ReviewAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Mixed Lineage Kinase Domain-Like Protein (MLKL): From Mechanisms to Therapeutic Opportunities.
Review in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
7 citing papers in PubMed.
- Mechanistic analysis of MLKL-driven cell survival.Cell death discovery · 2026Review
- Programmed cell death in cancer: targeting necroptosis to kill tumor cell.Cell death discovery · 2026Review
- Scaffold Hopping-Guided Design of Novel PIM-1 Inhibitors with Anticancer Activities.Molecules (Basel, Switzerland) · 2026Article
- To Die or Not to Die: How Sublethal Damage Rewires Cell Fate and Implications for Sepsis.Journal of inflammation research · 2026Review
- OTUD7B exacerbates atherosclerosis by promoting RIPK1-dependent vascular smooth muscle cell necroptosis.Frontiers in cardiovascular medicine · 2026Article
- Trigger Points of Necroptosis (RIPK1, RIPK3, and MLKL)-Promising Horizon or Blind Alley in Therapy of Colorectal Cancer?International journal of molecular sciences · 2025Review
- Mixed Lineage Kinase Domain-Like Protein (MLKL): From Mechanisms to Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
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.
Funding
Abstract
Lytic forms of regulated cell death (RCD) rely on the activation and recruitment of executioner proteins. The mixed lineage kinase domain-like protein (MLKL) acts as the executioner in the necroptosis pathway, transitioning from an inactive to active state through phosphorylation, oligomerization, membrane recruitment, and membrane insertion, ultimately forming membrane hotpots. These mechanisms involve protein-protein interactions between receptor-interacting protein kinase 3 (RIPK3) and MLKL, MLKL phosphorylation, protein-protein interactions between MLKL and MLKL, and MLKL-lipid interactions. In this review, the specificity of MLKL activation mechanisms is discussed across different species and describe the processes by which MLKL transitions from an auto-inhibited to a membrane-embedded state. The opportunities are further explored for targeting MLKL, including small molecule inhibitors and functionally interacting proteins.
Indexed as
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.