{"doi":"10.1183/09031936.98.12010221","title":"Transcription factors and asthma","abstract":"<jats:p>Asthma is characterized by the expression of multiple genes for inflammatory proteins, such as cytokines, enzymes, receptors and adhesion molecules. This is orchestrated by transcription factors, which are proteins that bind to the promoter regions of these genes and may be activated by inflammatory stimuli, such as cytokines. Several transcription factors are involved in asthmatic inflammation, including nuclear factor-kappaB (NF-kappaB), activator protein-1 (AP-1), nuclear factor of activated T-cells (NF-AT), cyclic AMP response element binding protein (CREB) and signal transduction-activated transcription factors (STAT). These transcription factors lead to coordinated expression of multiple inflammatory genes. There is increasing evidence that synergistic interaction of these transcription factors (e.g. NF-kappaB and AP-1) results in the optimal expression of particular genes, resulting in the specific inflammatory pattern seen in asthmatic airways. Transcription factors are a target for antiasthma therapy. Corticosteroids activate glucocorticoid receptors, which themselves are transcription factors, and interact with other transcription factors to inhibit their actions. The interaction between transcription factors may be important in amplifying and inhibiting the inflammatory process. Many transcription factors interact with a large co-activator molecule CREB-binding protein (CBP) that coordinates the activation of several transcription factors and controls transcription through the regulation of deoxyribonucleic acid coiling around histone residues in the chromatin structure. Understanding transcription factors in asthma has given new insights into the complex chronic inflammatory process, the mechanism of action of corticosteroids, and may lead to new approaches to therapy in the future.</jats:p>","journal":"European Respiratory Journal","year":1998,"id":22566,"datarank":11.816448642615761,"base_score":5.7745515455444085,"endowment":5.7745515455444085,"self_citation_contribution":0.8661827318316614,"citation_network_contribution":10.950265910784099,"self_endowment_contribution":0.8661827318316614,"citer_contribution":10.950265910784099,"corpus_percentile":null,"corpus_rank":null,"citation_count":321,"citer_count":200,"citers_with_citation_signal":200,"citers_with_endowment":200,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":141467,"name":"IM Adcock","orcid":null,"position":1,"is_corresponding":false},{"id":141466,"name":"PJ Barnes","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"base_score":5.7745515455444085,"endowment":5.7745515455444085,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"9701442","pmcid":null,"openalex_id":"https://openalex.org/W2110955240","authors":[],"funders":[],"total_grants":0,"fwci":8.0891,"citation_percentile":0.98143249,"influential_citations":11,"citation_trend":[{"year":2012,"count":9},{"year":2013,"count":9},{"year":2014,"count":5},{"year":2015,"count":5},{"year":2016,"count":10},{"year":2017,"count":5},{"year":2018,"count":7},{"year":2019,"count":4},{"year":2020,"count":5},{"year":2021,"count":3},{"year":2022,"count":4},{"year":2023,"count":4},{"year":2024,"count":7},{"year":2025,"count":7}],"oa_status":"bronze","license":null,"oa_locations":[{"url":"https://erj.ersjournals.com/content/erj/12/1/221.full.pdf","host_type":"journal"},{"url":"https://erj.ersjournals.com/content/erj/12/1/221.full.pdf","host_type":"BRONZE"},{"url":"https://erj.ersjournals.com/content/erj/12/1/221.full.pdf","host_type":"publisher"},{"url":"https://syndication.highwire.org/content/doi/10.1183/09031936.98.12010221","host_type":"publisher"},{"url":"https://doi.org/10.1183/09031936.98.12010221","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/9701442","host_type":"repository"}],"fields_of_study":["Cytokine Signaling Pathways and Interactions","NF-κB Signaling Pathways","IL-33, ST2, and ILC Pathways","Biology","Medicine","Asthma","Gene Expression","Humans","Inflammation Mediators","Transcription Factors"],"mesh_terms":["Asthma","Humans","Transcription Factors","Gene Expression","Inflammation Mediators"],"keywords":["Transcription coregulator","Transcription factor","E-box","CREB","Response element","General transcription factor","Sp3 transcription factor","TAF2","Activating transcription factor 2","PELP-1","Promoter","Cell biology","Activating transcription factor","Pioneer factor","Transcription (linguistics)","CREB-binding protein","Biology","Activator (genetics)","Enhancer","Gene expression","Nuclear receptor","Receptor","Gene","Genetics"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good health and well-being"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-06-07T13:22:58.452536Z","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,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}