For poly(A)-tail length to influence mRNA translational efficiency, poly(A)-binding protein (PABPC) must be limiting, mRNAs lacking PABPC must be stable, and translation initiation must be sensitive to PABPC levels.

LARP4 protects mRNAs against deadenylation over a wide range of poly(A) lengths but with most apparent functional impact on short lengths known to sensitize PABP binding and mRNA stability.

Noncanonical usage of stop codons in ciliates expands structurally flexible Q-rich domains and coevolves with codon usage biases to avoid triplet repeat disorders mediated by CAG/GTC replication slippage.

Poly(ADP-ribose) (PAR) Trackers (PAR-Ts) are optimized PAR sensors that allow the detection and quantification of PAR levels in extracts, living cells, and living tissues with high sensitivity, and with temporal and spatial precision, in many different experimental and biological systems.

In C. elegans and mouse neurons, the balance between poly(ADP-ribose) glycohydrolases and poly(ADP-ribose) polymerases regulates axon regeneration downstream of DLK-1/MAPKKK signaling.

Profiling of mRNA poly(A)-tail lengths and translational efficiencies provides new insights into posttranscriptional gene regulation in early Drosophila development.

The polyQ tract of pathogenic Huntingtin causes aggregation when expanded in Huntington’s disease, but its two flanking domains control its conformational landscape, proteostasis and neurotoxicity.

Human cullin-RING ligases are buffered to a much greater extent than had been previously appreciated, and the roles of ubiquitin chain extension enzymes are far more nuanced at physiological concentrations.

The RNA-binding protein, Zfp36, which is critical for resolving inflammation, inhibits the production of proinflammatory cytokines via modulation of the cytoplasmic poly(A)-binding protein.

The natural compounds cordycepin and mycophenolic acid stimulate alternative polyadenylation through opposing effects on transcriptional rate.