ReviewF1000Research2015
Post-translational control of RIPK3 and MLKL mediated necroptotic cell death.
Review in F1000Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 51 citations in OpenAlex.
- Redefining the Evolution of Pulpal Pathology: Inflammasomes as Central Integrative Hubs and Biological Switches Governing the Transition From Reversible to Irreversible Pulpal Inflammation Beyond Symptom-Based Classification.International endodontic journal · 2026Review
- Signaling pathways and ion channels in osteoarthritis: a review of recent advances.Frontiers in immunology · 2026Review
- MLKL Modulates Necroptosis and Neuroinflammation in a Mouse Model of MS.Inflammation · 2025Article
- Role of necroptosis in pulpitis: integration of bacterial infection, immune imbalance, and oxidative stress.PeerJ · 2025Review
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- Receptor-interacting protein 1 and 3 kinase activity are required for high-fat diet induced liver injury in mice.Frontiers in endocrinology · 2023Article
- Article
- No longer married to inflammasome signaling: the diverse interacting pathways leading to pyroptotic cell death.The Biochemical journal · 2022Review
- The role of necroptosis in disease and treatment.MedComm · 2021Review
- Mitochondrial Mechanisms of Necroptosis in Liver Diseases.International journal of molecular sciences · 2020Review
- Cell Death in Liver Diseases: A Review.International journal of molecular sciences · 2020Review
- FLIP(L): the pseudo-caspase.The FEBS journal · 2020Review
- Hepatic inflammation after burn injury is associated with necroptotic cell death signaling.The journal of trauma and acute care surgery · 2020Article
- TRAF2 protects against cerebral ischemia-induced brain injury by suppressing necroptosis.Cell death & disease · 2019Article
- Pyroptosis versus necroptosis: similarities, differences, and crosstalk.Cell death and differentiation · 2019Review
- When and how NK cell-induced programmed cell death benefits immunological protection against intracellular pathogen infection.Innate immunity · 2018Review
- The brace helices of MLKL mediate interdomain communication and oligomerisation to regulate cell death by necroptosis.Cell death and differentiation · 2018Article
- Non-Hematopoietic MLKL Protects AgainstFrontiers in immunology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several programmed lytic and necrotic-like cell death mechanisms have now been uncovered, including the recently described receptor interacting protein kinase-3 (RIPK3)-mixed lineage kinase domain-like (MLKL)-dependent necroptosis pathway. Genetic experiments have shown that programmed necrosis, including necroptosis, can play a pivotal role in regulating host-resistance against microbial infections. Alternatively, excess or unwarranted necroptosis may be pathological in autoimmune and autoinflammatory diseases. This review highlights the recent advances in our understanding of the post-translational control of RIPK3-MLKL necroptotic signaling. We discuss the critical function of phosphorylation in the execution of necroptosis, and highlight the emerging regulatory roles for several ubiquitin ligases and deubiquitinating enzymes. Finally, based on current evidence, we discuss the potential mechanisms by which the essential, and possibly terminal, necroptotic effector, MLKL, triggers the disruption of cellular membranes to cause cell lysis.
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Identifiers
What OpenQuestion holds
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.