The Whereabouts of microRNA Actions: Cytoplasm and Beyond

Leung, Anthony K.L.

doi:10.1016/j.tcb.2015.07.005

Cited by 164 publications

(137 citation statements)

References 96 publications

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“…This study strengthened the finding that the cellular abundance of miRNAs can be a poor indicator of their RNA-decay activity as already envisioned 4,5,24,50,51 . miRNA sequestration significantly reduces the active and free fraction of a given miRNA.…”

Section: Discussionsupporting

confidence: 83%

A non-coding function of TYRP1 mRNA promotes melanoma growth

et al. 2017

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Section: Discussionsupporting

confidence: 83%

A non-coding function of TYRP1 mRNA promotes melanoma growth

et al. 2017

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“…Other stressors that trigger SG formation—including arsenite, heat shock, and glucose deprivation—also trigger AGO2 poly-ADP-ribosylation [99]. The polymerases responsible for this post-translational modification are also recruited to SGs during stress, so their colocalization in SGs could be a means to post-translationally modify AGO2 and decrease this protein’s ability to support miRNA activity [100]. Another mechanism by which SG formation likely represses miRNAs is by repressing their synthesis.…”

Section: Stress Granules and Rna Degradationmentioning

confidence: 99%

Stress and the nonsense-mediated RNA decay pathway

Goetz

Wilkinson

2017

Cell. Mol. Life Sci.

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Cells respond to internal and external cellular stressors by activating stress response pathways that re-establish homeostasis. If homeostasis is not achieved in a timely manner, stress pathways trigger programmed cell death (apoptosis) to preserve organism integrity. A highly-conserved stress pathway is the unfolded protein response (UPR), which senses excessive amounts of unfolded proteins in the ER. While a physiologically beneficial pathway, the UPR requires tight regulation to provide a beneficial outcome and avoid deleterious consequences. Recent work has demonstrated that a conserved and highly selective RNA degradation pathway—Nonsense-Mediated RNA Decay (NMD)—serves as a major regulator of the UPR pathway. NMD degrades mRNAs encoding UPR components to prevent UPR activation in response to innocuous ER stress. In response to strong ER stress, NMD is inhibited by the UPR to allow for a full-magnitude UPR response. Recent studies have indicated that NMD also has other stress-related functions, including promoting the timely termination of the UPR to avoid apoptosis; NMD also regulates responses to non-ER stressors, including hypoxia, amino-acid deprivation, and pathogen infection. NMD regulates stress responses in species across the phylogenetic scale, suggesting it has conserved roles in shaping stress responses. Stress pathways are frequently constitutively activated or dysregulated in human disease, raising the possibility that “NMD therapy” may provide clinical benefit by downmodulating stress responses.

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“…Changing the length of the 3 0 UTR is believed to affect the stability, localization, transport, and even translation of the mRNA through altered interactions with microRNAs or other regulatory RNA binding proteins. [28][29][30][31][32] Several polyadenylation factors have been implicated in APA including CF1m 33,34 and CstF. 35,36 For example, knockdown of CF1m25 (CF1m25 KD) or CstF64 (CstF64 KD) has been shown to result in the activation of alternative poly(A) sites.…”

Section: Introductionmentioning

confidence: 99%

Coupling between alternative polyadenylation and alternative splicing is limited to terminal introns

et al. 2016

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Alternative polyadenylation has been implicated as an important regulator of gene expression. In some cases, alternative polyadenylation is known to couple with alternative splicing to influence last intron removal. However, it is unknown whether alternative polyadenylation events influence alternative splicing decisions at upstream exons. Knockdown of the polyadenylation factors CFIm25 or CstF64 in HeLa cells was used as an approach in identifying alternative polyadenylation and alternative splicing events on a genome-wide scale. Although hundreds of alternative splicing events were found to be differentially spliced in the knockdown of CstF64, genes associated with alternative polyadenylation did not exhibit an increased incidence of alternative splicing. These results demonstrate that the coupling between alternative polyadenylation and alternative splicing is usually limited to defining the last exon. The striking influence of CstF64 knockdown on alternative splicing can be explained through its effects on UTR selection of known splicing regulators such as hnRNP A2/B1, thereby indirectly influencing splice site selection. We conclude that changes in the expression of the polyadenylation factor CstF64 influences alternative splicing through indirect effects.

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The Whereabouts of microRNA Actions: Cytoplasm and Beyond

Cited by 164 publications

References 96 publications

A non-coding function of TYRP1 mRNA promotes melanoma growth

A non-coding function of TYRP1 mRNA promotes melanoma growth

Stress and the nonsense-mediated RNA decay pathway

Coupling between alternative polyadenylation and alternative splicing is limited to terminal introns

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