In normal physiology, host microRNAs (miRNAs) exported in extracellular vesicles (EVs) are involved in cell‐to‐cell communication and in maintaining homeostasis. Upon viral infection, the miRNA cargo of the EVs can be altered and enriched for specific (viral or host) miRNAs which influence immune responses in the recipient cell and alter the microenvironment.

Splicing dysfunction contributes to neurodegeneration and is a viable therapeutic target.

miR‐146a acts as a tumor suppressor microRNA (miRNA) in some cancers and as an oncogenic miRNA in others. Studies suggest that this miRNA is tumor suppressive in non‐small cell lung cancer cells. Pictured here are the genetic and epigenetic events responsible for miR‐146a repression in this disease, along with the cellular consequences of decreased miR‐146a expression. Direct miR‐146a target genes become overexpressed, leading to increased cell proliferation, invasion, metastasis, and cell survival.

Solution structure model showing a surface representation of the tandem zinc finger domain of human TTP. Zinc atoms are represented by green spheres, and the numbered RNA oligonucleotide by colored sticks. Shown underneath are the aligned domains from human (Hs) TTP, Drosophila (Dm) TIS11, and S. pombe (Sp) Zfs1.

Dynamic coupling of RNAPII transcription complex and RNA processing machinery is the first‐line of defense for nuclear RNA quality control.