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本文引用的文献

1
ETO, a target of t(8;21) in acute leukemia, interacts with the N-CoR and mSin3 corepressors.ETO是急性白血病中t(8;21)的一个靶点，它与N-CoR和mSin3共抑制因子相互作用。
Mol Cell Biol. 1998 Dec;18(12):7176-84. doi: 10.1128/MCB.18.12.7176.
2
The AML1-MTG8 leukemic fusion protein forms a complex with a novel member of the MTG8(ETO/CDR) family, MTGR1.AML1-MTG8白血病融合蛋白与MTG8（ETO/CDR）家族的一个新成员MTGR1形成复合物。
Mol Cell Biol. 1998 Feb;18(2):846-58. doi: 10.1128/MCB.18.2.846.
3
The t(8;21) fusion product, AML-1-ETO, associates with C/EBP-alpha, inhibits C/EBP-alpha-dependent transcription, and blocks granulocytic differentiation.t(8;21)融合产物AML-1-ETO与C/EBP-α结合，抑制C/EBP-α依赖的转录，并阻断粒细胞分化。
Mol Cell Biol. 1998 Jan;18(1):322-33. doi: 10.1128/MCB.18.1.322.
4
p53-dependent regulation of MDR1 gene expression causes selective resistance to chemotherapeutic agents.p53 依赖的 MDR1 基因表达调控导致对化疗药物的选择性耐药。
Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):11037-42. doi: 10.1073/pnas.94.20.11037.
5
Transcriptional regulation during myelopoiesis.髓系造血过程中的转录调控。
Mol Biol Rep. 1997 Aug;24(3):157-68. doi: 10.1023/a:1006859700409.
6
Acute myeloid leukemia in the elderly: assessment of multidrug resistance (MDR1) and cytogenetics distinguishes biologic subgroups with remarkably distinct responses to standard chemotherapy. A Southwest Oncology Group study.老年急性髓系白血病：多药耐药（MDR1）及细胞遗传学评估可区分对标准化疗反应显著不同的生物学亚组。一项西南肿瘤协作组研究。
Blood. 1997 May 1;89(9):3323-9.
7
Embryonic lethality and impairment of haematopoiesis in mice heterozygous for an AML1-ETO fusion gene.AML1-ETO融合基因杂合小鼠的胚胎致死性和造血功能损伤。
Nat Genet. 1997 Mar;15(3):303-6. doi: 10.1038/ng0397-303.
8
Functional characterization of ETV6 and ETV6/CBFA2 in the regulation of the MCSFR proximal promoter.ETV6和ETV6/CBFA2在巨噬细胞集落刺激因子受体（MCSFR）近端启动子调控中的功能特性
Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1949-54. doi: 10.1073/pnas.94.5.1949.
9
AML1A and AML1B can transactivate the human IL-3 promoter.AML1A和AML1B可反式激活人白细胞介素-3启动子。
J Immunol. 1997 Mar 1;158(5):2251-8.
10
The CBFbeta subunit is essential for CBFalpha2 (AML1) function in vivo.CBFβ亚基对于CBFα2（AML1）在体内的功能至关重要。
Cell. 1996 Nov 15;87(4):697-708. doi: 10.1016/s0092-8674(00)81389-6.

MYND基序是t(8;21)融合蛋白抑制多药耐药1启动子基础转录所必需的。

The MYND motif is required for repression of basal transcription from the multidrug resistance 1 promoter by the t(8;21) fusion protein.

作者信息

Lutterbach B, Sun D, Schuetz J, Hiebert S W

机构信息

Department of Biochemistry and the Vanderbilt Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37027, USA.

出版信息

Mol Cell Biol. 1998 Jun;18(6):3604-11. doi: 10.1128/MCB.18.6.3604.

DOI:10.1128/MCB.18.6.3604
PMID:9584201
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC108942/
Abstract

Chromosomal translocations in acute leukemia that affect the AML-1/CBFbeta transcription factor complex create dominant inhibitory proteins. However, the mechanisms by which these proteins act remain obscure. Here we demonstrate that the multidrug resistance 1 (MDR-1) promoter is a target for AML/ETO transcriptional repression. This repression is of basal, not activated, expression from the MDR-1 promoter and thus represents a new mechanism for AML/ETO function. We have defined two domains in AML/ETO that are required for repression of basal transcription from the MDR-1 promoter: a hydrophobic heptad repeat (HHR) motif and a conserved zinc finger (ZnF) domain termed the MYND domain. The HHR mediates formation of AML/ETO homodimers and AML/ETO-ETO heterodimers. Single serine substitutions at conserved cysteine residues within the predicted ZnFs also abrogate transcriptional repression. Finally, we observe that AML/ETO can also inhibit Ets-1 activation of the MDR-1 promoter, indicating that AML/ETO can disrupt both basal and Ets-1-dependent transcription. The fortuitous inhibition of MDR-1 expression in t(8;21)-containing leukemias may contribute to the favorable response of these patients to chemotherapeutic drugs.

摘要

急性白血病中影响AML-1/CBFβ转录因子复合体的染色体易位会产生显性抑制蛋白。然而，这些蛋白的作用机制仍不清楚。在此我们证明多药耐药1（MDR-1）启动子是AML/ETO转录抑制的靶点。这种抑制作用针对的是MDR-1启动子的基础表达而非激活表达，因此代表了AML/ETO发挥功能的一种新机制。我们已经确定了AML/ETO中两个抑制MDR-1启动子基础转录所需的结构域：一个疏水七肽重复（HHR）基序和一个被称为MYND结构域的保守锌指（ZnF）结构域。HHR介导AML/ETO同二聚体和AML/ETO-ETO异二聚体的形成。预测的ZnF内保守半胱氨酸残基处的单个丝氨酸取代也会消除转录抑制。最后，我们观察到AML/ETO还能抑制Ets-1对MDR-1启动子的激活，这表明AML/ETO可以破坏基础转录和Ets-1依赖的转录。在含有t(8;21)的白血病中MDR-1表达的偶然抑制可能有助于这些患者对化疗药物产生良好反应。