The DDX5/Dbp2 subfamily of DEAD-box RNA helicases

被引:69
|
作者
Xing, Zheng [1 ,2 ]
Ma, Wai Kit [3 ]
Tran, Elizabeth J. [1 ,2 ]
机构
[1] Purdue Univ, Dept Biochem, W Lafayette, IN 47906 USA
[2] Purdue Univ, Purdue Ctr Canc Res, W Lafayette, IN 47907 USA
[3] Cold Spring Harbor Lab, POB 100, Cold Spring Harbor, NY 11724 USA
基金
美国国家卫生研究院;
关键词
cancer; DEAD-box; gene regulation; helicase; RNA; PROLIFERATION IN-VITRO; JUNCTION CORE COMPLEX; GENE-EXPRESSION; RIBOSOME BIOGENESIS; CELL-PROLIFERATION; P68; DDX5; COOPERATIVE BINDING; PROTEOMIC ANALYSIS; PROTEIN MSS116P; ATP HYDROLYSIS;
D O I
10.1002/wrna.1519
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The mammalian DEAD-box RNA helicase DDX5, its paralog DDX17, and their orthologs in Saccharomyces cerevisiae and Drosophila melanogaster, namely Dbp2 and Rm62, define a subfamily of DEAD-box proteins. Members from this subfamily share highly conserved protein sequences and cellular functions. They are involved in multiple steps of RNA metabolism including mRNA processing, microRNA processing, ribosome biogenesis, RNA decay, and regulation of long noncoding RNA activities. The DDX5/Dbp2 subfamily is also implicated in transcription regulation, cellular signaling pathways, and energy metabolism. One emerging theme underlying the diverse cellular functions is that the DDX5/Dbp2 subfamily of DEAD-box helicases act as chaperones for complexes formed by RNA molecules and proteins (RNP) in vivo. This RNP chaperone activity governs the functions of various RNA species through their lifetime. Importantly, mammalian DDX5 and DDX17 are involved in cancer progression when overexpressed through alteration of transcription and signaling pathways, meaning that they are possible targets for cancer therapy. This article is categorized under: RNA Interactions with Proteins and Other Molecules > Protein-RNA Interactions: Functional Implications RNA Structure and Dynamics > Influence of RNA Structure in Biological Systems RNA Interactions with Proteins and Other Molecules > RNA-Protein Complexes
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页数:17
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