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作 者:Albert R.Wang Andrew M.Baschnagel Zijian Ni Sean R.Brennan Hypatia K.Newton Darya Buehler Christina Kendziorski Randall J.Kimple Gopal lyer
机构地区:[1]Department of Human Oncology,University of Wisconsin School of Medicine and Public Health,University of Wisconsin,Madison,WI 53705,USA [2]Department of Biomedical Engineering,University of Wisconsin-Madison,Madison,WI 53705,USA [3]University of Wisconsin Carbone Cancer Center,Madison,WI 53705,USA [4]Department of Biostatistics and Medical Informatics,University of Wisconsin-Madison,Madison,WI 53706,USA [5]Department of Biology,Tufts University,Medford,MA 02155,USA [6]Department of Pathology and Laboratory Medicine,University of Wisconsin School of Medicine and Public Health,University of Wisconsin,Madison,WI 53705,USA
出 处:《Genes & Diseases》2024年第3期140-143,共4页基因与疾病(英文)
基 金:funded in part by Astellas-Pfizer and was supported by the University of Wisconsin School of Medicine and Public Health and the University of Wisconsin Carbone Cancer Center Support Grant P30CA014520 and UW School of Medicine and Public Health(SMPH)and UWCCC grant to Gopal lyer;All lung cell lines except NCl-H3122 were received as research support as part of the ATCC Innovation Challenge.
摘 要:Androgen receptor(AR)is a major transcription factor that plays a role in inflammatory response including interleukin-6(IL6)signaling.1 While AR regulation through paracrine loop signaling in prostate tissue is well-studied,its impact through an IL6 autocrine loop in the lung has not been wellstudied despite the organ's response to respiratory viral infection.Chemical inhibition and RNA knockdown of AR identified a bZIP transcription factor MAF to be a common target of inflammation using these perturbations in lung cells.
关 键 词:INFLAMMATION LUNG RESPIRATORY
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