{"title":"Crosstalk between stress-induced NF-κB, p53 and HSF1 signaling pathways – review.","authors":"P. Widłak, Michalina Gramatyka, M. Kimmel","doi":"10.3182/20140824-6-ZA-1003.01054","DOIUrl":null,"url":null,"abstract":"Abstract The signaling pathways depending on NF-κB, p53 and HSF1 transcription factors are components of the cellular response to stress. NF-κB transcription factor regulates genes responsible for inflammation, immune response and cell survival. p53 either activates cell cycle arrest and DNA repair or induces apoptosis in cells with DNA damage. HSF1 activates under stress conditions and induces the heat shock response. All there pathways are essential for cancer and other human diseases. Here we review biological data on these signal transduction pathways and introduce complex crosstalk between these regulatory circuits as an apparent challenge for mathematical modeling.","PeriodicalId":13260,"journal":{"name":"IFAC Proceedings Volumes","volume":"1 1","pages":"11518-11523"},"PeriodicalIF":0.0000,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"IFAC Proceedings Volumes","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3182/20140824-6-ZA-1003.01054","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 5
Abstract
Abstract The signaling pathways depending on NF-κB, p53 and HSF1 transcription factors are components of the cellular response to stress. NF-κB transcription factor regulates genes responsible for inflammation, immune response and cell survival. p53 either activates cell cycle arrest and DNA repair or induces apoptosis in cells with DNA damage. HSF1 activates under stress conditions and induces the heat shock response. All there pathways are essential for cancer and other human diseases. Here we review biological data on these signal transduction pathways and introduce complex crosstalk between these regulatory circuits as an apparent challenge for mathematical modeling.