ArticleThe Journal of biological chemistry2012
Intermediate domain of receptor-interacting protein kinase 1 (RIPK1) determines switch between necroptosis and RIPK1 kinase-dependent apoptosis.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Hyperlipidemia induces hippocampal inflammation and loss of vascularity and can be rescued by silencing RIPK1.Scientific reports · 2026Article
- RNA splicing in cancer cell death regulation: shedding light on the molecular mechanisms and potential clinical applications.Cell death & disease · 2026Review
- Interconnected cell death pathways: central mechanisms and therapeutic targets in impaired follicular development of polycystic ovary syndrome.Journal of ovarian research · 2026Review
- Incoherent feedforward loop dominates the robustness and tunability of necroptosis biphasic, emergent, and coexistent dynamics.Fundamental research · 2026Article
- Novel anti-ITGA4 monoclonal antibody induces cell death via large pore formation in NK/T-cell lymphoma cells.Scientific reports · 2025Article
- 5-Iodotubercidin sensitizes cells to RIPK1-dependent necroptosis by interfering with NFκB signaling.Cell death discovery · 2023Article
- RIP1-dependent linear and nonlinear recruitments of caspase-8 and RIP3 respectively to necrosome specify distinct cell death outcomes.Protein & cell · 2021Article
- Necroptosis, pyroptosis and apoptosis: an intricate game of cell death.Cellular & molecular immunology · 2021Review
- Review
- Molecular Insights into the Mechanism of Necroptosis: The Necrosome As a Potential Therapeutic Target.Cells · 2019Review
- Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.Cell death and differentiation · 2018Review
- Necroptosis and ferroptosis are alternative cell death pathways that operate in acute kidney failure.Cellular and molecular life sciences : CMLS · 2017Article
- The degradation of mixed lineage kinase domain-like protein promotes neuroprotection after ischemic brain injury.Oncotarget · 2017Article
- Necroptosis in development, inflammation and disease.Nature reviews. Molecular cell biology · 2017Review
- Necroptosis: Mechanisms and Relevance to Disease.Annual review of pathology · 2017Review
- K45A mutation of RIPK1 results in poor necroptosis and cytokine signaling in macrophages, which impacts inflammatory responses in vivo.Cell death and differentiation · 2016Article
- Cell apoptosis, autophagy and necroptosis in osteosarcoma treatment.Oncotarget · 2016Review
- Terminalia Chebula provides protection against dual modes of necroptotic and apoptotic cell death upon death receptor ligation.Scientific reports · 2016Article
- DNA damage and the balance between survival and death in cancer biology.Nature reviews. Cancer · 2016Review
- A critical role for cellular inhibitor of protein 2 (cIAP2) in colitis-associated colorectal cancer and intestinal homeostasis mediated by the inflammasome and survival pathways.Mucosal immunology · 2016Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Receptor-interacting protein kinase 1 (RIPK1) is an important component of the tumor necrosis factor receptor 1 (TNFR1) signaling pathway. Depending on the cell type and conditions, RIPK1 mediates MAPK and NF-κB activation as well as cell death. Using a mutant form of RIPK1 (RIPK1ΔID) lacking the intermediate domain (ID), we confirm the requirement of this domain for activation of these signaling events. Moreover, expression of RIPK1ΔID resulted in enhanced recruitment of caspase-8 to the TNFR1 complex II component Fas-associated death domain (FADD), which allowed a shift from TNF-induced necroptosis to apoptosis in L929 cells. Addition of the RIPK1 kinase inhibitor necrostatin-1 strongly reduced recruitment of RIPK1 and caspase-8 to FADD and subsequent apoptosis, indicating a role for RIPK1 kinase activity in apoptotic complex formation. Our study shows that RIPK1 has an anti-apoptotic function residing in its ID and demonstrates a cellular system as an elegant genetic model for RIPK1 kinase-dependent apoptosis that, in contrast to the Smac mimetic model, does not rely on depletion of cellular inhibitor of apoptosis protein 1 and 2 (cIAP1/2).
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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.