dynamic chromatin remodeling of theExpand
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Multiple interactions recruit MLL1 and MLL1 fusion proteins to the HOXA9 locus in leukemogenesis.
MLL1 fusion proteins activate HoxA9 gene expression and cause aggressive leukemias that respond poorly to treatment, but how they recognize and stably bind to HoxA9 is not clearly understood. In aExpand
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Meis1 programs transcription of FLT3 and cancer stem cell character, using a mechanism that requires interaction with Pbx and a novel function of the Meis1 C-terminus.
Meis1 is a homeodomain transcription factor coexpressed with Hoxa9 in most human acute myeloid leukemias (AMLs). In mouse models of leukemia produced by Hoxa9, Meis1 accelerates leukemogenesis.Expand
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Chromatin remodeling and cancer, Part I: Covalent histone modifications.
Dynamic chromatin remodeling underlies many, if not all, DNA-templated biological processes, including gene transcription; DNA replication and repair; chromosome condensation; and segregation andExpand
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