Premature termination codon in mRNA (ribosome recognition) (PTC)

A **premature termination codon (PTC)** is a mutation within an mRNA coding sequence that converts a sense codon into a stop codon (UAA, UAG, UGA), leading the ribosome to halt translation prematurely[3][4]. When a ribosome encounters a PTC, translation is usually terminated, producing a truncated, often non-functional and potentially toxic protein. To reduce potential harm, eukaryotic cells utilize **nonsense-mediated mRNA decay (NMD)** and associated surveillance mechanisms to recognize and degrade PTC-containing transcripts[3][4][6]. Mechanistically, **release factors** (eRF1 in eukaryotes, RF1/RF2 in bacteria) mediate recognition of stop codons in the ribosomal A site, and failure of accurate recognition or the presence of mutations can result in disease[2][5]. Therapies focused on read-through of PTCs (e.g., aminoglycosides, ataluren, engineered tRNAs) aim to restore full-length protein synthesis in genetic disorders caused by nonsense mutations but face challenges including specificity, efficacy, and toxicity[5][7].\n\n**Summary of Issues:**\n- The target as phrased is not a unique molecular entity and combines a mutation type (PTC) and a cellular machine (ribosome).\n- It does not map cleanly to a single canonical gene or protein, making it an unsuitable entry for conventional drug target databases. \n- Focused, correct molecular targets may include: *eukaryotic release factor 1 (eRF1)*, *nonsense-mediated mRNA decay factors*, or mutant *mRNA* sequences harboring PTCs.

Other names

Nonsense codonPTCPremature stop codonNonsense mutation

Induce *read-through* of premature termination codons, allowing the ribosome to bypass the PTC and synthesize full-length protein\nModulate the efficiency of translation termination via interaction with ribosomal components or stop codon recognition\nInhibit or modify nonsense-mediated mRNA decay (NMD)