ArticleScientific reports2015
CNOT3 suppression promotes necroptosis by stabilizing mRNAs for cell death-inducing proteins.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Global Regulatory Functions of the Human CCR4-NOT Complex in mRNA Deadenylation and Decay.bioRxiv : the preprint server for biology · 2026Article
- Selective decay of interferon mRNAs controls antiviral immunity and innate memory.Molecular cell · 2026Article
- Identifying and targeting abnormal mitochondrial localization associated with psychosis.bioRxiv : the preprint server for biology · 2026Article
- CNOT11 depletion is associated with autophagy-related responses and IL-6-JAK-STAT signaling in cancer cells.Frontiers in cell and developmental biology · 2026Article
- Homeostatic regulation of nucleoporins is a central driver of nuclear pore biogenesis.Cell reports · 2025Article
- Specific tRNAs promote mRNA decay by recruiting the CCR4-NOT complex to translating ribosomes.Science (New York, N.Y.) · 2024Article
- Translation efficiency driven by CNOT3 subunit of the CCR4-NOT complex promotes leukemogenesis.Nature communications · 2024Article
- Targeting the up-regulated CNOT3 reverses therapeutic resistance and metastatic progression of EGFR-mutant non-small cell lung cancer.Cell death discovery · 2023Article
- Regulation of CCR4-NOT complex deadenylase activity and cellular responses by MK2-dependent phosphorylation of CNOT2.RNA biology · 2022Article
- MiRNA-124 regulates the sensitivity of renal cancer cells to cisplatin-induced necroptosis by targeting the CAPN4-CNOT3 axis.Translational andrology and urology · 2021Article
- Article
- Article
- Regulation of Fetal Genes by Transitions among RNA-Binding Proteins during Liver Development.International journal of molecular sciences · 2020Article
- The CCR4-NOT deadenylase complex safeguards thymic positive selection by down-regulating aberrant pro-apoptotic gene expression.Nature communications · 2020Article
- Review
- Loss of β-cell identity and diabetic phenotype in mice caused by disruption of CNOT3-dependent mRNA deadenylation.Communications biology · 2020Article
- The CCR4-NOT complex maintains liver homeostasis through mRNA deadenylation.Life science alliance · 2020Article
- The Ccr4-Not complex monitors the translating ribosome for codon optimality.Science (New York, N.Y.) · 2020Article
- Essential functions of the CNOT7/8 catalytic subunits of the CCR4-NOT complex in mRNA regulation and cell viability.RNA biology · 2020Article
- The CCR4-NOT Deadenylase Complex Maintains Adipocyte Identity.International journal of molecular sciences · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CCR4-NOT complex is conserved in eukaryotes and is involved in mRNA metabolism, though its molecular physiological roles remain to be established. We show here that CNOT3-depleted mouse embryonic fibroblasts (MEFs) undergo cell death. Levels of other complex subunits are decreased in CNOT3-depleted MEFs. The death phenotype is rescued by introduction of wild-type (WT), but not mutated CNOT3, and is not suppressed by the pan-caspase inhibitor, zVAD-fluoromethylketone. Gene expression profiling reveals that mRNAs encoding cell death-related proteins, including receptor-interacting protein kinase 1 (RIPK1) and RIPK3, are stabilized in CNOT3-depleted MEFs. Some of these mRNAs bind to CNOT3, and in the absence of CNOT3 their poly(A) tails are elongated. Inhibition of RIPK1-RIPK3 signaling by a short-hairpin RNA or a necroptosis inhibitor, necrostatin-1, confers viability upon CNOT3-depleted MEFs. Therefore, we conclude that CNOT3 targets specific mRNAs to prevent cells from being disposed to necroptotic death.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.