{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,10]],"date-time":"2026-04-10T09:10:14Z","timestamp":1775812214237,"version":"3.50.1"},"reference-count":57,"publisher":"Canadian Science Publishing","issue":"2","license":[{"start":{"date-parts":[[2020,4,1]],"date-time":"2020-04-01T00:00:00Z","timestamp":1585699200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Biochem. Cell Biol."],"published-print":{"date-parts":[[2020,4]]},"abstract":"<jats:p> Mitochondria affect cellular functions alone or in cooperation with other cellular organelles. Recent research has demonstrated the close relationship of mitochondria with the endoplasmic reticulum (ER), both at the physical and the functional level. In an effort to define the combined effect of mitochondrial dysfunction (MD) and ER stress in the proinflammatory activities of macrophages, the human macrophage-like monocytic leukemia cell line THP-1 was treated with mitochondrial electron transport chain (ETC) blockers, and changes in the cellular responses upon stimulation by interferon (IFN)-\u03b3 were analyzed. Inducing mitochondrial dysfunction (MD) with ETC blockers resulted in suppression of IFN-induced activation of JAK1 and STAT1\/3, as well as the expression of STAT1-regulated genes. In addition, experiments utilizing pharmacological modulators of adenosine 5\u2032-monophosphate (AMP)-activated protein kinase (AMPK) and liver kinase B1 (LKB1)-deficient HeLa cells demonstrated that these suppressive effects are mediated by the LKB1\u2013AMPK pathway. Treatment with pharmacological inhibitors of ER stress sensors failed to affect these processes, thus indicating that involvement of ER stress is not required. These results indicate that MD, induced by blocking the ETC, affects IFN-induced activation of JAK\u2013STAT and associated inflammatory changes in THP-1 cells through the LKB1\u2013AMPK pathway independently of ER stress. <\/jats:p>","DOI":"10.1139\/bcb-2019-0088","type":"journal-article","created":{"date-parts":[[2019,5,9]],"date-time":"2019-05-09T21:47:51Z","timestamp":1557438471000},"page":"137-144","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":23,"title":["Mitochondrial dysfunction regulates the JAK\u2013STAT pathway via LKB1-mediated AMPK activation ER-stress-independent manner"],"prefix":"10.1139","volume":"98","author":[{"given":"Dong-Yeon","family":"Kim","sequence":"first","affiliation":[{"name":"School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu 41566, Republic of Korea."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Su-Geun","family":"Lim","sequence":"additional","affiliation":[{"name":"School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu 41566, Republic of Korea."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kyoungho","family":"Suk","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Brain Science & Engineering Institute, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu 41944, Republic of Korea."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Won-Ha","family":"Lee","sequence":"additional","affiliation":[{"name":"School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu 41566, Republic of Korea."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"refg1\/ref1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.0900228"},{"key":"refg2\/ref2","unstructured":"Ahmad, M., and Kahwaji, C.I. 2018. 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