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作 者:Xian-Hui Ning Bing Han Ye Peng Shao-Wu Yin
机构地区:[1]College of Marine Science and Engineering,Nanjing Normal University,Nanjing,Jiangsu 210023,China [2]CAS Key Laboratory of Experimental Marine Biology,Center for Ocean Mega-Science,Institute of Oceanology,Chinese Academy of Sciences,Qingdao,Shandong 266071,China [3]Co-Innovation Center for Marine Bio-Industry Technology of Jiangsu Province,Lianyungang,Jiangsu 222005,China
出 处:《Zoological Research》2024年第1期25-35,共11页动物学研究(英文)
基 金:supported by the National Natural Science Foundation of China(42006082);Natural Science Foundation of Jiangsu Province of China(BK20221323);“JBGS”Project of Seed Industry Revitalization in Jiangsu Province(JBGS[2021]034);State Key Laboratory of Developmental Biology of Freshwater Fish(2021KF009)。
摘 要:Long non-coding RNAs(lncRNAs)function as key modulators in mammalian immunity,particularly due to their involvement in lncRNA-mediated competitive endogenous RNA(ceRNA)crosstalk.Despite their recognized significance in mammals,research on lncRNAs in lower vertebrates remains limited.In the present study,we characterized the first immune-related lncRNA(pol-lnc78)in the teleost Japanese flounder(Paralichthys olivaceus).Results indicated that pol-lnc78 acted as a ceRNA for pol-miR-n199-3p to target the sterile alpha and armadillo motif-containing protein(SARM),the fifth discovered member of the Toll/interleukin 1(IL-1)receptor(TIR)adaptor family.This ceRNA network regulated the antibacterial responses of flounder via the Toll-like receptor(TLR)signaling pathway.Specifically,SARM acted as a negative regulator and exacerbated bacterial infection by inhibiting the expression of inflammatory cytokines IL-1βand tumor necrosis factor-α(TNF-α).Pol-miR-n199-3p reduced SARM expression by specifically interacting with the 3’untranslated region(UTR),thereby promoting SARM-dependent inflammatory cytokine expression and protecting the host against bacterial dissemination.Furthermore,pol-lnc78 sponged pol-miR-n199-3p to ameliorate the inhibition of SARM expression.During infection,the negative regulators pol-lnc78 and SARM were significantly down-regulated,while pol-miR-n199-3p was significantly up-regulated,thus favoring host antibacterial defense.These findings provide novel insights into the mechanisms underlying fish immunity and open new horizons to better understand ceRNA crosstalk in lower vertebrates.
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