ETO, a Target of t(8;21) in Acute Leukemia, Makes Distinct Contacts with Multiple Histone Deacetylases and Binds mSin3A through Its Oligomerization Domain
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James R. Downing | Hironori Harada | J. Downing | N. Lenny | J. Nip | S. Hiebert | B. Lutterbach | H. Harada | Scott W. Hiebert | Joseph M. Amann | John Nip | David K. Strom | Bart Lutterbach | Noel Lenny | Shari Meyers | S. Meyers | J. Amann | D. Strom
[1] M. Grez,et al. Multiple Regions of ETO Cooperate in Transcriptional Repression* , 2001, The Journal of Biological Chemistry.
[2] B. Hug,et al. Oligomerization of ETO Is Obligatory for Corepressor Interaction , 2001, Molecular and Cellular Biology.
[3] P G Pelicci,et al. Histone deacetylase-targeted treatment restores retinoic acid signaling and differentiation in acute myeloid leukemia. , 2001, Cancer research.
[4] J. Qin,et al. Both corepressor proteins SMRT and N‐CoR exist in large protein complexes containing HDAC3 , 2000, The EMBO journal.
[5] C. Glass,et al. The histone deacetylase-3 complex contains nuclear receptor corepressors. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[6] James D. Winkler,et al. Cloning and Characterization of a Novel Human Class I Histone Deacetylase That Functions as a Transcription Repressor* , 2000, The Journal of Biological Chemistry.
[7] A. Friedman,et al. Exogenous cdk4 overcomes reducedcdk4 RNA and inhibition of G1 progression in hematopoietic cells expressing a dominant-negative CBF – a model for overcoming inhibition of proliferation by CBF oncoproteins , 2000, Oncogene.
[8] S. Minucci,et al. Oligomerization of RAR and AML1 transcription factors as a novel mechanism of oncogenic activation. , 2000, Molecular cell.
[9] R. Shiekhattar,et al. A core SMRT corepressor complex containing HDAC3 and TBL1, a WD40-repeat protein linked to deafness. , 2000, Genes & development.
[10] J. Licht,et al. The ETO Protein Disrupted in t(8;21)-Associated Acute Myeloid Leukemia Is a Corepressor for the Promyelocytic Leukemia Zinc Finger Protein , 2000, Molecular and Cellular Biology.
[11] James R. Downing,et al. Expression of the AML-1 Oncogene Shortens the G1Phase of the Cell Cycle* , 2000, The Journal of Biological Chemistry.
[12] E. Miska,et al. Nuclear receptor corepressors partner with class II histone deacetylases in a Sin3-independent repression pathway. , 2000, Genes & development.
[13] R. Evans,et al. Isolation of a novel histone deacetylase reveals that class I and class II deacetylases promote SMRT-mediated repression. , 2000, Genes & development.
[14] S. Hiebert,et al. The inv(16) encodes an acute myeloid leukemia 1 transcriptional corepressor. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[15] J. Downing,et al. Both TEL and AML-1 Contribute Repression Domains to the t(12;21) Fusion Protein , 1999, Molecular and Cellular Biology.
[16] S. Schreiber,et al. Three proteins define a class of human histone deacetylases related to yeast Hda1p. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[17] J. Davis,et al. ETO-2, a new member of the ETO-family of nuclear proteins , 1999, Oncogene.
[18] S. Minucci,et al. Aberrant Recruitment of the Nuclear Receptor Corepressor-Histone Deacetylase Complex by the Acute Myeloid Leukemia Fusion Partner ETO , 1998, Molecular and Cellular Biology.
[19] C. Glass,et al. ETO, a Target of t(8;21) in Acute Leukemia, Interacts with the N-CoR and mSin3 Corepressors , 1998, Molecular and Cellular Biology.
[20] P. Pandolfi,et al. Therapeutic targeting of transcription in acute promyelocytic leukemia by use of an inhibitor of histone deacetylase. , 1998, Journal of the National Cancer Institute.
[21] T. Hoshino,et al. ETO, fusion partner in t(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDAC1 complex. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[22] T. Nagase,et al. The partner gene of AML1 in t(16;21) myeloid malignancies is a novel member of the MTG8(ETO) family. , 1998, Blood.
[23] J. Schuetz,et al. The MYND Motif Is Required for Repression of Basal Transcription from the Multidrug Resistance 1 Promoter by the t(8;21) Fusion Protein , 1998, Molecular and Cellular Biology.
[24] Y. Ito,et al. Negative regulation of granulocytic differentiation in the myeloid precursor cell line 32Dcl3 by ear-2, a mammalian homolog of Drosophila seven-up, and a chimeric leukemogenic gene, AML1/ETO. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[25] N. Nomura,et al. The AML1-MTG8 Leukemic Fusion Protein Forms a Complex with a Novel Member of the MTG8(ETO/CDR) Family, MTGR1 , 1998, Molecular and Cellular Biology.
[26] J. Downing,et al. The t(8;21) Fusion Product, AML-1–ETO, Associates with C/EBP-α, Inhibits C/EBP-α-Dependent Transcription, and Blocks Granulocytic Differentiation , 1998, Molecular and Cellular Biology.
[27] J. Downing,et al. The t(8;21) fusion product, AML-1-ETO, associates with C/EBP-alpha, inhibits C/EBP-alpha-dependent transcription, and blocks granulocytic differentiation. , 1998, Molecular and cellular biology.
[28] B. O’Malley,et al. Gene silencing by chicken ovalbumin upstream promoter-transcription factor I (COUP-TFI) is mediated by transcriptional corepressors, nuclear receptor-corepressor (N-CoR) and silencing mediator for retinoic acid receptor and thyroid hormone receptor (SMRT). , 1997, Molecular endocrinology.
[29] Wen‐Ming Yang,et al. Histone Deacetylases Associated with the mSin3 Corepressor Mediate Mad Transcriptional Repression , 1997, Cell.
[30] S. Schreiber,et al. Nuclear Receptor Repression Mediated by a Complex Containing SMRT, mSin3A, and Histone Deacetylase , 1997, Cell.
[31] Stuart L Schreiber,et al. Histone Deacetylase Activity Is Required for Full Transcriptional Repression by mSin3A , 1997, Cell.
[32] J. Cleveland,et al. E2F-1 cooperates with topoisomerase II inhibition and DNA damage to selectively augment p53-independent apoptosis , 1997, Molecular and cellular biology.
[33] N. Speck,et al. CBFβ-SMMHC, expressed in M4Eo AML, reduced CBF DNA-binding and inhibited the G1 to S cell cycle transition at the restriction point in myeloid and lymphoid cells , 1997, Oncogene.
[34] P. Marks,et al. Cell cycle regulatory proteins are targets for induced differentiation of transformed cells: Molecular and clinical studies employing hybrid polar compounds. , 1996, International journal of hematology.
[35] J L Cleveland,et al. E2F-1:DP-1 induces p53 and overrides survival factors to trigger apoptosis , 1995, Molecular and cellular biology.
[36] N. Lenny,et al. Functional domains of the t(8;21) fusion protein, AML-1/ETO. , 1995, Oncogene.
[37] J. Rowley,et al. AML1 and the 8;21 and 3;21 translocations in acute and chronic myeloid leukemia. , 1995, Blood.
[38] R. Mann,et al. Identification of homeotic target genes in Drosophila melanogaster including nervy, a proto-oncogene homologue. , 1995, Genetics.
[39] H. Drabkin,et al. The ETO portion of acute myeloid leukemia t(8;21) fusion transcript encodes a highly evolutionarily conserved, putative transcription factor. , 1994, Cancer research.
[40] F. Collins,et al. Fusion between transcription factor CBF beta/PEBP2 beta and a myosin heavy chain in acute myeloid leukemia. , 1993, Science.
[41] M. Ohki,et al. The t(8;21) translocation in acute myeloid leukemia results in production of an AML1‐MTG8 fusion transcript. , 1993, The EMBO journal.
[42] R. Tjian,et al. Molecular cloning and functional analysis of Drosophila TAF110 reveal properties expected of coactivators , 1993, Cell.
[43] H. Drabkin,et al. 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. , 1992, Blood.
[44] M. Gossen,et al. Tight control of gene expression in mammalian cells by tetracycline-responsive promoters. , 1992, Proceedings of the National Academy of Sciences of the United States of America.
[45] M. Ohki,et al. t(8;21) breakpoints on chromosome 21 in acute myeloid leukemia are clustered within a limited region of a single gene, AML1. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[46] R A Laskey,et al. S phase of the cell cycle. , 1989, Science.
[47] M. Ohki,et al. t ( 8 ; 21 ) breakpoints on chromosome 21 in acute myeloid leukemia are clustered within a limited region of a single gene , AMLJ ( chromosomal translocation / cancer genetics , 2022 .