<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhang X</submitter><funding>NIEHS NIH HHS</funding><funding>Foundation for the National Institutes of Health</funding><funding>NCI NIH HHS</funding><pagination>116753</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11065478</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>481</volume><pubmed_abstract>Exposure to nickel, an environmental respiratory toxicant, is associated with lung diseases including asthma, pulmonary fibrosis, bronchitis and cancers. Our previous studies have shown that a majority of the nickel-induced transcriptional changes are persistent and do not reverse even after the termination of exposure. This suggested transcriptional memory, wherein the cell 'remembers' past nickel exposure. Transcriptional memory, due to which the cells respond more robustly to a previously encountered stimulus has been identified in a number of organisms. Therefore, transcriptional memory has been described as an adaptive mechanism. However, transcriptional memory caused by environmental toxicant exposures has not been well investigated. Moreover, how the transcriptional memory caused by</pubmed_abstract><journal>Toxicology and applied pharmacology</journal><pubmed_title>Nickel-induced transcriptional memory in lung epithelial cells promotes interferon signaling upon nicotine exposure.</pubmed_title><pmcid>PMC11065478</pmcid><funding_grant_id>R01 ES031937</funding_grant_id><funding_grant_id>T32 ES007324</funding_grant_id><funding_grant_id>P30 CA016087</funding_grant_id><funding_grant_id>R01 ES031402</funding_grant_id><pubmed_authors>Jose CC</pubmed_authors><pubmed_authors>Katari M</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Tan T</pubmed_authors><pubmed_authors>Bradford B</pubmed_authors><pubmed_authors>Cuddapah S</pubmed_authors><pubmed_authors>Baweja S</pubmed_authors><pubmed_authors>Lee HW</pubmed_authors><pubmed_authors>Kim N</pubmed_authors></additional><is_claimable>false</is_claimable><name>Nickel-induced transcriptional memory in lung epithelial cells promotes interferon signaling upon nicotine exposure.</name><description>Exposure to nickel, an environmental respiratory toxicant, is associated with lung diseases including asthma, pulmonary fibrosis, bronchitis and cancers. Our previous studies have shown that a majority of the nickel-induced transcriptional changes are persistent and do not reverse even after the termination of exposure. This suggested transcriptional memory, wherein the cell 'remembers' past nickel exposure. Transcriptional memory, due to which the cells respond more robustly to a previously encountered stimulus has been identified in a number of organisms. Therefore, transcriptional memory has been described as an adaptive mechanism. However, transcriptional memory caused by environmental toxicant exposures has not been well investigated. Moreover, how the transcriptional memory caused by</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Dec</publication><modification>2026-06-01T07:15:19.993Z</modification><creation>2026-04-08T10:21:01.134Z</creation></dates><accession>S-EPMC11065478</accession><cross_references><pubmed>37951547</pubmed><doi>10.1016/j.taap.2023.116753</doi></cross_references></HashMap>