microRNAs can serve as a surveillance system to repress nonsense mRNAs by recognizing miRNA-responsive elements in the open reading frame region downstream of the premature termination codon.
microRNA-1 plays an essential role in the development and functioning of the heart by ensuring that genes for striated, rather than smooth, muscle are expressed there.
In invertebrate and vertebrate models of Spinal Muscular Atrophy, diminished SMN protein causes Gemin3-dependent decreases in microRNA function, leading to upregulated M2 muscarinic receptor and deleterious consequences.
Coordinated microRNAs activity induced by VEGF represses cell proliferation and favors cell migration at the onset of sprouting angiogenesis in endothelial cells.
The deletion of Ddx6 results in the translational upregulation, but not transcript stabilization, of microRNA targets in embryonic stem cells while largely phenocopying the overall impact of global microRNA loss.
A cell-free reaction that reconstitutes the selective sorting of a miRNA into exosomes reveals an RNA-binding protein, YBX1, as a critical sorting factor.
In the liver, microRNAs exert widespread functions in the modulation of phases and amplitudes of clock-controlled gene expression, but their influence on the core clock is remarkably mild.
MicroRNA-based direct conversion of human fibroblasts to neurons is applicable to fibroblasts from donors ranging in age from neonatal to centenarian, allowing the generation of neurons that maintain the age-associated signatures of the starting fibroblasts.
