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In this review, we consider the emerging evidence that cellular metabolic activity contributes to gene expression and cell fate decisions through metabolite-dependent effects on chromatin organization.</jats:p>","journal":"Journal of Cell Biology","year":2018,"id":588226,"datarank":5.869313046749787,"base_score":5.438079308923196,"endowment":5.438079308923196,"self_citation_contribution":0.8157118963384794,"citation_network_contribution":5.053601150411308,"self_endowment_contribution":0.8157118963384794,"citer_contribution":5.053601150411308,"corpus_percentile":null,"corpus_rank":null,"citation_count":229,"citer_count":200,"citers_with_citation_signal":184,"citers_with_endowment":184,"datacite_reuse_total":4,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":611838,"name":"Craig B. 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Many of the chemical modifications that decorate DNA and histones are adducts derived from intermediates of cellular metabolic pathways. In addition, several of the enzymes that can remove these marks use metabolites as part of their enzymatic reaction. These observations have led to the hypothesis that fluctuations in metabolite levels influence the deposition and removal of chromatin modifications. In this review, we consider the emerging evidence that cellular metabolic activity contributes to gene expression and cell fate decisions through metabolite-dependent effects on chromatin organization.</jats:p>","is_dataset_classified":null,"base_score":0.0,"endowment":0.0,"datacite_reuse_total":4,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"29760106","pmcid":"PMC6028552","openalex_id":null,"authors":[],"funders":[{"funder_name":"Damon Runyon Cancer Research Foundation","grant_id":"DFS-23-17","title":null},{"funder_name":"Memorial Sloan Kettering Cancer Center","grant_id":"P30 CA008748","title":null},{"funder_name":"National Institutes of Health","grant_id":"2P30CA008748-43","title":"MOUSE GENETICS"},{"funder_name":"Hope Funds for Cancer Research","grant_id":"","title":null}],"total_grants":4,"fwci":null,"citation_percentile":null,"influential_citations":4,"citation_trend":[],"oa_status":"bronze","license":"CC BY NC SA","oa_locations":[{"url":"https://rupress.org/jcb/article-pdf/217/7/2247/1378862/jcb_201803061.pdf","host_type":"HYBRID"},{"url":"https://rupress.org/jcb/article-pdf/217/7/2247/1378862/jcb_201803061.pdf","host_type":"publisher"},{"url":"https://rupress.org/jcb/article-pdf/217/7/2247/1613915/jcb_201803061.pdf","host_type":"publisher"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/6028552","host_type":"repository"},{"url":"https://europepmc.org/articles/PMC6028552","host_type":"Europe_PMC"},{"url":"https://europepmc.org/articles/PMC6028552?pdf=render","host_type":"Europe_PMC"},{"url":"https://doi.org/10.1083/jcb.201803061","host_type":""},{"url":"https://pubmed.ncbi.nlm.nih.gov/29760106","host_type":""},{"url":"http://dx.doi.org/10.1083/jcb.201803061","host_type":""},{"url":"https://dx.doi.org/10.1083/jcb.201803061","host_type":""}],"fields_of_study":["Medicine","Biology","Chemistry","0301 basic medicine","0303 health sciences","03 medical and health sciences"],"mesh_terms":["Chromatin","Humans","Histones","Chromatin Assembly and Disassembly","Gene Expression Regulation","Epigenesis, Genetic","Cell Lineage","Metabolic Networks and Pathways"],"keywords":["Histones","Gene Expression Regulation","Reviews","Humans","Cell Lineage","Chromatin Assembly and Disassembly","Chromatin","Metabolic Networks and Pathways","Epigenesis, Genetic"],"sdg_mappings":[],"linked_datasets":[{"doi":"10.6084/m9.figshare.24124008.v1","title":"Additional file 1 of H3K18 lactylation of senescent microglia potentiates brain aging and Alzheimer's disease through the NFκB signaling pathway","publisher":"figshare","resource_type":"JournalArticle"},{"doi":"10.6084/m9.figshare.24124008","title":"Additional file 1 of H3K18 lactylation of senescent microglia potentiates brain aging and Alzheimer's disease through the NFκB signaling pathway","publisher":"figshare","resource_type":"JournalArticle"},{"doi":"10.6084/m9.figshare.24124011.v1","title":"Additional file 2 of H3K18 lactylation of senescent microglia potentiates brain aging and Alzheimer's disease through the NFκB signaling pathway","publisher":"figshare","resource_type":"JournalArticle"},{"doi":"10.6084/m9.figshare.24124011","title":"Additional file 2 of H3K18 lactylation of senescent microglia potentiates brain aging and Alzheimer's disease through the NFκB signaling pathway","publisher":"figshare","resource_type":"JournalArticle"}],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-07-19T20:08:28.592955Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}