<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chandrakesan P</submitter><funding>NCI NIH HHS</funding><pagination>33485-33498</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2963366</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>285(43)</volume><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</pubmed_abstract><journal>The Journal of biological chemistry</journal><pubmed_title>Novel changes in NF-{kappa}B activity during progression and regression phases of hyperplasia: role of MEK, ERK, and p38.</pubmed_title><pmcid>PMC2963366</pmcid><funding_grant_id>R01 CA097959</funding_grant_id><funding_grant_id>CA114264</funding_grant_id><funding_grant_id>R01 CA114264</funding_grant_id><funding_grant_id>R01 CA 97959</funding_grant_id><funding_grant_id>R01 CA131413</funding_grant_id><funding_grant_id>R21 CA131936</funding_grant_id><pubmed_authors>Peleg S</pubmed_authors><pubmed_authors>Ahmed I</pubmed_authors><pubmed_authors>Sarkar S</pubmed_authors><pubmed_authors>Umar S</pubmed_authors><pubmed_authors>Chandrakesan P</pubmed_authors><pubmed_authors>Singh P</pubmed_authors><pubmed_authors>Anwar T</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Novel changes in NF-{kappa}B activity during progression and regression phases of hyperplasia: role of MEK, ERK, and p38.</name><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</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Oct</publication><modification>2025-04-26T11:27:22.859Z</modification><creation>2019-03-27T00:35:05Z</creation></dates><accession>S-EPMC2963366</accession><cross_references><pubmed>20710027</pubmed><doi>10.1074/jbc.m110.129353</doi><doi>10.1074/jbc.M110.129353</doi></cross_references></HashMap>