Excess expression of the Gadd45 mRNA accounts for lethality when nonsense-mediated decay is lost in Drosophila and mammalian cells, revealing that this pathway is a critical gene regulatory mechanism.

RNA polymerase II generates numerous transcript isoforms, including transcripts initiating downstream of the START codon, that are efficiently degraded by the nonsense-mediated mRNA decay pathway.

The RNA-binding protein PTBP1 is recruited to sites near stop codons in retroviral and human mRNAs, shielding them from detection and degradation by the nonsense-mediated mRNA decay pathway.

A whole-genome siRNA screen identifies ICE1 as a factor required for accurate sensing and quality control of mRNAs containing premature stop codons.

Casein kinase I, a pivotal kinase in the circadian clock encoded by ck-1a, is positively regulated by a novel RNA-binding protein that protects ck-1a transcripts from nonsense-mediated decay.

Inhibition of nonsense-mediated decay turns immunologically cold tumors hot by increasing the amount of mutant RNA leading to an increase in T-cell-targetable neoantigens on the cell surface.

Expression of the disease gene DUX4 inhibits RNA quality control in skeletal muscle, thereby stabilizing thousands of aberrant RNAs, including its own transcript.

Nonstop mRNA decay degrades mRNAs with a premature stop codon after such mRNAs are targeted by the nonsense-mediated decay machinery.

Cryo-EM reveals the regulation of RUVBL1 and RUVBL2 AAA-ATPases by DHX34, a helicase involved in nonsense-mediated mRNA decay (NMD), and suggests mechanisms for how RUVBL1 and RUVBL2 function in NMD.

The nonsense-mediated RNA decay (NMD) branch-specific factor UPF3B influences olfactory sensory neuron cell populations, the olfactory receptor repertoire, and antimicrobial gene expression.