Control of translation and mRNA degradation by miRNAs and siRNAs.

By M. A. Valencia-Sanchez, Jidong Liu, Gregory J. Hannon, R. Parker. Genes & Development, 2006

2,131 citations recorded by the source corpus.

The control of translation and mRNA degradation is an important part of the regulation of gene expression. It is now clear that small RNA molecules are common and effective modulators of gene expression in many eukaryotic cells. These small RNAs that control gene expression can be either endogenous or exogenous micro RNAs (miRNAs) and short interfering RNAs (siRNAs) and can affect mRNA degradation and translation, as well as chromatin structure, thereby having impacts on transcription rates. In this review, we discuss possible mechanisms by which miRNAs control translation and mRNA degradation. An emerging theme is that miRNAs, and siRNAs to some extent, target mRNAs to the general eukaryotic machinery for mRNA degradation and translation control.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/016896770295b80ba404dc3e8e294040b5c4df3f

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Citations in the corpus

Argonaute proteins: key players in RNA silencing (2008, background): “Factors that are suggested to be important are those responsible for regulating the stability and turnover rate of the targeted RNA and/or the miRNA–target comple”
Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives (2011, background): “In addition, the recently discovered microRNAs, which bind to messenger RNAs to interfere with their translational process, play a significant role in the regulation of gene and protein expressions and hence a variety of biological processes (430, 551, 585).”
Argonaute2 complexes carry a population of circulating microRNAs independent of vesicles in human plasma (2011, background): “Our finding of Ago2– miRNA complexes in the circulation raises the interesting possibility that, as the core catalytic component of the miRNAinduced silencing complex (22), these complexes may be poised to regulate gene expression in recipient cells.”
XRN 5’→3’ exoribonucleases: Structure, mechanisms and functions (2013, background): “More often,miRNA function in animal cells is associatedwith translational inhibition and the corresponding targets undergo deadenylation-dependent decay by XRN1 [34,36,83,84].”
DGCR8 is essential for microRNA biogenesis and silencing of embryonic stem cell self-renewal (2007, background): “miRNAs are well suited to perform this task by inhibiting the translation of several target”
The MicroRNA miR-124 promotes neuronal differentiation by triggering brain-specific alternative pre-mRNA splicing. (2007, background): “miRNAs are 22 nt noncoding RNAs that play important roles in the posttranscriptional regulation of gene expression (Bartel, 2004; Kim, 2005; Kloosterman and Plasterk, 2006; Valencia-Sanchez et al., 2006).”
MicroRNA expression alterations are linked to tumorigenesis and non-neoplastic processes in pancreatic ductal adenocarcinoma (2007, background): “Upon binding to their target RNAs, miRNAs cause posttranscriptional gene silencing by either cleaving the target mRNA or by inhibiting the translation process (Valencia-Sanchez et al., 2006).”
P bodies: at the crossroads of post-transcriptional pathways (2007, background): “jpg" NDATA ITEM> ]> Eukaryotic gene expression involves several post-transcriptional events that share mRNA as a common substrat”
mRNA degradation by miRNAs and GW182 requires both CCR4:NOT deadenylase and DCP1:DCP2 decapping complexes. (2006, background): “…components of P-bodies in yeast and/or human cells include the CCR4:NOT deadenylase complex, auxiliary decapping factors (e.g., the LSm1–7 complex and Pat1p/Mtr1p), the cap-binding protein eIF4E, and the RNA helicase Dhh1/Me31B involved in translational repression (Valencia-Sanchez et al. 2006).”
Dysregulation of cardiogenesis, cardiac conduction, and cell cycle in mice lacking miRNA-1-2. (2007, background): “These would represent targets regulated at the level of mRNA stability rather than via translational inhibition (Valencia-Sanchez et al., 2006).”