ReviewCell death and differentiation2023
MLKL post-translational modifications: road signs to infection, inflammation and unknown destinations.
Review in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Uncovering Necroptosis in Alzheimer's Disease: A Systematic Review of Evidence Across Experimental Models.Cellular and molecular neurobiology · 2025Pooled it
- Targeting AIF to trigger RIPKs/MLKL necroptosis: a disulfiram-based strategy to reverse paclitaxel resistance in ovarian cancer.Cell communication and signaling : CCS · 2026Article
- Necroptosis in Down Syndrome.Cell death & disease · 2026Article
- Ubiquitination and autophagy in host-pathogen interactions: from immune surveillance to therapeutic targeting.Nature reviews. Immunology · 2026Review
- RIP kinase inhibition with Necrostatin-1 improves human marginal mass islet graft survival and function for the management of type 1 diabetes.Cell death & disease · 2026Article
- Autoinhibitory control of MLKL governs pseudokinase domain phosphorylation and oligomerization during necroptosis.Cell reports · 2026Article
- FKBP5 Mediates Alveolar Fibroblast Necroptosis During Acute Respiratory Distress Syndrome.Cell proliferation · 2026Article
- EnterotoxigenicFrontiers in immunology · 2026Article
- Research Prospects for Necroptosis in Inflammatory Diseases: A Bibliometric Analysis.Current medicinal chemistry · 2026Review
- Integrating necroptosis and immune landscapes: a multi-omics-derived NecropImmScore stratifies prognosis and therapy in ovarian cancer.Cancer immunology, immunotherapy : CII · 2025Article
- Disrupting membranes, controlling cell fate: the role of pore-forming proteins in cell death and therapy.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
- Autophagy disruption and mitochondrial stress precede photoreceptor necroptosis in multiple mouse models of inherited retinal disorders.Nature communications · 2025Article
- Epigenetic Inactivation of RIPK3-Dependent Necroptosis Augments Cisplatin Chemoresistance in Human Osteosarcoma.International journal of molecular sciences · 2025Article
- Epigenetic modulation of RIPK3 by transglutaminase 2-dependent serotonylation of H3K4me3 affects necroptosis.Cellular and molecular life sciences : CMLS · 2025Article
- Erythronecroptosis: an overview of necroptosis or programmed necrosis in red blood cells.Molecular and cellular biochemistry · 2024Review
- Targeting necroptosis: a promising avenue for respiratory disease treatment.Cell communication and signaling : CCS · 2024Review
- The importance of murine phospho-MLKL-S345 in situ detection for necroptosis assessment in vivo.Cell death and differentiation · 2024Article
- Dying in self-defense: cell death signaling in animals and plants.Cell death and differentiation · 2024Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis is a caspase-independent modality of cell death that requires the activation of the executioner MLKL. In the last ten years the field gained a substantial amount of evidence regarding its involvement in host response to pathogens, TNF-induced inflammatory diseases as well as pathogen recognition receptors (PRR)-induced inflammation. However, there are still a lot of questions that remain unanswered. While it is clear that there are specific events needed to drive MLKL activation, substantial differences between human and mouse MLKL not only highlight different evolutionary pressure, but also provide potential insights on alternative modalities of activation. While in TNF-induced necroptosis it is clear the involvement of the RIPK3 mediated phosphorylation, it still remains to be understood how certain inflammatory in vivo phenotypes are not equally rescued by either RIPK3 or MLKL loss. Moreover, the plethora of different reported phosphorylation events on MLKL, even in cells that do not express RIPK3, suggest indeed that there is more to MLKL than RIPK3-mediated activation, not only in the execution of necroptosis but perhaps in other inflammatory conditions that include IFN response. The recent discovery of MLKL ubiquitination has highlighted a new checkpoint in the regulation of MLKL activation and the somewhat conflicting evidence reported certainly require some untangling. In this review we will highlight the recent findings on MLKL activation and involvement to pathogen response with a specific focus on MLKL post-translational modifications, in particular ubiquitination. This review will highlight the outstanding main questions that have risen from the last ten years of research, trying at the same time to propose potential avenues of research.
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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.