AML1-Evi-1 specifically transforms hematopoietic stem cells through fusion of the entire Evi-1 sequence to AML1

No abstract is available for this paper.

• Publication year

  2008

• Venue

  Leukemia

• Publication date

  2008-06-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1038/leu.2008.53PMID 18337762
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• AML1 deletion in adult mice causes splenomegaly and lymphomas

  2006cited by this paper
• Dimerization of MLL fusion proteins and FLT3 activation synergize to induce multiple-lineage leukemogenesis.

  2005cited by this paper
• Oligomerization of Evi-1 regulated by the PR domain contributes to recruitment of corepressor CtBP

  2005cited by this paper
• The distal zinc finger domain of AML1/MDS1/EVI1 is an oligomerization domain involved in induction of hematopoietic differentiation defects in primary cells in vitro.

  2005cited by this paper
• Both AML1 and EVI1 oncogenic components are required for the cooperation of AML1/MDS1/EVI1 with BCR/ABL in the induction of acute myelogenous leukemia in mice

  2004cited by this paper
• AML-1 is required for megakaryocytic maturation and lymphocytic differentiation, but not for maintenance of hematopoietic stem cells in adult hematopoiesis

  2004cited by this paper
• MOZ-TIF2, but not BCR-ABL, confers properties of leukemic stem cells to committed murine hematopoietic progenitors.

  2004cited by this paper
• Loss of Runx1 perturbs adult hematopoiesis and is associated with a myeloproliferative phenotype.

  2004cited by this paper
• Similar MLL-associated leukemias arising from self-renewing stem cells and short-lived myeloid progenitors.

  2003cited by this paper
• MOZ-TIF2-induced acute myeloid leukemia requires the MOZ nucleosome binding motif and TIF2-mediated recruitment of CBP.

  2003cited by this paper
• The leukemia-associated transcription repressor AML1/MDS1/EVI1 requires CtBP to induce abnormal growth and differentiation of murine hematopoietic cells

  2002cited by this paper
• Expression of a conditional AML1-ETO oncogene bypasses embryonic lethality and establishes a murine model of human t(8;21) acute myeloid leukemia.

  2002cited by this paper
• The t(3;21) fusion product, AML1/Evi-1 blocks AML1-induced transactivation by recruiting CtBP

  2002cited by this paper
• AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutations

  2001cited by this paper
• Interaction of EVI1 with cAMP-responsive Element-binding Protein-binding Protein (CBP) and p300/CBP-associated Factor (P/CAF) Results in Reversible Acetylation of EVI1 and in Co-localization in Nuclear Speckles*

  2001cited by this paper
• Evi-1 Transforming and Repressor Activities Are Mediated by CtBP Co-repressor Proteins*

  2001cited by this paper
• The corepressor CtBP interacts with Evi-1 to repress transforming growth factor beta signaling.

  2001cited by this paper
• Analysis of the role of AML1-ETO in leukemogenesis, using an inducible transgenic mouse model.

  2000cited by this paper
• The Evi‐1 oncoprotein inhibits c‐Jun N‐terminal kinase and prevents stress‐induced cell death

  2000cited by this paper
• Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AML.

  2000cited by this paper
• The oncoprotein Evi-1 represses TGF-β signalling by inhibiting Smad3

  1998cited by this paper
• The t(3;21) fusion product, AML1/Evi-1, interacts with Smad3 and blocks transforming growth factor-beta-mediated growth inhibition of myeloid cells.

  1998cited by this paper
• The oncoprotein Evi-1 represses TGF-beta signalling by inhibiting Smad3.

  1998cited by this paper
• The chimeric genes AML1/MDS1 and AML1/EAP inhibit AML1B activation at the CSF1R promoter, but only AML1/MDS1 has tumor-promoter properties.

  1996cited by this paper
• The t(8;21) fusion protein interferes with AML-1B-dependent transcriptional activation

  1995cited by this paper
• The AML1/Evi-1 fusion protein in the t(3;21) translocation exhibits transforming activity on Rat1 fibroblasts with dependence on the Evi-1 sequence.

  1995cited by this paper
• Dual functions of the AML1/Evi-1 chimeric protein in the mechanism of leukemogenesis in t(3;21) leukemias

  1995cited by this paper
• Generation of the AML1‐EVI‐1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia.

  1994cited by this paper
• Evi-1 raises AP-1 activity and stimulates c-fos promoter transactivation with dependence on the second zinc finger domain.

  1994cited by this paper
• Consistent intergenic splicing and production of multiple transcripts between AML1 at 21q22 and unrelated genes at 3q26 in (3;21)(q26;q22) translocations.

  1994cited by this paper
• Identification of AML-1 and the (8;21) translocation protein (AML-1/ETO) as sequence-specific DNA-binding proteins: the runt homology domain is required for DNA binding and protein-protein interactions

  1993cited by this paper
• Identification of breakpoints in t(8;21) acute myelogenous leukemia and isolation of a fusion transcript, AML1/ETO, with similarity to Drosophila segmentation gene, runt.

  1992cited by this paper
• t(8;21) breakpoints on chromosome 21 in acute myeloid leukemia are clustered within a limited region of a single gene, AML1.

  1991cited by this paper

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  2021cites this paper
• KDM4B promotes acute myeloid leukemia associated with AML1‐ETO by regulating chromatin accessibility

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• Expression of Evi-1 Gene in Leukaemia: Diagnostic and Prognostic Perspective

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  2016cites this paper
• Identification of common and distinct epigenetic re-programming properties of Core-Binding Factor (CBF) Fusion Proteins

  2016cites this paper
• Identification of common and distinct epigenetic re-programming properties of Core-Binding Factor (CBF) Fusion Proteins

  2016cites this paper
• RUNX1-Evi-1 fusion gene inhibited differentiation and apoptosis in myelopoiesis: an in vivo study

  2015cites this paper
• Caractérisation clinique et moléculaire de nouvelles translocations chromosomiques ciblant le gène RUNX1 dans les leucémies aiguës de l’adulte

  2012cites this paper
• Fadd and Skp2 are possible downstream targets of RUNX1-EVI1

  2012cites this paper
• EVI1‐mediated down regulation of MIR449A is essential for the survival of EVI1 positive leukaemic cells

  2011cites this paper
• Evi-1 is a transcriptional target of mixed-lineage leukemia oncoproteins in hematopoietic stem cells.

  2011cites this paper
• EVI-1 interacts with histone methyltransferases SUV39H1 and G9a for transcriptional repression and bone marrow immortalization

  2010cites this paper
• The Orphan Nuclear Receptor Nurr1 Restricts the Proliferation of Hematopoietic Stem Cells

  2010cites this paper
• Overexpression or knock‐down of runt‐related transcription factor 1 affects BCR‐ABL‐induced proliferation and migration in vitro and leukemogenesis in vivo in mice

  2009cites this paper
• Pbx1 is a downstream target of Evi-1 in hematopoietic stem/progenitors and leukemic cells

  2009cites this paper
• Identification of the Downstream Effector Genes Involved in HOXB4-Induced Expansion of Hematopoietic Progenitor Cells

  2009cites this paper
• Role of the RUNX1‐EVI1 fusion gene in leukemogenesis

  2008cites this paper