Oligomerization of Evi-1 regulated by the PR domain contributes to recruitment of corepressor CtBP

No abstract is available for this paper.

• Publication year

  2005

• Venue

  Oncogene

• Publication date

  2005-09-08

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1038/sj.onc.1208754PMID 15897867
• 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.

• Dimerization: a versatile switch for oncogenesis.

  2004cited by this paper
• Prognostically useful gene-expression profiles in acute myeloid leukemia.

  2004cited by this paper
• Dimerization contributes to oncogenic activation of MLL chimeras in acute leukemias.

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• High EVI1 expression predicts poor survival in acute myeloid leukemia: a study of 319 de novo AML patients.

  2003cited by this paper
• Dimerization of MLL fusion proteins immortalizes hematopoietic cells.

  2003cited by this paper
• Oncogenic receptor tyrosine kinase in leukemia.

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

  2002cited by this paper
• Histone methyltransferases, diet nutrients and tumour suppressors

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• The Human Candidate Tumor Suppressor Gene HIC1 Recruits CtBP through a Degenerate GLDLSKK Motif

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• The corepressor CtBP interacts with Evi-1 to repress transforming growth factor beta signaling.

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

  2001cited by this paper
• Mutations of the Smad4 gene in acute myelogeneous leukemia and their functional implications in leukemogenesis

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• The Evi‐1 oncoprotein inhibits c‐Jun N‐terminal kinase and prevents stress‐induced cell death

  2000cited by this paper
• Acquisition of oncogenic potential by RAR chimeras in acute promyelocytic leukemia through formation of homodimers.

  2000cited by this paper
• Oligomerization of RAR and AML1 transcription factors as a novel mechanism of oncogenic activation.

  2000cited by this paper
• MDS1/EVI1 enhances TGF-β1 signaling and strengthens its growth-inhibitory effect, but the leukemia-associated fusion protein AML1/MDS1/EVI1, product of the t(3;21), abrogates growth-inhibition in response to TGF-β1

  1999cited by this paper
• MLL rearrangements in haematological malignancies: lessons from clinical and biological studies

  1999cited by this paper
• Formation of PML/RARα high molecular weight nuclear complexes through the PML coiled-coil region is essential for the PML/RARα-mediated retinoic acid response

  1999cited by this paper
• The transcription factor Evi-1.

  1999cited by this paper
• Formation of PML/RAR alpha high molecular weight nuclear complexes through the PML coiled-coil region is essential for the PML/RAR alpha-mediated retinoic acid response.

  1999cited by this paper
• The oncoprotein Evi-1 represses TGF-beta signalling by inhibiting Smad3.

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

  1998cited by this paper
• The PR Domain of the Rb-binding Zinc Finger Protein RIZ1 Is a Protein Binding Interface and Is Related to the SET Domain Functioning in Chromatin-mediated Gene Expression*

  1998influential reference
• Smad proteins exist as monomers in vivo and undergo homo‐ and hetero‐oligomerization upon activation by serine/threonine kinase receptors

  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
• Crystal structure of the BTB domain from PLZF.

  1998cited by this paper
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  1997cited by this paper
• Intergenic splicing of MDS1 and EVI1 occurs in normal tissues as well as in myeloid leukemia and produces a new member of the PR domain family.

  1996cited by this paper
• Partnership between DPC4 and SMAD proteins in TGF-β signalling pathways

  1996cited by this paper
• Structurally altered Evi-1 protein generated in the 3q21q26 syndrome.

  1996cited by this paper
• Increased Evi-1 expression is frequently observed in blastic crisis of chronic myelocytic leukemia.

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  1996cited by this paper
• Partnership between DPC4 and SMAD proteins in TGF-beta signalling pathways.

  1996cited 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
• The retinoblastoma protein binds to RIZ, a zinc-finger protein that shares an epitope with the adenovirus E1A protein.

  1995influential reference
• 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
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• Efficient selection for high-expression transfectants with a novel eukaryotic vector

  1991cited by this paper

• EVI1 protein interaction dynamics: targetable for therapeutic intervention?

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• Emerging Roles of PRDM Factors in Stem Cells and Neuronal System: Cofactor Dependent Regulation of PRDM3/16 and FOG1/2 (Novel PRDM Factors)

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• EVI1 carboxy-terminal phosphorylation is ATM-mediated and sustains transcriptional modulation and self-renewal via enhanced CtBP1 association

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• Lethal neonatal bone marrow failure syndrome with multiple congenital abnormalities, including limb defects, due to a constitutional deletion of 3′ MECOM

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• Deletion of Mecom in mouse results in early-onset spinal deformity and osteopenia.

  2014cites this paper
• stem cell function is critical for long-term hematopoietic

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  2013cites this paper
• Expression, function and regulation of Evi-1 during embryonic avian development.

  2013cites this paper
• Caractérisation clinique et moléculaire de nouvelles translocations chromosomiques ciblant le gène RUNX1 dans les leucémies aiguës de l’adulte

  2012cites this paper
• The Increased Expression of Integrin α6 (ITGA6) Enhances Drug Resistance in EVI1high Leukemia

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• Roles of transforming growth factor-β in graft-versus-host and graft-versus-tumor effects.

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

  2011cites this paper
• PR-domain-containing Mds1-Evi1 is critical for long-term hematopoietic stem cell function.

  2011cites this paper
• The role of Runx1/AML1 and Evi‐1 in the regulation of hematopoietic stem cells

  2010cites this paper
• EVI-1 interacts with histone methyltransferases SUV39H1 and G9a for transcriptional repression and bone marrow immortalization

  2010cites this paper
• Evaluation of EVI1 and EVI1s (Delta324) as potential therapeutic targets in ovarian cancer.

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