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The CCR4\u2010NOT complex is central to this process, interacting with ribosomes when the A and E sites are unoccupied, a state that arises when a nonoptimal codon with low tRNA availability is at the A site. This triggers recruitment of decay factors, reducing the stability of transcripts enriched in such codons. In humans, codon\u2010mediated mRNA decay is less well\u2010understood. Recent research has identified a related but distinct mechanism called P\u2010site tRNA\u2010mediated decay (PTMD). Unlike yeast, human CCR4\u2010NOT recruitment depends on specific arginine codons (CGG, CGA, or AGG) at the P site and slow decoding at the A site, allowing E\u2010site vacancy and CNOT3\u2010dependent binding. Through analysis of public datasets, we explored the characteristics of human transcripts enriched in PTMD codons. Interestingly, these codons are mostly found in transcripts with longer half\u2010lives. This suggests that, rather than targeting already unstable mRNAs as in yeast, PTMD in humans selectively reduces the stability of otherwise long\u2010lived transcripts, indicating a regulatory role distinct from the decay associated with codon usage.<\/jats:p>","DOI":"10.1002\/2211-5463.70277","type":"journal-article","created":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T11:07:52Z","timestamp":1781262472000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Transcripts enriched in codons that trigger P\u2010site\n                    <scp>tRNA<\/scp>\n                    \u2010mediated\n                    <scp>mRNA<\/scp>\n                    decay possess stable\n                    <scp>mRNA<\/scp>"],"prefix":"10.1002","author":[{"given":"Rodolfo Lopes","family":"Carneiro","sequence":"first","affiliation":[{"name":"Programa de Biologia Estrutural, Instituto de Bioqu\u00edmica M\u00e9dica Leopoldo de Meis 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