CNOT11 is a structural subunit of the CCR4-NOT complex, the primary mRNA deadenylase responsible for bulk mRNA degradation and regulated mRNA decay in eukaryotes 1. As part of the N-terminal module with CNOT1 and CNOT10, CNOT11 functions as a protein-protein interaction platform rather than directly catalyzing deadenylation 2. Its conserved antenna domain recruits regulatory proteins like GGNBP2 and enables complex engagement with ribosome-associated decay pathways 32. CNOT11 is essential for CNOT10 association with the complex and participates in multiple cellular processes including miRNA-mediated repression, translational regulation, and transcription control 1. Mechanistically, CNOT11 acts as a molecular relay in tubulin mRNA decay, where ribosomal nascent polypeptide recognition is linked to deadenylase recruitment through protein-protein interactions 3. Disease relevance is evident through mutations in CNOT11-interacting partner GGNBP2, which impair chromosome 2 and cause intellectual disability and retinitis pigmentosa 3. Additionally, CNOT11 participates in innate immune responses by regulating cytoplasmic dsRNA sensing and type I interferon signaling 4, suggesting involvement in autoimmune and autoinflammatory pathways.