ArticleJournal of nature and science2018
Necroptosis: MLKL Polymerization.
Article in Journal of nature and science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 33 citations in OpenAlex.
- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
- Research progress on programmed cell death of cardiomyocytes in pressure-overload hypertrophic cardiomyopathy.Apoptosis : an international journal on programmed cell death · 2025Review
- Mixed Lineage Kinase Domain-Like Protein (MLKL): From Mechanisms to Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Mitochondrial dysfunction is a major cause of thromboinflammation and inflammatory cell death in critical illnesses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- MLKL as an emerging machinery for modulating organelle dynamics: regulatory mechanisms, pathophysiological significance, and targeted therapeutics.Frontiers in pharmacology · 2025Review
- Autophagy and autophagic cell death in sepsis: friend or foe?Journal of intensive care · 2024Review
- From Crypts to Cancer: A Holistic Perspective on Colorectal Carcinogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Stimulation of Hemolysis and Eryptosis by β-Caryophyllene Oxide.Life (Basel, Switzerland) · 2023Article
- Necroptosis executioner MLKL plays pivotal roles in agonist-induced platelet prothrombotic responses and lytic cell death in a temporal order.Cell death and differentiation · 2023Article
- Article
- Cell Death Triggers Induce MLKL Cleavage in Multiple Myeloma Cells, Which may Promote Cell Death.Frontiers in oncology · 2022Article
- Protein acylation by saturated very long chain fatty acids and endocytosis are involved in necroptosis.Cell chemical biology · 2021Article
- Viral Induced Protein Aggregation: A Mechanism of Immune Evasion.International journal of molecular sciences · 2021Review
- Review
- MLKL in cancer: more than a necroptosis regulator.Cell death and differentiation · 2021Review
- A narrative review of the role of necroptosis in liver disease: a double-edged sword.Annals of translational medicine · 2021Review
- RIP3 mediates TCN-induced necroptosis through activating mitochondrial metabolism and ROS production in chemotherapy-resistant cancers.American journal of cancer research · 2021Article
- Peptide-Based TNF-α-Binding Decoy Therapy Mitigates Lipopolysaccharide-Induced Liver Injury in Mice.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Optimal concentration of necrostatin-1 for protecting against hippocampal neuronal damage in mice with status epilepticus.Neural regeneration research · 2020Article
- Review
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 1 institution in 1 country.
Funding
Abstract
Necroptosis is a subtype of regulated necrosis that occurs when caspases are inhibited or fail to activate. Stimulus of cell death receptors results in a signaling cascade that triggers caspase independent, immunogenic cell death. The core pathway relies on receptor interacting protein kinase (RIPK) 1 and 3, which interact through their receptor homotypic interacting motif (RHIM) domains, and form amyloid-like structures termed the necrosome. RIPK3 recruits and phosphorylates mixed lineage kinase domain-like pseudokinase (MLKL), the terminal mediator in the necroptotic pathway. MLKL polymerizes to form a second amyloid-like structure that causes cell membrane disruption resulting in cell death. Although the core necroptosis pathway has been elucidated, the details of MLKL membrane translocation and membrane disruption remain an open area of research.
Indexed as
Identifiers
30294675PMC6173486W2809939144What 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.