EVI1 and hematopoietic disorders: History and perspectives

被引：80

作者：

Nucifora, G ^{[1
]}

Laricchia-Robbio, L ^{[1
]}

Senyuk, V ^{[1
]}

机构：

[1] Univ Illinois, Dept Pathol, Chicago, IL 60607 USA

来源：

GENE | 2006年 / 368卷

关键词：

EVI1 (ecotropic viral integration site 1); human leukemia; murine myeloid leukemia; ecotropic retrovirus;

D O I：

10.1016/j.gene.2005.09.020

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

The ecotropic viral integration site I (EVII) gene was identified almost 20 years ago as the integration site of an ecotropic retrovirus leading to murine myeloid leukemia. Since its identification, EVII has slowly been recognized as one of the most aggressive oncogenes associated with human leukemia. Despite the effort of many investigators, still very little is known about this gene. The mechanism by which EVII operates in the transformation of hematopoietic cells is not known, but it is clear that EVII upregulates cell proliferation, impairs cell differentiation, and induces cell transformation. In this review, we summarize the biochemical properties of EVII and the effects of EVII in biological models. (c) 2005 Elsevier B.V. All rights reserved.

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页码：1 / 11

页数：11

相关论文

共 72 条

[1] Establishment of an undifferentiated leukemia cell line (Kasumi-3) with t(3;7)(q27;q22) and activation of the EVI1 gene [J].

Asou, H ;

Suzukawa, K ;

Kita, K ;

Nakase, K ;

Ueda, H ;

Morishita, K ;

Kamada, N .

JAPANESE JOURNAL OF CANCER RESEARCH, 1996, 87 (03) :269-274

[2] The Evi-1 proto-oncogene encodes a transcriptional repressor activity associated with transformation [J].

Bartholomew, C ;

Kilbey, A ;

Clark, AM ;

Walker, M .

ONCOGENE, 1997, 14 (05) :569-577

[3]

BORDEREAUX D, 1990, ONCOGENE, V5, P925

[4] EVI1 abrogates interferon-α response by selectively blocking PML induction [J].

Buonamici, S ;

Li, DL ;

Mikhail, FM ;

Sassano, A ;

Platanias, LC ;

Colamonici, O ;

Anastasi, J ;

Nucifora, G .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (01) :428-436

[5] EVI1 induces myelodysplastic syndrome in mice [J].

Buonamici, S ;

Li, DL ;

Chi, YQ ;

Zhao, R ;

Wang, XR ;

Brace, L ;

Ni, HY ;

Saunthararajah, Y ;

Nucifora, G .

JOURNAL OF CLINICAL INVESTIGATION, 2004, 114 (05) :713-719

[6]

CALMELS B, 2005, BLOOD 0602

[7] 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 [J].

Chakraborty, S ;

Senyuk, V ;

Sitailo, S ;

Chi, YQ ;

Nucifora, G .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (48) :44936-44943

[8] EVI1 promotes cell proliferation by interacting with BRG1 and blocking the repression of BRG1 on E2F1 activity [J].

Chi, YQ ;

Senyuk, V ;

Chakraborty, S ;

Nucifora, G .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (50) :49806-49811

[9] 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 [J].

Cuenco, GM ;

Ren, RB .

ONCOGENE, 2004, 23 (02) :569-579

[10] Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: A model for human AML [J].

Cuenco, GM ;

Nucifora, G ;

Ren, R .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (04) :1760-1765

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