ArticleFrontiers in cell and developmental biology2015
A novel function of RIP1 in postnatal development and immune homeostasis by protecting against RIP3-dependent necroptosis and FADD-mediated apoptosis.
Article in Frontiers in cell and developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- RIPK1 ubiquitination regulates its kinase-independent function in development and inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Monogenic disorders of the TNF signalling pathway.Nature reviews. Rheumatology · 2026Review
- Research trends, hot spots and prospects for necroptosis in the field of neuroscience.Neural regeneration research · 2021Article
- RIPK1-Associated Inborn Errors of Innate Immunity.Frontiers in immunology · 2021Review
- The PANoptosome: A Deadly Protein Complex Driving Pyroptosis, Apoptosis, and Necroptosis (PANoptosis).Frontiers in cellular and infection microbiology · 2020Review
- Review
- Ubiquitination of RIPK1 suppresses programmed cell death by regulating RIPK1 kinase activation during embryogenesis.Nature communications · 2019Article
- RIP1/RIP3-regulated necroptosis as a target for multifaceted disease therapy (Review).International journal of molecular medicine · 2019Review
- Caspase-8-dependent control of NK- and T cell responses during cytomegalovirus infection.Medical microbiology and immunology · 2019Review
- RIPK1 can mediate apoptosis in addition to necroptosis during embryonic development.Cell death & disease · 2019Article
- Loss of periodontal ligament fibroblasts by RIPK3-MLKL-mediated necroptosis in the progress of chronic periodontitis.Scientific reports · 2019Article
- TRADD regulates perinatal development and adulthood survival in mice lacking RIPK1 and RIPK3.Nature communications · 2019Article
- Dominant Negative FADD/MORT1 Inhibits the Development of Intestinal Intraepithelial Lymphocytes With a Marked Defect on CD8αα+TCRγδ+ T Cells.Frontiers in immunology · 2018Article
- Mechanisms of RIPK3-induced inflammation.Immunology and cell biology · 2017Review
- Kinase-independent function of RIP1, critical for mature T-cell survival and proliferation.Cell death & disease · 2016Article
- MLKL and FADD Are Critical for Suppressing Progressive Lymphoproliferative Disease and Activating the NLRP3 Inflammasome.Cell reports · 2016Article
- Necroptosis-independent signaling by the RIP kinases in inflammation.Cellular and molecular life sciences : CMLS · 2016Review
- The diverse role of RIP kinases in necroptosis and inflammation.Nature immunology · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
RIP1 is an adaptor kinase originally identified as being able to associate with TNFR1 and Fas, and is later shown to be involved in signaling induced by TLRs. Major signaling pathways regulated by RIP1 include necroptosis, apoptosis, and pro-survival/inflammation NF-κB activation. Previous studies show that RIP1 deficiency has no effect on mouse embryogenesis, but blocks postnatal development. This phenotype could not readily be explained, since mice lacking TNFR1, Fas, or TLRs show no apparent developmental defect. Certain types of RIP1-deficient cells are hypersensitive to TNF-induced apoptosis. However, in our previous study, deletion of the apoptotic adaptor protein, FADD, provides marginal improvement of postnatal development of rip1 (-/-) mice. Remarkably, the current data shows that haploid insufficiency of RIP3, a known mediator of necroptosis, allowed survival of rip1 (-/-) fadd (-/-) mice beyond weaning age, although the resulting rip1(-/-)fadd(-/-) rip3(+/-) mice were significant smaller in size and weight. Moreover, complete absence of RIP3 further improved postnatal development of the resulting rip1 (-/-) fadd (-/-) rip3 (-/-) mice, which display normal size and weight. In such triple knockout (TKO) mice, lymphocytes underwent normal development, but progressively accumulated as mice age. This lymphoproliferative (lpr) disease in TKO mice is, however, less severe than that of fadd(-/-)rip3 (-/-) double knockout mice. In total, the data show that the postnatal developmental defect in rip1 (-/-) mice is due in part to FADD-mediated apoptosis as well as RIP3-dependent necroptosis. Moreover, the function of RIP1 contributes to development of lpr diseases.
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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.