ArticleCell chemical biology2021
Protein acylation by saturated very long chain fatty acids and endocytosis are involved in necroptosis.
Article in Cell chemical biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- Lipid Metabolic Labeling to Study Site- and Lipid-Specific Long-ChainACS chemical biology · 2026Article
- Protein Palmitoylation as a Molecular Switch Linking Regulated Cell Death and Disease.Biomolecules · 2026Review
- Identification of human MLKL Cys184 and HSPBP1 Cys201 as novel cellular targets for necroptosis.Cell death & disease · 2026Article
- Spatiotemporal profiling of modification-specific proteome secretion uncovers an itaconation-activated tyrosine kinase.Nature communications · 2025Article
- Loss of ADAM15 prevents necroptosis induction by partial RIPK1 degradation due to enhanced TNF-R1 surface expression and basal caspase-8 activation.Cell communication and signaling : CCS · 2025Article
- Posttranslational modifications of phosphodiesterase type 4 enzymes represent novel points for therapeutic targeting.The FEBS journal · 2025Review
- Tegavivint triggers TECR-dependent nonapoptotic cancer cell death.Nature chemical biology · 2025Article
- Palmitic acid and palmitoylation in cancer: Understanding, insights, and challenges.Innovation (Cambridge (Mass.)) · 2025Review
- Necroptosis in cancer: insight from epigenetic, post-transcriptional and post-translational modifications.Journal of hematology & oncology · 2025Review
- Anticancer Quinolinol Small Molecules Target Multiple Pathways to Promote Cell Death and Eliminate Melanoma Cells Resistant to BRAF Inhibitors.Molecules (Basel, Switzerland) · 2025Article
- S-acylation in apoptotic and non-apoptotic cell death: a central regulator of membrane dynamics and protein function.Biochemical Society transactions · 2025Review
- Divergent roles of RIPK3 and MLKL in high-fat diet-induced obesity and MAFLD in mice.Life science alliance · 2025Article
- Inhibitors identify an auxiliary role for mTOR signalling in necroptosis execution downstream of MLKL activation.The Biochemical journal · 2024Article
- Crosstalk between metabolism and cell death in tumorigenesis.Molecular cancer · 2024Review
- Amino acid and protein specificity of protein fatty acylation inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Soluble TREM2 ameliorates tau phosphorylation and cognitive deficits through activating transgelin-2 in Alzheimer's disease.Nature communications · 2023Article
- Click chemistry-based enrichment strategy for tracing cellular fatty acid metabolism by LC-MS/MS.Journal of pharmaceutical analysis · 2023Article
- SREBP activation contributes to fatty acid accumulations in necroptosis.RSC chemical biology · 2023Article
- High-quality and robust protein quantification in large clinical/pharmaceutical cohorts with IonStar proteomics investigation.Nature protocols · 2023Review
- Breaking bad: necroptosis in the pathogenesis of gastrointestinal diseases.Frontiers in immunology · 2023Review
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Necroptosis is a form of cell death characterized by receptor-interacting protein kinase activity and plasma membrane permeabilization via mixed-lineage kinase-like protein (MLKL). This permeabilization is responsible for the inflammatory properties of necroptosis. We previously showed that very long chain fatty acids (VLCFAs) are functionally involved in necroptosis, potentially through protein fatty acylation. Here, we define the scope of protein acylation by saturated VLCFAs during necroptosis. We show that MLKL and phosphoMLKL, key for membrane permeabilization, are exclusively acylated during necroptosis. Reducing the levels of VLCFAs decreases their membrane recruitment, suggesting that acylation by VLCFAs contributes to their membrane localization. Acylation of phosphoMLKL occurs downstream of phosphorylation and oligomerization and appears to be, in part, mediated by ZDHHC5 (a palmitoyl transferase). We also show that disruption of endosomal trafficking increases cell viability during necroptosis, possibly by preventing recruitment, or removal, of phosphoMLKL from the plasma membrane.
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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.