CNOT10

Last update 08 May 2025

Basic Info

Synonyms

CCR4-NOT transcription complex subunit 10, CNOT10, FLJ12890

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Introduction

Component of the CCR4-NOT complex which is one of the major cellular mRNA deadenylases and is linked to various cellular processes including bulk mRNA degradation, miRNA-mediated repression, translational repression during translational initiation and general transcription regulation. Additional complex functions may be a consequence of its influence on mRNA expression. Is not required for association of CNOT7 to the CCR4-NOT complex.

100 Clinical Results associated with CNOT10

100 Translational Medicine associated with CNOT10

0 Patents (Medical) associated with CNOT10

Literatures (Medical) associated with CNOT10

22 Nov 2024·Science Immunology

GGNBP2 regulates MDA5 sensing triggered by self double-stranded RNA following loss of ADAR1 editing

Article

Author: Chalk, Alistair M. ; Goradia, Ankita ; Simpson, Kaylene J. ; Heraud-Farlow, Jacki E. ; Guallar, Diana ; Li, Qin ; Escudero, Adriana ; Nikolic, Iva ; Walkley, Carl R. ; Hu, Shi-Bin ; Li, Jin Billy ; Fidalgo, Miguel ; Taylor, Scott R. ; Sun, Tao

Adenosine-to-inosine (A-to-I) editing of double-stranded RNA (dsRNA) by ADAR1 is an essential modifier of the immunogenicity of cellular dsRNA. The role of MDA5 in sensing unedited cellular dsRNA and the downstream activation of type I interferon (IFN) signaling are well established. However, we have an incomplete understanding of pathways that modify the response to unedited dsRNA. We performed a genome-wide CRISPR screen and showed that GGNBP2, CNOT10, and CNOT11 interact and regulate sensing of unedited cellular dsRNA. We found that GGNBP2 acts between dsRNA transcription and its cytoplasmic sensing by MDA5. GGNBP2 loss prevented induction of type I IFN and autoinflammation after the loss of ADAR1 editing activity by modifying the subcellular distribution of endogenous A-to-I editing substrates and reducing cytoplasmic dsRNA load. These findings reveal previously undescribed pathways to modify diseases associated with ADAR mutations and may be determinants of response or resistance to small-molecule ADAR1 inhibitors.

01 Feb 2024·Theriogenology

Differential transcript usage across mammalian oocytes at the germinal vesicle and metaphase II stages

Article

Author: Puthier, Denis ; Chokeshaiusaha, Kaj ; Nguyen, Catherine ; Sananmuang, Thanida

Ongoing progress in mRNA-Sequencing technologies has significantly contributed to the refinement of assisted reproductive technologies. However, the prior investigations have predominantly concentrated on alterations in overall gene expression levels, thereby leaving a considerable gap in our understanding of the influence of transcript isoform expression on fundamental cellular mechanisms of oocytes. Given the efficacy of differential transcript usage (DTU) analysis to address such knowledge, we conducted comprehensive DTU analysis utilizing mRNA-Seq datasets of germinal vesicle (GV) and metaphase II (MII) oocytes across six mammalian species from the SRA database, including cow, donkey, horse, human, mouse, and pig. To further illuminate the roles of these genes, we also conducted a rigorous Gene Ontology (GO) term enrichment analysis. While the DTU analysis of each species exhibited several genes with alterations in their transcript isoform usage, referred to as DTU genes, this study focused on only ten cross-species DTU genes sharing among a minimum of five distinct species (FDR≤0.05). These cross-species DTU genes were as follows: ABCF1, CDC6, CFAP36, CNOT10, DNM3, IWS1, NBN, NDEL1, RAD50 and ZCCHC17. GO term enrichment analysis unveiled the alignment of these cross-species DTU gene functions with RNA and cell-cycle control mechanisms across diverse mammalian species, thereby suggesting their vital roles during oocyte maturation. Further exploration of the transcript isoforms of these genes hence bore the potential to uncover novel transcript isoform markers for future reproductive technologies in both human and animal contexts.

01 Jan 2023·Cell Reports

The human CNOT1-CNOT10-CNOT11 complex forms a structural platform for protein-protein interactions

Article

Author: Séraphin, Bertrand ; Mauxion, Fabienne ; Basquin, Jérôme ; Ozgur, Sevim ; Rame, Marion ; Albrecht, Jana ; Schäfer, Ingmar ; Conti, Elena

The evolutionary conserved CCR4-NOT complex functions in the cytoplasm as the main mRNA deadenylase in both constitutive mRNA turnover and regulated mRNA decay pathways. The versatility of this complex is underpinned by its modular multi-subunit organization, with distinct structural modules actuating different functions. The structure and function of all modules are known, except for that of the N-terminal module. Using different structural approaches, we obtained high-resolution data revealing the architecture of the human N-terminal module composed of CNOT1, CNOT10, and CNOT11. The structure shows how two helical domains of CNOT1 sandwich CNOT10 and CNOT11, leaving the most conserved domain of CNOT11 protruding into solvent as an antenna. We discovered that GGNBP2, a protein identified as a tumor suppressor and spermatogenic factor, is a conserved interacting partner of the CNOT11 antenna domain. Structural and biochemical analyses thus pinpoint the N-terminal CNOT1-CNOT10-CNOT11 module as a conserved protein-protein interaction platform.

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CNOT10

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