{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T14:53:12Z","timestamp":1787237592482,"version":"build-2736575974"},"reference-count":54,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2024,10,26]],"date-time":"2024-10-26T00:00:00Z","timestamp":1729900800000},"content-version":"vor","delay-in-days":299,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100002701","name":"Ministry of Education","doi-asserted-by":"publisher","award":["2017R1A6A3A11034242"],"award-info":[{"award-number":["2017R1A6A3A11034242"]}],"id":[{"id":"10.13039\/501100002701","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002701","name":"Ministry of Education","doi-asserted-by":"publisher","award":["2017R1A6A1A03015642"],"award-info":[{"award-number":["2017R1A6A1A03015642"]}],"id":[{"id":"10.13039\/501100002701","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002701","name":"Ministry of Education","doi-asserted-by":"publisher","award":["2020R1A6C101A191"],"award-info":[{"award-number":["2020R1A6C101A191"]}],"id":[{"id":"10.13039\/501100002701","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2024,1]]},"abstract":"<jats:p>\n                    Inflammation is a vital immune defense mechanism regulated by Toll\u2010like receptors (TLRs) and the nuclear factor\u2010kappa B (NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B) pathway. TANK\u2010binding kinase 1 (TBK1) is central to immunity and inflammation and influences antiviral responses and cellular processes. However, the precise role of TBK1 in modulating the NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B pathway through interactions with other proteins, such as spleen tyrosine kinase (Syk), remains poorly understood. As dysregulation of TBK1 and NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B can lead to a variety of diseases, they are important therapeutic targets. In this work, inflammatory processes involving the TBK1\u2010Syk\u2010NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B pathway were elucidated using lipopolysaccharide (LPS)\u2010induced macrophages; human embryonic kidney 293 (HEK293) cells overexpressing MyD88, TBK1, and Syk proteins and their mutants; and real\u2010time polymerase chain reaction (PCR), immunoblotting analyses, and kinase assays. TBK1 was activated in LPS\u2010, poly I:C\u2010, and Pam3CSK\u2010stimulated macrophages. Transcript levels of\n                    <jats:italic>TNF<\/jats:italic>\n                    ,\n                    <jats:italic>NOS2<\/jats:italic>\n                    , and\n                    <jats:italic>IL1B<\/jats:italic>\n                    were increased in cells overexpressing TBK1 but not in cells overexpressing TBK1 K38A. The transcription of\n                    <jats:italic>TNF<\/jats:italic>\n                    ,\n                    <jats:italic>NOS2<\/jats:italic>\n                    , and\n                    <jats:italic>IL1B<\/jats:italic>\n                    and NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B luciferase activity were inhibited by silencing TBK1 in LPS\u2010stimulated RAW264.7 cells and MyD88\u2010transfected HEK293 cells. Syk was the key mediator of the TBK1\u2010dependent NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B pathway and bound directly to the coiled coil domain of TBK1, which was necessary to activate Syk and the Syk\u2010p85 pathway. This research advances the understanding of the role of TBK1 in NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B signaling, emphasizing Syk as a key mediator. The interaction between TBK1 and Syk has potential for precise immune modulation that can be applied to treat immune\u2010related disorders.\n                  <\/jats:p>","DOI":"10.1155\/2024\/8634515","type":"journal-article","created":{"date-parts":[[2024,10,26]],"date-time":"2024-10-26T06:35:17Z","timestamp":1729924517000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Functional Involvement of TANK\u2010Binding Kinase 1 in the MyD88\u2010Dependent NF\u2010\n                    <i>\u03ba<\/i>\n                    B Pathway Through Syk"],"prefix":"10.1155","volume":"2024","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4730-9801","authenticated-orcid":false,"given":"Han Gyung","family":"Kim","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7881-9599","authenticated-orcid":false,"given":"Ji Hye","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0925-2242","authenticated-orcid":false,"given":"Tao","family":"Yu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8141-9927","authenticated-orcid":false,"given":"Jae 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