MLL fusion proteins preferentially regulate a subset of wild-type MLL target genes in the leukemic genome. - Test2 - elhamkhani - TriplyDB

MLL fusion proteins preferentially regulate a subset of wild-type MLL target genes in the leukemic genome.

MLL fusion proteins preferentially regulate a subset of wild-type MLL target genes in the leukemic genome.

http://www.wikidata.org/entity/Q35083272

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Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia Structure-function analyses of the human SIX1–EYA2 complex reveal insights into metastasis and BOR syndrome A SALL4/MLL/HOXA9 pathway in murine and human myeloid leukemogenesis Degree of recruitment of DOT1L to MLL-AF9 defines level of H3K79 Di- and tri-methylation on target genes and transformation potential.Allosteric inhibitors of the Eya2 phosphatase are selective and inhibit Eya2-mediated cell migration.MicroRNA-30a regulates zebrafish myogenesis through targeting the transcription factor Six1 Replication Study: Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia.EWS/FLI1 regulates EYA3 in Ewing sarcoma via modulation of miRNA-708, resulting in increased cell survival and chemoresistance.Requirement for CDK6 in MLL-rearranged acute myeloid leukemia.Base-pair resolution DNA methylation sequencing reveals profoundly divergent epigenetic landscapes in acute myeloid leukemia.The molecular mechanics of mixed lineage leukemia.Small-molecular modulators of cancer-associated epigenetic mechanisms.Two decades of leukemia oncoprotein epistasis: the MLL1 paradigm for epigenetic deregulation in leukemia.The SIX1-EYA transcriptional complex as a therapeutic target in cancer.PU.1 is essential for MLL leukemia partially via crosstalk with the MEIS/HOX pathway.Targeting DOT1L and HOX gene expression in MLL-rearranged leukemia and beyond Cell cycle control in acute myeloid leukemia.AF4 uses the SL1 components of RNAP1 machinery to initiate MLL fusion- and AEP-dependent transcription.Aberrant expression of homeobox gene SIX1 in Hodgkin lymphoma.Higher expression levels of the HOXA9 gene, closely associated with MLL-PTD and EZH2 mutations, predict inferior outcome in acute myeloid leukemia.Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1l.PBX3 and MEIS1 Cooperate in Hematopoietic Cells to Drive Acute Myeloid Leukemias Characterized by a Core Transcriptome of the MLL-Rearranged Disease The phosphatase-transcription activator EYA1 is targeted by anaphase-promoting complex/Cdh1 for degradation at M-to-G1 transition.Menin-MLL inhibitors block oncogenic transformation by MLL-fusion proteins in a fusion partner-independent manner.The trithorax protein partner menin acts in tandem with EZH2 to suppress C/EBPα and differentiation in MLL-AF9 leukemia.MLL1 and MLL1 fusion proteins have distinct functions in regulating leukemic transcription program An MLL-dependent network sustains hematopoiesis.Distinct pathways regulated by menin and by MLL1 in hematopoietic stem cells and developing B cells.Epigenetic roles of MLL oncoproteins are dependent on NF-κB CDK6 binds and promotes the degradation of the EYA2 protein MLL fusion proteins link transcriptional coactivators to previously active CpG-rich promoters.The bone marrow niche, stem cells, and leukemia: impact of drugs, chemicals, and the environment.The EYA-SO/SIX complex in development and disease.Menin as a hub controlling mixed lineage leukemia.Molecular and Epigenetic Mechanisms of MLL in Human Leukemogenesis.Six1: a critical transcription factor in tumorigenesis.Mechanisms of mixed-lineage leukemia.Initiation of MLL-rearranged AML is dependent on C/EBPα The leukemogenic fusion gene MLL-AF9 alters microRNA expression pattern and inhibits monoblastic differentiation via miR-511 repression.Epigenetic modifiers in normal and malignant hematopoiesis.

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P2860

MLL fusion proteins preferentially regulate a subset of wild-type MLL target genes in the leukemic genome.

http://www.wikidata.org/entity/Q35083272

description

2011 nî lūn-bûn

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2011 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2011 թվականի ապրիլին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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MLL fusion proteins preferenti ...... genes in the leukemic genome.

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MLL fusion proteins preferenti ...... genes in the leukemic genome.

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MLL fusion proteins preferenti ...... genes in the leukemic genome.

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MLL fusion proteins preferenti ...... genes in the leukemic genome.

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Fuhong He

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George Wu

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Hongkai Ji

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Jingfang Dong

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Joseph J Kaberlein

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Jun Wu

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Michael J Thirman

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Qian-Fei Wang

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Roger T Luo

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Ryan Mattison

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P2860

PML/RARalpha targets promoter regions containing PU.1 consensus and RARE half sites in acute promyelocytic leukemia

Pro isomerization in MLL1 PHD3-bromo cassette connects H3K4me readout to CyP33 and HDAC-mediated repression

The PAF complex synergizes with MLL fusion proteins at HOX loci to promote leukemogenesis

Global and Hox-specific roles for the MLL1 methyltransferase

The elongation domain of ELL is dispensable but its ELL-associated factor 1 interaction domain is essential for MLL-ELL-induced leukemogenesis

Hoxa9 and Meis1 are key targets for MLL-ENL-mediated cellular immortalization

Retrovirus-mediated gene transfer of MLL-ELL transforms primary myeloid progenitors and causes acute myeloid leukemias in mice

AGTR1 overexpression defines a subset of breast cancer and confers sensitivity to losartan, an AGTR1 antagonist

Haematopoietic malignancies caused by dysregulation of a chromatin-binding PHD finger

Structure of the MLL CXXC domain-DNA complex and its functional role in MLL-AF9 leukemia.

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21518926

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