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2014学年春季学期系列学术讲座之八
题目：From RNA editing to RNA silencing: How ADAR1 responds to stress
报告人：Kazuko Nishikura
Professor, The Wistar Institute, Philadelphia, PA
时间：2014年5月16日（周五），13:00-14:30 PM
地点：威廉希尔一楼邓祐才报告厅
Adenosine deaminases acting on RNA (ADARs) are involved in RNA editing that converts adenosine residues to inosine specifically in double-stranded RNAs (dsRNA) (1). This A-to-I RNA editing pathway and the RNA interference (RNAi) pathway seem to interact antagonistically by competing for their common dsRNA substrates. For instance, A-to-I editing of certain microRNA (miRNA) precursors by ADAR1 and ADAR2 inhibits their processing to mature miRNAs (2). Recent studies unexpectedly revealed the presence of a completely different type of interaction between the RNA editing mechanism and the RNAi machinery (3). ADAR1 forms a complex via direct protein-protein interaction with Dicer, an RNase III gene family member involved in the RNAi mechanism. ADAR1 in the Dicer complex promotes pre-miRNA cleavage by Dicer and facilitates loading of miRNA onto RNA-induced silencing complexes, giving rise to an unsuspected stimulative function of ADAR1 on miRNA processing and RNAi mechanisms. ADAR1 differentiates its functions in RNA editing and RNAi by formation of either ADAR1-ADAR1 homodimer or Dicer-ADAR1 heterodimer complexes. Expression of miRNAs is globally inhibited in ADAR1 null mouse embryos, which in turn alters expression of their target genes and may contribute to their embryonic lethal phenotype. Current efforts are focused on identification of the mechanism that switches ADAR1 function from RNA editing to RNA silencing.
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