ReviewNature reviews. Molecular cell biology2023
Pore-forming proteins as drivers of membrane permeabilization in cell death pathways.
Review in Nature reviews. Molecular cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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Who cites it
104 citing papers in PubMed.
- Article
- PTEN-L inhibits mitophagy and GSDME-dependent pyroptosis via Parkin dephosphorylation.EMBO reports · 2026Article
- Mitochondrial dysfunction and oxidative stress in OSAHS and associated comorbidities: Mechanism and potential targeted therapeutic strategies.Redox biology · 2026Review
- Microplastic-Induced DRP1-BAX Interaction Contributes to Mitochondrial Apoptosis in Lung Epithelial Cells.Environment & health (Washington, D.C.) · 2026Article
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- BOK beyond apoptosis: pyrimidine metabolism and ATR dependence in p53-deficient lung cancer.Cell death and differentiation · 2026Article
- Formic acid released by intratumoralActa pharmaceutica Sinica. B · 2026Article
- Molecular mechanism of pore formation by Plasmodium Perforin-like Protein 2.Nature communications · 2026Article
- The novel agent VP79s synergistically enhances venetoclax activity in multiple myeloma cells.Investigational new drugs · 2026Article
- Direct visualization of native GSDMD pores reveals lipid-driven stabilization during pyroptosis.Science advances · 2026Article
- Redirecting TRIM21 with TRIMTACs for the targeted degradation of multimeric proteins.The FEBS journal · 2026Review
- Integrated Stress Response and Drug-Induced Acute Kidney Injury: Involvement of Activating ATF4-STAT1-GBP2 Signaling.Journal of the American Society of Nephrology : JASN · 2026Article
- BIRC6 prevents GSDME-mediated pyroptosis and promotes cisplatin resistance via a non-canonical UBC domain-dependent steric hindrance.Cell communication and signaling : CCS · 2026Article
- Overexpression of SIRT3 ameliorates calcium oxalate crystal-induced renal necroptosis by suppressing the TNF-α/RIPK3/P-MLKL pathway.Translational andrology and urology · 2026Article
- Bon appétit, your phagocyte.Cell death discovery · 2026Review
- IFN-I Induces Keratinocytes Necroptosis via ZBP1-MLKL Axis in Oral Lichen Planus.Inflammation · 2026Article
- Physiological and Metabolic Mechanisms ofJournal of fungi (Basel, Switzerland) · 2026Article
- Necroptosis in both tumour and stromal compartments determines responsiveness to immunogenic cell death-based immunotherapy.Nature communications · 2026Article
- Tackling cuproptosis: from metabolic rewiring to therapeutic exploitation in cancer.Cellular & molecular immunology · 2026Review
- Engineered Escherichia coli as a microbial cell factory for intracellular protein delivery: strains, vectors, mechanisms, and therapeutic applications.Microbial cell factories · 2026Review
44 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulated cell death (RCD) relies on activation and recruitment of pore-forming proteins (PFPs) that function as executioners of specific cell death pathways: apoptosis regulator BAX (BAX), BCL-2 homologous antagonist/killer (BAK) and BCL-2-related ovarian killer protein (BOK) for apoptosis, gasdermins (GSDMs) for pyroptosis and mixed lineage kinase domain-like protein (MLKL) for necroptosis. Inactive precursors of PFPs are converted into pore-forming entities through activation, membrane recruitment, membrane insertion and oligomerization. These mechanisms involve protein-protein and protein-lipid interactions, proteolytic processing and phosphorylation. In this Review, we discuss the structural rearrangements incurred by RCD-related PFPs and describe the mechanisms that manifest conversion from autoinhibited to membrane-embedded molecular states. We further discuss the formation and maturation of membrane pores formed by BAX/BAK/BOK, GSDMs and MLKL, leading to diverse pore architectures. Lastly, we highlight commonalities and differences of PFP mechanisms involving BAX/BAK/BOK, GSDMs and MLKL and conclude with a discussion on how, in a population of challenged cells, the coexistence of cell death modalities may have profound physiological and pathophysiological implications.
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