The AML1-ETO fusion protein promotes the expansion of human hematopoietic stem cells

Blood

Volumn 99, Issue 1, 2002, Pages 15-23

  Mulloy, James C ^a   Cammenga, Jörg ^b   MacKenzie, Karen L ^b   Berguido, Francisco J ^b   Moore, Malcolm A S ^b   Nimer, Stephen D ^b  

^a MEMORIAL SLOAN KETTERING CANCER CENTER   (United States)

^b Box 575 ^*

Author keywords

[No Author keywords available]

Indexed keywords

CD34 ANTIGEN; GREEN FLUORESCENT PROTEIN; HYBRID PROTEIN; RETROVIRUS VECTOR;

ACUTE GRANULOCYTIC LEUKEMIA; ACUTE LEUKEMIA; ARTICLE; CHROMOSOME TRANSLOCATION; COLONY FORMING UNIT C; DNA BINDING; FLOW CYTOMETRY; HEMATOPOIESIS; HEMATOPOIETIC STEM CELL; HUMAN; HUMAN CELL; LEUKEMIA CELL; LEUKEMOGENESIS; NONHUMAN; PRIORITY JOURNAL; PROTEIN PROTEIN INTERACTION;

EID: 0036095217     PISSN: 00064971     EISSN: None     Source Type: Journal    
DOI: 10.1182/blood.V99.1.15     Document Type: Article

References (33)

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3. AML1, the target of multiple chromosomal translocations in human leukemia, is essential for normal fetal liver hematopoiesis
4. Disruption of the Cbfa2 gene causes necrosis and hemorrhaging in the central nervous system and blocks definitive hematopoiesis
5. The CBFbeta subunit is essential for CBFalpha2 (AML1) function in vivo
6. Hematopoiesis in the fetal liver is impaired by targeted mutagenesis of a gene encoding a non-DNA binding sub-unit of the transcription factor, polyomavirus enhancer binding protein 2/core binding factor
7. Absence of fetal liver hematopoiesis in mice deficient in transcriptional coactivator core binding factor beta
8. Role of the transcription factor AML-1 in acute leukemia and hematopoietic differentiation
9. ETO, a target of t(8;21) in acute leukemia, interacts with the N-CoR and mSin3 corepressors
10. Aberrant recruitment of the nuclear receptor corepressor-histone deacetylase complex by the acute myeloid leukemia fusion partner ETO
11. ETO fusion partner int(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDAC1 complex
12. The AML1-MTG8 leukemic fusion protein forms a complex with a novel member of the MTG8(ETO/CDR) family, MTGR1
13. An acute myeloid leukemia gene, AML1, regulates hemopoietic myeloid cell differentiation and transcriptional activation antagonistically by two alternative spliced forms
14. The t(8;21) fusion product, AML-I-ETO, associates with C/EBP-alpha, inhibits C/EBP-alpha-dependent transcription, and blocks granulocytic differentiation
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16. Expression of a knocked-in AML1-ETO leukemia gene inhibits the establishment of normal definitive hematopoiesis and directly generates dysplastic hematopoietic progenitors
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24. The t(8;21) fusion protein, AML1/ETO, transforms NIH3T3 cells and activates AP-1
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27. Analysis of genes under the downstream control of the t(8;21) fusion protein AML1-MTG8: Overexpression of the TIS11b (ERF-1, cMG1) gene induces myeloid cell proliferationin response to G-CSF
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