ArticleMolecular and cellular biology2019
Importance of the Conserved Carboxyl-Terminal CNOT1 Binding Domain to Tristetraprolin Activity
Article in Molecular and cellular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Selective decay of interferon mRNAs controls antiviral immunity and innate memory.Molecular cell · 2026Article
- ZFP36 Family Proteins as Critical Regulators of Inflammation, Immune Cell Development, and Antiviral Responses.Vaccines · 2026Review
- CNOT10 is involved in the TTP-mediated AU-rich element-containing mRNA metabolism, independent of mRNA decay regulation.RNA (New York, N.Y.) · 2026Article
- Phosphorylation-dependent tuning of mRNA deadenylation rates.Nature structural & molecular biology · 2026Article
- Multivalent interactions with CCR4-NOT and PABPC1 determine mRNA repression efficiency by tristetraprolin.Nature communications · 2025Article
- ZFP36L1 and ZFP36L2 reduce cyclin D1 expression by decreasing expression of E2F1 and long 3'UTR isoform of CCND1 transcripts.Molecular and cellular biochemistry · 2025Article
- In Vitro Reconstitution of the Drosophila melanogaster CCR4-NOT Complex to Assay Deadenylation.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Synergistic roles of tristetraprolin family members in myeloid cells in the control of inflammation.Life science alliance · 2024Article
- Regulation of mRNA stability contributes to the function of innate lymphoid cells in various diseases.Frontiers in immunology · 2023Review
- ZFP36 ring finger protein like 1 significantly suppresses human coronavirus OC43 replication.PeerJ · 2023Article
- Clinical implications of tristetraprolin (TTP) modulation in the treatment of inflammatory diseases.Pharmacology & therapeutics · 2022Review
- The Conserved CNOT1 Interaction Motif of Tristetraprolin Regulates ARE-mRNA Decay Independently of the p38 MAPK-MK2 Kinase Pathway.Molecular and cellular biology · 2022Article
- Backbone and sidechainBiomolecular NMR assignments · 2022Article
- TTP-mediated regulation of mRNA stability in immune cells contributes to adaptive immunity, immune tolerance and clinical applications.RNA biology · 2021Review
- A post-transcriptional regulon controlled by TtpA, the single tristetraprolin family member expressed in Dictyostelium discoideum.Nucleic acids research · 2021Article
- The Plasmodium NOT1-G paralogue is an essential regulator of sexual stage maturation and parasite transmission.PLoS biology · 2021Article
- The functional characterization of phosphorylation of tristetraprolin at C-terminal NOT1-binding domain.Journal of inflammation (London, England) · 2021Article
- Regulation of mRNA stability by RBPs and noncoding RNAs contributing to the pathogenicity of Th17 cells.RNA biology · 2021Review
- Tristetraprolin, a Potential Safeguard Against Carcinoma: Role in the Tumor Microenvironment.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Tristetraprolin (TTP) is an anti-inflammatory protein that modulates the stability of certain cytokine/chemokine mRNAs. After initial high-affinity binding to AU-rich elements in 3' untranslated regions of target mRNAs, mediated through its tandem zinc finger (TZF) domain, TTP promotes the deadenylation and ultimate decay of target transcripts. These transcripts and their encoded proteins accumulate abnormally in TTP knockout (KO) mice, leading to a severe inflammatory syndrome. To assess the importance of the highly conserved C-terminal CNOT1 binding domain (CNBD) of TTP to the TTP deficiency phenotype in mice, we created a mouse model in which TTP lacked its CNBD. CNBD deletion mice exhibited a less severe phenotype than the complete TTP KO mice. In macrophages, the stabilization of target transcripts seen in KO mice was partially normalized in the CNBD deletion mice. In cell-free experiments, recombinant TTP lacking its CNBD could still activate target mRNA deadenylation by purified recombinant
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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.