implications for mechanisms of pathogenesis familial platelet disorder with predisposition to acute myelogenous leukemia: In vitro analyses of known and novel RUNX1/AML1 mutations in dominant

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  2013

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  Biology, Medicine

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• Structural analyses of DNA recognition by the AML1/Runx-1 Runt domain and its allosteric control by CBFbeta.

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• Dimerization with PEBP2β protects RUNX1/AML1 from ubiquitin–proteasome‐mediated degradation

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• Requirement of Runx1/AML1/PEBP2αB for the generation of haematopoietic cells from endothelial cells

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• Dominant-negative mutations of CEBPA, encoding CCAAT/enhancer binding protein-α (C/EBPα), in acute myeloid leukemia

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• Susceptibility gene for familial acute myeloid leukemia associated with loss of 5q and/or 7q is not localized on the commonly deleted portion of 5q

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• Structural basis for the heterodimeric interaction between the acute leukaemia‐associated transcription factors AML1 and CBFβ

  2000cited by this paper
• High incidence of biallelic point mutations in the Runt domain of the AML1/PEBP2 alpha B gene in Mo acute myeloid leukemia and in myeloid malignancies with acquired trisomy 21.

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• Accommodating haploinsufficient tumour suppressor genes in Knudson's model

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• Mutations of the AML1 gene in myelodysplastic syndrome and their functional implications in leukemogenesis.

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• Immunoglobulin motif DNA recognition and heterodimerization of the PEBP2/CBF Runt domain

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• Role of the transcription factor AML-1 in acute leukemia and hematopoietic differentiation.

  2000cited by this paper
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  2000cited by this paper
• Transcriptional Regulation of the Transforming Growth Factor-β-inducible Mouse Germ Line Ig α Constant Region Gene by Functional Cooperation of Smad, CREB, and AML Family Members*

  2000cited by this paper
• C-kit mutations in core binding factor leukemias.

  2000cited by this paper
• Haploinsufficiency of CBFA2 causes familial thrombocytopenia with propensity to develop acute myelogenous leukaemia

  1999cited by this paper
• CBFA1 mutation analysis and functional correlation with phenotypic variability in cleidocranial dysplasia.

  1999cited by this paper
• Biallelic and heterozygous point mutations in the runt domain of the AML1/PEBP2alphaB gene associated with myeloblastic leukemias.

  1999cited by this paper
• Cleidocranial dysplasia: clinical and molecular genetics

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• Molecular basis of tissue‐specific gene expression mediated by the Runt domain transcription factor PEBP2/CBF

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• Mutation analysis of core binding factor A1 in patients with cleidocranial dysplasia.

  1999cited by this paper
• Identification of an upstream enhancer containing an AML1 site in the human myeloperoxidase (MPO) gene.

  1998cited by this paper
• Familial gastrointestinal stromal tumours with germline mutation of the KIT gene

  1998cited by this paper
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  1998cited by this paper
• Retention of wild‐type p53 in tumors from p53 heterozygous mice: reduction of p53 dosage can promote cancer formation

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• Expression of a knocked-in AML1-ETO leukemia gene inhibits the establishment of normal definitive hematopoiesis and directly generates dysplastic hematopoietic progenitors.

  1998cited by this paper
• Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors.

  1998cited by this paper
• The AML1-MTG8 Leukemic Fusion Protein Forms a Complex with a Novel Member of the MTG8(ETO/CDR) Family, MTGR1

  1998cited by this paper
• Evidence for genetic homogeneity in a familial platelet disorder with predisposition to acute myelogenous leukemia (FPD/AML)

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• Cytoplasmic Sequestration of the Polyomavirus Enhancer Binding Protein 2 (PEBP2)/Core Binding Factor α (CBFα) Subunit by the Leukemia-Related PEBP2/CBFβ-SMMHC Fusion Protein Inhibits PEBP2/CBF-Mediated Transactivation

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  1997cited by this paper
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• Platelet alpha granule deficiency associated with decreased P-selectin and selective impairment of thrombin-induced activation in a new patient with gray platelet syndrome (alpha-storage pool deficiency).

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• The genetics of familial leukemia

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• Disruption of the Cbfa2 gene causes necrosis and hemorrhaging in the central nervous system and blocks definitive hematopoiesis.

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  1996cited by this paper
• Failure of embryonic hematopoiesis and lethal hemorrhages in mouse embryos heterozygous for a knocked-in leukemia gene CBFB-MYH11.

  1996cited by this paper
• Linkage of a familial platelet disorder with a propensity to develop myeloid malignancies to human chromosome 21q22.1-22.2.

  1996cited by this paper
• Regulation of GM-CSF gene transcription by core-binding factor.

  1996cited by this paper
• The AML1/ETO fusion protein blocks transactivation of the GM-CSF promoter by AML1B.

  1995cited by this paper
• Transactivation of the Moloney murine leukemia virus and T-cell receptor beta-chain enhancers by cbf and ets requires intact binding sites for both proteins

  1995cited by this paper
• The t(8;21) fusion protein interferes with AML-1B-dependent transcriptional activation

  1995cited by this paper
• Subcellular localization of the alpha and beta subunits of the acute myeloid leukemia-linked transcription factor PEBP2/CBF

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• An acute myeloid leukemia gene, AML1, regulates hemopoietic myeloid cell differentiation and transcriptional activation antagonistically by two alternative spliced forms.

  1995cited by this paper
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  1994cited by this paper
• The molecular basis of human piebaldism.

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• Decreased content and surface expression of alpha-granule membrane protein GMP-140 in one of two types of platelet alpha delta storage pool deficiency.

  1991cited by this paper
• The "megaprimer" method of site-directed mutagenesis.

  1990cited by this paper
• Studies of a familial platelet disorder

  1985cited by this paper
• Heterogeneity in storage pool deficiency: studies on granule-bound substances in 18 patients including variants deficient in alpha-granules, platelet factor 4, beta-thromboglobulin, and platelet-derived growth factor.

  1979cited by this paper
• A fatal myeloproliferative syndrome in a family with thrombocytopenia and platelet dysfunction

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• A familialdefect in platelet function associated with imapired release of adenosine diphosphate.

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