ArticleCell metabolism2015
s-Adenosylmethionine Levels Govern Innate Immunity through Distinct Methylation-Dependent Pathways.
Article in Cell metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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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.
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Who cites it
85 citing papers in PubMed, 147 citations in OpenAlex.
- Disruption of methionine metabolism drives erythroid cell fate reprogramming by remodeling the H3K4me3 landscape.The Journal of clinical investigation · 2026Article
- Vitamin BNature communications · 2026Article
- Oxidation Products of S-Adenosyl Methionine Probed by Infrared Multiple Photon Dissociation Spectroscopy.Chemphyschem : a European journal of chemical physics and physical chemistry · 2026Article
- dCas9-metabolic enzyme fusions modulate global and locus-specific gene expression.bioRxiv : the preprint server for biology · 2026Article
- Retrotransposons in Bone and Joint Diseases.FASEB bioAdvances · 2026Review
- WDR-5 exhibits H3K4 methylation-independent activity during embryonic development in C. elegans.Epigenetics & chromatin · 2026Article
- Endozoicomonas acroporae enhances coral thermal resilience through host-microbe coordination.The ISME journal · 2026Article
- Distinct S-adenosylmethionine synthases link phosphatidylcholine to mitochondrial function and stress survival.PLoS biology · 2025Article
- Vitamin BResearch square · 2025Article
- The chromatin remodeler LET-418/Mi-2 regulates the intracellular pathogen response in the C. elegans intestine.BMC genomics · 2025Article
- Parental S-adenosylmethionine diet defines offspring immune response via histone H3K4me3 complex and Endoplasmic Reticulum UPR.Cell communication and signaling : CCS · 2025Article
- Patterns of pathogenesis in innate immunity: insights from C. elegans.Nature reviews. Immunology · 2025Review
- Methionine cycle in C. elegans serotonergic neurons regulates diet-dependent behaviour and longevity through neuron-gut signaling.Nature communications · 2025Article
- From Nutrient to Nanocarrier: The Multifaceted Role of Vitamin B12 in Drug Delivery.International journal of molecular sciences · 2025Review
- Chromatin and epigenetics in aging biology.Genetics · 2025Review
- Conserved chromatin regulators control the transcriptional immune response to intracellular pathogens in Caenorhabditis elegans.PLoS genetics · 2025Article
- Endosomal catabolism of phosphatidylinositol 4,5-bisphosphate is fundamental in building resilience against pathogens.Protein & cell · 2025Article
- Review
- Lysosome-related organelle integrity suppresses TIR-1 aggregation to restrain toxic propagation of p38 innate immunity.Cell reports · 2024Article
- Nutritional vitamin B12 regulates RAS/MAPK-mediated cell fate decisions through one-carbon metabolism.Nature communications · 2024Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
s-adenosylmethionine (SAM) is the sole methyl donor modifying histones, nucleic acids, and phospholipids. Its fluctuation affects hepatic phosphatidylcholine (PC) synthesis or may be linked to variations in DNA or histone methylation. Physiologically, low SAM is associated with lipid accumulation, tissue injury, and immune responses in fatty liver disease. However, molecular connections among SAM limitation, methyltransferases, and disease-associated phenotypes are unclear. We find that low SAM can activate or attenuate Caenorhabditis elegans immune responses. Immune pathways are stimulated downstream of PC production on a non-pathogenic diet. In contrast, distinct SAM-dependent mechanisms limit survival on pathogenic Pseudomonas aeruginosa. C. elegans undertakes a broad transcriptional response to pathogens and we find that low SAM restricts H3K4me3 at Pseudomonas-responsive promoters, limiting their expression. Furthermore, this response depends on the H3K4 methyltransferase set-16/MLL. Thus, our studies provide molecular links between SAM and innate immune functions and suggest that SAM depletion may limit stress-induced gene expression.
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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.