ArticleThe Journal of experimental medicine2015
CNOT3 contributes to early B cell development by controlling Igh rearrangement and p53 mRNA stability.
Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
- A Chemical-Genetic Interaction Matrix Reveals Drug Mechanism and Genetic Architecture.bioRxiv : the preprint server for biology · 2026Article
- Posttranscriptional control of the B cell receptor by HuR is essential for innate B cell maintenance and function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- mRNA stability fine-tunes gene expression in the developing cortex to control neurogenesis.PLoS biology · 2025Article
- Specific tRNAs promote mRNA decay by recruiting the CCR4-NOT complex to translating ribosomes.Science (New York, N.Y.) · 2024Article
- UPF1 plays critical roles in early B cell development.Nature communications · 2024Article
- Csk restrains BCR-mediated ROS production and contributes to germinal center selection and affinity maturation.The Journal of experimental medicine · 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
- The splicing regulators TIA1 and TIAL1 are required for the expression of the DNA damage repair machinery during B cell lymphopoiesis.Cell reports · 2022Article
- Regulation of CCR4-NOT complex deadenylase activity and cellular responses by MK2-dependent phosphorylation of CNOT2.RNA biology · 2022Article
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- Exit from germinal center to become quiescent memory B cells depends on metabolic reprograming and provision of a survival signal.The Journal of experimental medicine · 2021Article
- Regulation of Early Lymphocyte DevelopmentFrontiers in immunology · 2021Review
- 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
- Control of Early B Cell Development by the RNA NCell reports · 2020Article
- The CCR4-NOT complex maintains liver homeostasis through mRNA deadenylation.Life science alliance · 2020Article
- Essential functions of the CNOT7/8 catalytic subunits of the CCR4-NOT complex in mRNA regulation and cell viability.RNA biology · 2020Article
Corrections and comments
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Authors and funding
14 authors at 8 institutions in 5 countries.
Funding
Abstract
The CCR4-NOT deadenylase complex plays crucial roles in mRNA decay and translational repression induced by poly(A) tail shortening. Although the in vitro activities of each component of this complex have been well characterized, its in vivo role in immune cells remains unclear. Here we show that mice lacking the CNOT3 subunit of this complex, specifically in B cells, have a developmental block at the pro- to pre-B cell transition. CNOT3 regulated generation of germline transcripts in the VH region of the immunoglobulin heavy chain (Igh) locus, compaction of the locus, and subsequent Igh gene rearrangement and destabilized tumor suppressor p53 mRNA. The developmental defect in the absence of CNOT3 could be partially rescued by ablation of p53 or introduction of a pre-rearranged Igh transgene. Thus, our data suggest that the CCR4-NOT complex regulates B cell differentiation by controlling Igh rearrangement and destabilizing p53 mRNA.
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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.