ReviewCold Spring Harbor perspectives in biology2020
The Evolutionary Origins of Programmed Cell Death Signaling.
Review in Cold Spring Harbor perspectives in biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Pyroptosis in Patients with Ovarian Dysfunction and Infertility: Molecular Mechanisms and Therapeutics.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- VqLecRKV.4 and VqBAK1 Modulate Grapevine Resistance to Powdery Mildew by Regulating Dynamic Balance of ROS.Plant biotechnology journal · 2026Article
- Bioinformatics analyses reveal the role of RIPK1 in clear cell renal cell carcinoma.BMC cancer · 2026Article
- Cell death and its interaction with mitochondrial dysfunction in pathogenesis of acute pancreatitis: a comprehensive review.Apoptosis : an international journal on programmed cell death · 2026Review
- Radial astroglia cooperate with microglia to clear neuronal cell bodies during zebrafish optic tectum development.Cell reports · 2025Article
- Evolutionary and Functional Analysis of Caspase-8 and ASC Interactions to Drive Lytic Cell Death, PANoptosis.Molecular biology and evolution · 2025Article
- Bringing together but staying apart: decisive differences in animal and fungal mitochondrial inner membrane fusion.Biological reviews of the Cambridge Philosophical Society · 2025Review
- Article
- Pufferfish gasdermin Ea is a significant player in the defense against bacterial pathogens.Marine life science & technology · 2024Article
- Endosperm cell death: roles and regulation in angiosperms.Journal of experimental botany · 2024Review
- What are the 100 most cited fungal genera?Studies in mycology · 2024Article
- het-B allorecognition in Podospora anserina is determined by pseudo-allelic interaction of genes encoding a HET and lectin fold domain protein and a PII-like protein.PLoS genetics · 2024Article
- Article
- Looking outside the box: a comparative cross-kingdom view on the cell biology of the three major lineages of eukaryotic multicellular life.Cellular and molecular life sciences : CMLS · 2023Review
- The VEGFR/PDGFR tyrosine kinase inhibitor, ABT-869, blocks necroptosis by targeting RIPK1 kinase.The Biochemical journal · 2023Article
- Paradoxical roles for programmed cell death signaling during viral infection of the central nervous system.Current opinion in neurobiology · 2022Review
- Clearing Your Mind: Mechanisms of Debris Clearance After Cell Death During Neural Development.Annual review of neuroscience · 2022Review
- Article
- The Ancient Origins of Death Domains Support the 'Original Sin' Hypothesis for the Evolution of Programmed Cell Death.Journal of molecular evolution · 2022Article
- New insights into the evolutionary dynamic and lineage divergence of gasdermin E in metazoa.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
1 author.
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Abstract
Programmed cell death (PCD) pathways are found in many phyla, ranging from developmentally programmed apoptosis in animals to cell-autonomous programmed necrosis pathways that limit the spread of biotrophic pathogens in multicellular assemblies. Prominent examples for the latter include animal necroptosis and pyroptosis, plant hypersensitive response (HR), and fungal heterokaryon incompatibility (HI) pathways. PCD pathways in the different kingdoms show fundamental differences in execution mechanism, morphology of the dying cells, and in the biological sequelae. Nevertheless, recent studies have revealed remarkable evolutionary parallels, including a striking sequence relationship between the "HeLo" domains found in the pore-forming components of necroptosis and some types of plant HR and fungal HI pathways. Other PCD execution components show cross-kingdom conservation as well, or are derived from prokaryotic ancestors. The currently available data suggest a model, wherein the primordial eukaryotic PCD pathway used proteins similar to present-day plant R-proteins and caused necrotic cell death by direct action of Toll and IL-1 receptor (TIR) and HeLo-like domains.
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