We are analyzing https://link.springer.com/article/10.1007/s13238-011-1092-4.

Title:
The role of the CNOT1 subunit of the CCR4-NOT complex in mRNA deadenylation and cell viability | Protein & Cell
Description:
The human CCR4-NOT deadenylase complex consists of at least nine enzymatic and non-enzymatic subunits. Accumulating evidence suggests that the non-enzymatic subunits are involved in the regulation of mRNA deadenylation, although their precise roles remain to be established. In this study, we addressed the function of the CNOT1 subunit by depleting its expression in HeLa cells. Flow cytometric analysis revealed that the sub G1 fraction was increased in CNOT1-depleted cells. Virtually, the same level of the sub G1 fraction was seen when cells were treated with a mixture of siRNAs targeted against all enzymatic subunits, suggesting that CNOT1 depletion induces apoptosis by destroying the CCR4-NOT-associated deadenylase activity. Further analysis revealed that CNOT1 depletion leads to a reduction in the amount of other CCR4-NOT subunits. Importantly, the specific activity of the CNOT6L immunoprecipitates-associated deadenylase from CNOT1-depleted cells was less than that from control cells. The formation of P-bodies, where mRNA decay is reported to take place, was largely suppressed in CNOT1-depleted cells. Therefore, CNOT1 has an important role in exhibiting enzymatic activity of the CCR4-NOT complex, and thus is critical in control of mRNA deadenylation and mRNA decay. We further showed that CNOT1 depletion enhanced CHOP mRNA levels and activated caspase-4, which is associated with endoplasmic reticulum ER stress-induced apoptosis. Taken together, CNOT1 depletion structurally and functionally deteriorates the CCR4-NOTcomplex and induces stabilization of mRNAs, which results in the increment of translation causing ER stress-mediated apoptosis. We conclude that CNOT1 contributes to cell viability by securing the activity of the CCR4-NOT deadenylase.
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Topics {✒️}

nuclear receptor-mediated transcription rna-mediated gene silencing related subjects privacy choices/manage cookies human rcd-1 reveals reveals molecular insights apoptosis induced programmed cell death cellular signaling pathways not1 mediates recruitment impairs cell growth main content log messenger rna occur antiproliferative protein tob cnot2 depletion disrupts cnot1 depletion leads cnot1 depletion structurally european economic area accumulating evidence suggests coding sequence composition distinct expression patterns mice lacking cnot7 endoplasmic reticulum er stress unfolded protein response conditions privacy policy p-body formation cytoplasmic processing bodies gene expression accepting optional cookies cnot1-depleted cells mrna degradation p27kip1 mrna level precise roles remain dcp2 decapping complexes recombinant human ccr4 search search tadashi yamamoto journal finder publish p-bodies mol biol 303 protein cell 1 protein cell 2 mol cell 6 exhibiting enzymatic activity behm-ansmant article ito deadenylase complex consists author correspondence cell viability

Questions {❓}

The eukaryotic Ccr4-not complex: a regulatory platform integrating mRNA metabolism with cellular signaling pathways?

Schema {🗺️}

WebPage:
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         headline:The role of the CNOT1 subunit of the CCR4-NOT complex in mRNA deadenylation and cell viability
         description:The human CCR4-NOT deadenylase complex consists of at least nine enzymatic and non-enzymatic subunits. Accumulating evidence suggests that the non-enzymatic subunits are involved in the regulation of mRNA deadenylation, although their precise roles remain to be established. In this study, we addressed the function of the CNOT1 subunit by depleting its expression in HeLa cells. Flow cytometric analysis revealed that the sub G1 fraction was increased in CNOT1-depleted cells. Virtually, the same level of the sub G1 fraction was seen when cells were treated with a mixture of siRNAs targeted against all enzymatic subunits, suggesting that CNOT1 depletion induces apoptosis by destroying the CCR4-NOT-associated deadenylase activity. Further analysis revealed that CNOT1 depletion leads to a reduction in the amount of other CCR4-NOT subunits. Importantly, the specific activity of the CNOT6L immunoprecipitates-associated deadenylase from CNOT1-depleted cells was less than that from control cells. The formation of P-bodies, where mRNA decay is reported to take place, was largely suppressed in CNOT1-depleted cells. Therefore, CNOT1 has an important role in exhibiting enzymatic activity of the CCR4-NOT complex, and thus is critical in control of mRNA deadenylation and mRNA decay. We further showed that CNOT1 depletion enhanced CHOP mRNA levels and activated caspase-4, which is associated with endoplasmic reticulum ER stress-induced apoptosis. Taken together, CNOT1 depletion structurally and functionally deteriorates the CCR4-NOTcomplex and induces stabilization of mRNAs, which results in the increment of translation causing ER stress-mediated apoptosis. We conclude that CNOT1 contributes to cell viability by securing the activity of the CCR4-NOT deadenylase.
         datePublished:2011-10-06T00:00:00Z
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ScholarlyArticle:
      headline:The role of the CNOT1 subunit of the CCR4-NOT complex in mRNA deadenylation and cell viability
      description:The human CCR4-NOT deadenylase complex consists of at least nine enzymatic and non-enzymatic subunits. Accumulating evidence suggests that the non-enzymatic subunits are involved in the regulation of mRNA deadenylation, although their precise roles remain to be established. In this study, we addressed the function of the CNOT1 subunit by depleting its expression in HeLa cells. Flow cytometric analysis revealed that the sub G1 fraction was increased in CNOT1-depleted cells. Virtually, the same level of the sub G1 fraction was seen when cells were treated with a mixture of siRNAs targeted against all enzymatic subunits, suggesting that CNOT1 depletion induces apoptosis by destroying the CCR4-NOT-associated deadenylase activity. Further analysis revealed that CNOT1 depletion leads to a reduction in the amount of other CCR4-NOT subunits. Importantly, the specific activity of the CNOT6L immunoprecipitates-associated deadenylase from CNOT1-depleted cells was less than that from control cells. The formation of P-bodies, where mRNA decay is reported to take place, was largely suppressed in CNOT1-depleted cells. Therefore, CNOT1 has an important role in exhibiting enzymatic activity of the CCR4-NOT complex, and thus is critical in control of mRNA deadenylation and mRNA decay. We further showed that CNOT1 depletion enhanced CHOP mRNA levels and activated caspase-4, which is associated with endoplasmic reticulum ER stress-induced apoptosis. Taken together, CNOT1 depletion structurally and functionally deteriorates the CCR4-NOTcomplex and induces stabilization of mRNAs, which results in the increment of translation causing ER stress-mediated apoptosis. We conclude that CNOT1 contributes to cell viability by securing the activity of the CCR4-NOT deadenylase.
      datePublished:2011-10-06T00:00:00Z
      dateModified:2011-10-06T00:00:00Z
      pageStart:755
      pageEnd:763
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      keywords:
         deadenylation
         CCR4-NOT
         small interfering RNA
         P-bodies
         apoptosis
         Biochemistry
         general
         Protein Science
         Cell Biology
         Stem Cells
         Human Genetics
         Developmental Biology
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      affiliation:
            name:University of Tokyo
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               name:Division of Oncology, Department of Cancer Biology, Institute of Medical Science, University of Tokyo, Tokyo, Japan
               type:PostalAddress
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      affiliation:
            name:University of Tokyo
            address:
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               type:PostalAddress
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      affiliation:
            name:University of Tokyo
            address:
               name:Division of Oncology, Department of Cancer Biology, Institute of Medical Science, University of Tokyo, Tokyo, Japan
               type:PostalAddress
            type:Organization
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      name:Division of Oncology, Department of Cancer Biology, Institute of Medical Science, University of Tokyo, Tokyo, Japan
      name:Division of Oncology, Department of Cancer Biology, Institute of Medical Science, University of Tokyo, Tokyo, Japan
      name:Cell Signal Unit, Okinawa Institute of Science and Technology, 1919-1, Okinawa, Japan

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