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作 者:Aikebaier Reheman Xiaojian Cao Yifan Wang Xi Nie Gang Cao Wei Zhou Bing Yang Yingying Lei Weipan Zhang Muhammad Ahsan Naeem Xi Chen
机构地区:[1]State Key Laboratory of Agricultural Microbiology,College of Veterinary Medicine,Huazhong Agricultural University,Wuhan 430070,China [2]College of Animal Science and Technology,Tarim University,Alar 843300,China [3]Bio-Medical Center,Huazhong Agricultural University,Wuhan 430070,China [4]Department of Basic Sciences(Pharmacology),University of Veterinary and Animal Sciences(Narowal Campus),Lahore 54000,Pakistan
出 处:《Animal Diseases》2023年第4期275-285,共11页动物疾病(英文)
基 金:funded by the National Natural Science Foundation of China(Grant No.31602061,U21A20259,31872470);the National Key Research and Development Program of China(Grant No.2021YFD1800401).
摘 要:Mycobacterium tuberculosis(M.tuberculosis)can replicate in the macrophage by interfering with many host protein functions.While it is far from known these host proteins for controlling M.tuberculosis infection.Herein,we infected macrophages including THP-1 and Raw264.7 cells with M.tuberculosis and identified the differentially expressed genes(DEGs)in the interferon signaling pathway.Among them,2'-5'oligoadenylate synthetase-like(OASL)underwent the greatest upregulation in M.tuberculosis-infected macrophages.Knockdown of the expression of OASL attenuated M.tuberculosis survival in macrophages.Further,bioinformatics analysis revealed the potential interaction axis of OASL-TAB3-RvO127,which was further validated by the yeast-two-hybrid(Y2H)assay and Co-IP.This interaction axis might regulate the M.tuberculosis survival and proliferation in macrophages.The study reveals a possible role of OASL during M.tuberculosis infection as a target to control its propagation.
关 键 词:Mycobacterium tuberculosis INTERFERON Interferon stimulated genes OASL
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