{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chandrakesan P"],"funding":["NCI NIH HHS"],"pagination":["33485-33498"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2963366"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["285(43)"],"pubmed_abstract":["Utilizing the Citrobacter rodentium-induced transmissible murine colonic hyperplasia (TMCH) model, we measured hyperplasia and NF-κB activation during progression (days 6 and 12 post-infection) and regression (days 20-34 post-infection) phases of TMCH. NF-κB activity increased at progression in conjunction with bacterial attachment and translocation to the colonic crypts and decreased 40% by day 20. NF-κB activity at days 27 and 34, however, remained 2-3-fold higher than uninfected control. Expression of the downstream target gene CXCL-1/KC in the crypts correlated with NF-κB activation kinetics. Phosphorylation of cellular IκBα kinase (IKK)α/β (Ser(176/180)) was elevated during progression and regression of TMCH. Phosphorylation (Ser(32/36)) and degradation of IκBα, however, contributed t"],"journal":["The Journal of biological chemistry"],"pubmed_title":["Novel changes in NF-{kappa}B activity during progression and regression phases of hyperplasia: role of MEK, ERK, and p38."],"pmcid":["PMC2963366"],"funding_grant_id":["R01 CA097959","CA114264","R01 CA114264","R01 CA 97959","R01 CA131413","R21 CA131936"],"pubmed_authors":["Peleg S","Ahmed I","Sarkar S","Umar S","Chandrakesan P","Singh P","Anwar T","Wang Y"],"additional_accession":[]},"is_claimable":false,"name":"Novel changes in NF-{kappa}B activity during progression and regression phases of hyperplasia: role of MEK, ERK, and p38.","description":"Utilizing the Citrobacter rodentium-induced transmissible murine colonic hyperplasia (TMCH) model, we measured hyperplasia and NF-κB activation during progression (days 6 and 12 post-infection) and regression (days 20-34 post-infection) phases of TMCH. NF-κB activity increased at progression in conjunction with bacterial attachment and translocation to the colonic crypts and decreased 40% by day 20. NF-κB activity at days 27 and 34, however, remained 2-3-fold higher than uninfected control. Expression of the downstream target gene CXCL-1/KC in the crypts correlated with NF-κB activation kinetics. Phosphorylation of cellular IκBα kinase (IKK)α/β (Ser(176/180)) was elevated during progression and regression of TMCH. Phosphorylation (Ser(32/36)) and degradation of IκBα, however, contributed t","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 Oct","modification":"2025-04-26T11:27:22.859Z","creation":"2019-03-27T00:35:05Z"},"accession":"S-EPMC2963366","cross_references":{"pubmed":["20710027"],"doi":["10.1074/jbc.m110.129353","10.1074/jbc.M110.129353"]}}