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Cited by 62RNA Research and SplicingMicroRNA in disease regulationRNA regulation and disease

Functional Interactions Between microRNAs and RNA Binding Proteins

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Jiang, Peng, Coller, Hilary·2012·MicroRNA e
DOI 10.2174/2211536611201010070PMC PMC5123774
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Abstract

Ensuring the appropriate spatial-temporal control of protein abundance requires careful control of transcript levels. This process is regulated at many steps, including the rate at which transcripts decay. microRNAs (miRNAs) and RNA Binding Proteins (RBPs) represent two important regulators of transcript degradation. We review here recent literature that suggests these two regulators of transcript decay may functionally interact. Some studies have reported an excess of miRNA binding sites surrounding the positions at which RBPs bind. Experimental reports focusing on a particular transcript have identified instances in which RBPs and miRNAs compete for the same target sites, and instances in which the binding of a RBP makes a miRNA recognition site more accessible to the RISC complex. Further, miRNAs and RBPs use similar enzymes for degradation of target transcripts and the degradation of the target transcripts occurs in similar subcellular compartments. In addition to miRNA-RBP interactions involving transcript decay, RBPs have also been reported to facilitate the processing of pri-miRNAs to their final form. We summarize here several possible mechanisms through which miRNA-RBP interactions may occur.

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  • RBPs can compete for binding to microRNA, thereby having either synergistic or opposing effects on RNA stability.

    “In addition, RBPs can compete for binding to microRNA, thereby having either synergistic or opposing effects on RNA stability [38,39,40].”

    From Untranslated Region Sequences and the Efficacy of mRNA Vaccines against Tuberculosis (2024) · cites this paper as [39]

    The Introduction says RBPs and miRNAs can act synergistically or oppose each other in transcript decay. The section ‘Competition for the Same Binding Position’ describes competition for sites on target mRNAs as antagonistic, not competition for binding to the microRNA itself or competition that produces synergy. Page numbers are unavailable in our copy. (LLM, conf=0.88)

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Authors
Jiang, P., & Coller, H.
Affiliations
Princeton University (US)
Corresponding author
Coller, Hilary
ORCID
Venue
MicroRNA e
Publisher
Bentham Science Publishers Ltd.
Published
2012-09-01
Volume
1
Issue
1
Pages
70-79
ISSN
2211-5366 (ISSN-L)
DOI
10.2174/2211536611201010070
PMC
PMC5123774
OpenAlex
W2325353427
Cited by
62
References
7
Citations by year
2026: 5 · 2025: 5 · 2024: 7 · 2023: 2 · 2022: 9 · 2021: 6 · 2020: 6 · 2019: 5 · 2018: 3 · 2017: 3 · 2016: 4 · 2015: 5 · 2013: 2
FWCI
0.21
Type
journal article
Language
en
Open access
Locations
  • MicroRNA (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of General Medical Sciences (R01GM081686, R01GM086465)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA regulation and disease
Keywords
microRNA, RNA-binding proteins, RNA degradation, microRNA binding sites, pri-miRNA processing, post-transcriptional regulation
MeSH terms
Animals, Binding Sites, Gene Expression Regulation, Humans, Models, Molecular, RNA-Binding Proteins, Genome, RNA Stability, MicroRNAs

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