{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang Y"],"funding":["National Institute of Diabetes and Digestive and Kidney Diseases","NIDDK NIH HHS","Michigan Metabolomics and Obesity Center","University of Michigan Center for Gastrointestinal Research","Michigan Diabetes Research and Training Center"],"pagination":["e71318"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12680040"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["39(23)"],"pubmed_abstract":["NF-κB-inducing kinase (NIK) is selectively upregulated in cholangiocytes during chronic liver disease, but its role in disease progression is poorly understood. We here show that cholangiocyte-specific overexpression of NIK (NIK<sup>Tg</sup>) exacerbates liver disease progression. NIK<sup>Tg</sup> mice were generated using a CK19-CreERT/loxp system. NIK<sup>Tg</sup> and wild-type control (NIK<sup>Con</sup>) mice were treated with thioacetamide (TAA) or 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) to induce liver disease. In a separate cohort, mice were allowed a 2-week recovery period following 4 weeks of TAA administration. NIK was also ablated in human HuCC-T1 cholangiocyte cultures (HuCC-T1<sup>NIK-/-</sup>), and either wild-type NIK or the NIK<sup>G885R</sup> mutant (defective in ac"],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["Biliary NF-κB-Inducing Kinase Promotes Ductular Reaction, Inflammation, and Fibrosis and Impedes Liver Disease Resolution."],"pmcid":["PMC12680040"],"funding_grant_id":["R01 DK114220","DK089503","R01 DK141559","NIDDK P30DK034933","NIH DK020572","R01 DK130111"],"pubmed_authors":["Kang Q","Rui L","Nikooie R","Wang Y"],"additional_accession":[]},"is_claimable":false,"name":"Biliary NF-κB-Inducing Kinase Promotes Ductular Reaction, Inflammation, and Fibrosis and Impedes Liver Disease Resolution.","description":"NF-κB-inducing kinase (NIK) is selectively upregulated in cholangiocytes during chronic liver disease, but its role in disease progression is poorly understood. We here show that cholangiocyte-specific overexpression of NIK (NIK<sup>Tg</sup>) exacerbates liver disease progression. NIK<sup>Tg</sup> mice were generated using a CK19-CreERT/loxp system. NIK<sup>Tg</sup> and wild-type control (NIK<sup>Con</sup>) mice were treated with thioacetamide (TAA) or 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) to induce liver disease. In a separate cohort, mice were allowed a 2-week recovery period following 4 weeks of TAA administration. NIK was also ablated in human HuCC-T1 cholangiocyte cultures (HuCC-T1<sup>NIK-/-</sup>), and either wild-type NIK or the NIK<sup>G885R</sup> mutant (defective in ac","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-06-05T22:26:52.762Z","creation":"2026-05-22T03:15:23.87Z"},"accession":"S-EPMC12680040","cross_references":{"pubmed":["41348430"],"doi":["10.1096/fj.202502014RRR"]}}