期刊
JOURNAL OF INTERFERON AND CYTOKINE RESEARCH
卷 34, 期 4, 页码 275-288出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/jir.2013.0147
关键词
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资金
- NIH [AI077556]
- VA Merit Award
- NIH T32 Cancer Biology Training Grant
- National Cancer Institute [T32CA154274]
RNase-L is a mediator of type 1 interferon-induced antiviral activity that has diverse and critical cellular roles, including the regulation of cell proliferation, differentiation, senescence and apoptosis, tumorigenesis, and the control of the innate immune response. Although RNase-L was originally shown to mediate the endonucleolytic cleavage of both viral and ribosomal RNAs in response to infection, more recent evidence indicates that RNase-L also functions in the regulation of cellular mRNAs as an important mechanism by which it exerts its diverse biological functions. Despite this growing body of work, many questions remain regarding the roles of mRNAs as RNase-L substrates. This review will survey known and putative mRNA substrates of RNase-L, propose mechanisms by which it may selectively cleave these transcripts, and postulate future clinical applications.
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