ArticleCell reports2020
Constitutive Interferon Attenuates RIPK1/3-Mediated Cytokine Translation.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Noncanonical feedback loop between "RIP3-MLKL" and "4EBP1-eIF4E" promotes neuronal necroptosis.MedComm · 2025Article
- RIPK1 inhibition mitigates neuroinflammation and rescues depressive-like behaviors in a mouse model of LPS-induced depression.Cell communication and signaling : CCS · 2024Article
- Regulation of Zfp36 by ISGF3 and MK2 restricts the expression of inflammatory cytokines during necroptosis stimulation.Cell death & disease · 2024Article
- IAPs and RIPK1 mediate LPS-induced cytokine production in healthy subjects and Crohn's disease.Clinical and experimental immunology · 2024Article
- Endothelial RIPK1 protects artery bypass graft against arteriosclerosis by regulating SMC growth.Science advances · 2023Article
- RIPK1-dependent necroptosis promotes vasculogenic mimicry formation via eIF4E in triple-negative breast cancer.Cell death & disease · 2023Article
- TMEM25 inhibits monomeric EGFR-mediated STAT3 activation in basal state to suppress triple-negative breast cancer progression.Nature communications · 2023Article
- Targeting RIPK1 kinase for modulating inflammation in human diseases.Frontiers in immunology · 2023Review
- RIPK1 and RIPK3 inhibitors: potential weapons against inflammation to treat diabetic complications.Frontiers in immunology · 2023Review
- Human ZBP1 induces cell death-independent inflammatory signaling via RIPK3 and RIPK1.EMBO reports · 2022Article
- Nucleotide receptors mediate protection against neonatal sepsis and meningitis caused by alpha-hemolysin expressing Escherichia coli K1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- RIPK3 signaling and its role in the pathogenesis of cancers.Cellular and molecular life sciences : CMLS · 2021Review
- Genetic inhibition of RIPK3 ameliorates functional outcome in controlled cortical impact independent of necroptosis.Cell death & disease · 2021Article
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- RIPK1 activation mediates neuroinflammation and disease progression in multiple sclerosis.Cell reports · 2021Article
- Identification of PBMC-based molecular signature associational with COVID-19 disease severity.Heliyon · 2021Article
- RIPK protein kinase family: Atypical lives of typical kinases.Seminars in cell & developmental biology · 2021Review
- Regulation of Autophagic Signaling by Mechanical Loading and Inflammation in Human PDL Fibroblasts.International journal of molecular sciences · 2020Article
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Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
Receptor-interacting protein kinase 1 (RIPK1) and 3 (RIPK3) are well known for their capacity to drive necroptosis via mixed-lineage kinase-like domain (MLKL). Recently, RIPK1/3 kinase activity has been shown to drive inflammation via activation of MAPK signaling. However, the regulatory mechanisms underlying this kinase-dependent cytokine production remain poorly understood. In the present study, we establish that the kinase activity of RIPK1/3 regulates cytokine translation in mouse and human macrophages. Furthermore, we show that this inflammatory response is downregulated by type I interferon (IFN) signaling, independent of type I IFN-promoted cell death. Specifically, low-level constitutive IFN signaling attenuates RIPK-driven activation of cap-dependent translation initiation pathway components AKT, mTORC1, 4E-BP and eIF4E, while promoting RIPK-dependent cell death. Altogether, these data characterize constitutive IFN signaling as a regulator of RIPK-dependent inflammation and establish cap-dependent translation as a crucial checkpoint in the regulation of cytokine production.
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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.