ReviewCellular and molecular life sciences : CMLS2016
An outline of necrosome triggers.
Review in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
78 citing papers in PubMed, 127 citations in OpenAlex.
- Amygdalin synergizes with the TNF-α monoclonal antibody infliximab to modulate HSP90 and related necro-inflammatory/oxidative stress pathways in a rat model of hepatic I/R.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- De novo cyclic peptides allow visualisation of the monomeric and functional amyloid conformations of the kinase RIPK3.The Biochemical journal · 2026Article
- PANoptosis as a Potential Therapeutic Target in Drug-Induced Liver Injury: A Narrative Review.Journal of inflammation research · 2026Review
- Resonance assignments of the human receptor interacting protein kinase 1 (RIPK1) in its fibrillar conformation.Biomolecular NMR assignments · 2025Article
- Structural basis for amyloid fibril assembly by the master cell-signaling regulator receptor-interacting protein kinase 1.Nature communications · 2025Article
- Pharmacological targeting of caspase-8/c-FLIPCommunications biology · 2025Article
- Elucidating the dual roles of apoptosis and necroptosis in diabetic wound healing: implications for therapeutic intervention.Burns & trauma · 2025Review
- Targeting TNFR1-driven necroptosis in breast cancer.EXCLI journal · 2025Review
- PANoptosis: a new insight into the mechanism of ischaemia-reperfusion injury.Burns & trauma · 2025Review
- HSPA8 inhibitors augment cancer chemotherapeutic effectiveness via potentiating necroptosis.Molecular biology of the cell · 2024Article
- Spatiotemporal Control of Inflammatory Lytic Cell Death Through Optogenetic Induction of RIPK3 Oligomerization.Journal of molecular biology · 2024Article
- Immunogenic cell death in cancer: targeting necroptosis to induce antitumour immunity.Nature reviews. Cancer · 2024Review
- Exploration of Potential Therapeutic Targets of Shentong Zhuyu Decoction for Ankylosing Spondylitis Based on Network Pharmacology and Molecular Docking.Journal of inflammation research · 2024Article
- Current evidence and therapeutic implication of PANoptosis in cancer.Theranostics · 2024Review
- SMAC Mimetics for the Treatment of Lung Carcinoma: Present Development and Future Prospects.Mini reviews in medicinal chemistry · 2024Review
- Different Ways to Die: Cell Death Pathways and Their Association With Spinal Cord Injury.Neurospine · 2023Article
- Cell death and inflammation during obesity: "Know my methods, WAT(son)".Cell death and differentiation · 2023Review
- Manipulation of Host Cell Death Pathways by Herpes Simplex Virus.Current topics in microbiology and immunology · 2023Article
- Higher Mixed lineage Kinase Domain-like protein (MLKL) is associated with worst overall survival in adult-type diffuse glioma patients.PloS one · 2023Article
- Advances in mechanism and regulation of PANoptosis: Prospects in disease treatment.Frontiers in immunology · 2023Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis was initially identified as a backup cell death program when apoptosis is blocked. However, it is now recognized as a cellular defense mechanism against infections and is presumed to be a detrimental factor in several pathologies driven by cell death. Necroptosis is a prototypic form of regulated necrosis that depends on activation of the necrosome, which is a protein complex in which receptor interacting protein kinase (RIPK) 3 is activated. The RIP homotypic interaction motif (RHIM) is the core domain that regulates activation of the necrosome. To date, three RHIM-containing proteins have been reported to activate the kinase activity of RIPK3 within the necrosome: RIPK1, Toll/IL-1 receptor domain-containing adaptor inducing IFN-β (TRIF), and DNA-dependent activator of interferon regulatory factors (DAI). Here, we review and discuss commonalities and differences of the increasing number of activators of the necrosome. Since the discovery that activation of mixed lineage kinase domain-like (MLKL) by RIPK3 kinase activity is crucial in necroptosis, interest has increased in monitoring and therapeutically targeting their activation. The availability of new phospho-specific antibodies, pharmacologic inhibitors, and transgenic models will allow us to further document the role of necroptosis in degenerative, inflammatory and infectious diseases.
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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.