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The molecular signature of oncofusion proteins in acute myeloid leukemia
被引:77
|作者:
Martens, Joost H. A.
[1
]
Stunnenberg, Henk G.
[1
]
机构:
[1] Radboud Univ Nijmegen, Dept Mol Biol, Fac Sci, Nijmegen Ctr Mol Life Sci, NL-6500 HB Nijmegen, Netherlands
关键词:
Acute myeloid leukemia;
Oncofusion protein;
Transcriptional regulation;
Epigenetic;
ACUTE PROMYELOCYTIC LEUKEMIA;
SERUM RESPONSE FACTOR;
ACUTE LYMPHOBLASTIC-LEUKEMIA;
MYOSIN HEAVY-CHAIN;
GENE-EXPRESSION;
FUSION PROTEIN;
TRANSCRIPTION FACTOR;
RAR-ALPHA;
HISTONE DEACETYLASE;
HEMATOPOIETIC-CELLS;
D O I:
10.1016/j.febslet.2010.04.002
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Acute myeloid leukemia (AML) associated translocations often cause gene fusions that encode onco-fusion proteins. Although many of the breakpoints involved in chromosomal translocations have been cloned, in most cases the role of the chimeric proteins in tumorigenesis is not elucidated. Here we will discuss the fusion proteins of the 4 most common translocations associated with AML as well as the common molecular mechanisms that these four and other fusion proteins utilize to transform progenitor cells. Intriguingly, although the individual partners within the fusion proteins represent a wide variety of cellular functions, at the molecular level many commodities can be found. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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页码:2662 / 2669
页数:8
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