Under starvation conditions, anti-carD antisense RNA and Clp protease work together to decrease the CarD level to mediate the adaptation and survival of mycobacterial cells.

Genome-wide analysis reveals novel functions for a post-translational modification to the carboxy-terminal domain (CTD) of RNA Polymerase II in mammals.

C9ORF72 antisense repeat expanded RNAs activate PKR/eIF2α dependent integrated stress response and cause neuronal toxicity independent of DPR proteins.

Allele-specific expression, natural antisense transcripts, and developmental gene expression, but not RNA editing or developmental hourglass, act in concert to shape the transcriptome during the fruiting body formation of complex multicellular fungi.

Phosphorylation of tyrosine 1 in the carboxy-terminal domain (CTD) of the largest subunit of RNA Polymerase (RNAP) II functions to stabilize this domain, and facilitates turnover of upstream antisense RNAs.

Functional characterization of a pair of cis-encoded antisense RNAs reveals a role for RNase III and antisense regulation in the biogenesis and regulatory activity of a bacterial virulence factor-regulating small RNA.

The ability to target transcripts from high-copy regions of the genome is an emergent property of a minimal RNA interference system.

A viral RNA has been identified as a specific MDA5 agonist in cells infected with encephalomyocarditis virus.

CRISPR interference (CRISPRi), which uses small guide RNAs to target catalytically dead Cas9 protein to chromatin, disrupts existing transcription units and generates new sites for initiation and termination of transcription on both strands of DNA.

NET-seq analysis of 41 S. cerevisiae transcription regulatory factors uncovers their differential and opposing effects on Pol II transcription elongation and antisense transcription, revealing that wild-type transcription is balanced by the joint impact of many regulators.