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dc.contributor.author양철수-
dc.date.accessioned2017-03-07T04:48:23Z-
dc.date.available2017-03-07T04:48:23Z-
dc.date.issued2015-06-
dc.identifier.citationJOURNAL OF IMMUNOLOGY, v. 194, NO 11, Page. 5355-5365en_US
dc.identifier.issn0022-1767-
dc.identifier.issn1550-6606-
dc.identifier.urihttp://www.jimmunol.org/content/194/11/5355-
dc.identifier.urihttp://hdl.handle.net/20.500.11754/25892-
dc.description.abstractMicroRNAs (miRNAs) are small noncoding nucleotides that play critical roles in the regulation of diverse biological functions, including the response of host immune cells. Autophagy plays a key role in activating the antimicrobial host defense against Mycobacterium tuberculosis. Although the pathways associated with autophagy must be tightly regulated at a posttranscriptional level, the contribution of miRNAs and whether they specifically influence the activation of macrophage autophagy during M. tuberculosis infection are largely unknown. In this study, we demonstrate that M. tuberculosis infection of macrophages leads to increased expression of miRNA-125a-3p (miR-125a), which targets UV radiation resistance-associated gene (UVRAG), to inhibit autophagy activation and antimicrobial responses to M. tuberculosis. Forced expression of miR-125a significantly blocked M. tuberculosis-induced activation of autophagy and phagosomal maturation in macrophages, and inhibitors of miR-125a counteracted these effects. Both TLR2 and MyD88 were required for biogenesis of miR-125a during M. tuberculosis infection. Notably, activation of the AMP-activated protein kinase significantly inhibited the expression of miR-125a in M. tuberculosisinfected macrophages. Moreover, either overexpression of miR-125a or silencing of UVRAG significantly attenuated the antimicrobial effects of macrophages against M. tuberculosis. Taken together, these data indicate that miR-125a regulates the innate host defense by inhibiting the activation of autophagy and antimicrobial effects against M. tuberculosis through targeting UVRAG.en_US
dc.description.sponsorshipThis work was supported by National Research Foundation of Korea Grant 2007-0054932 funded by the Korean government (Ministry of Science, ICT and Future Planning) at Chungnam National University and by National Research Foundation of Korea Grant 2011-0027459 funded by the Korean government (Ministry of Education and Science Technology).en_US
dc.language.isoenen_US
dc.publisherAMER ASSOC IMMUNOLOGISTSen_US
dc.subjectPHAGOSOME MATURATIONen_US
dc.subjectDEFENSE-MECHANISMen_US
dc.subjectPROTEIN-KINASEen_US
dc.subjectHOST-DEFENSEen_US
dc.subjectTUBERCULOSISen_US
dc.subjectPATHWAYen_US
dc.subjectIMMUNITYen_US
dc.subjectTARGETSen_US
dc.subjectSYSTEMen_US
dc.subjectCELLSen_US
dc.titleMicroRNA-125a Inhibits Autophagy Activation and Antimicrobial Responses during Mycobacterial Infectionen_US
dc.typeArticleen_US
dc.relation.no11-
dc.relation.volume194-
dc.identifier.doi10.4049/jimmunol.1402557-
dc.relation.page5355-5365-
dc.relation.journalJOURNAL OF IMMUNOLOGY-
dc.contributor.googleauthorKim, Jin Kyung-
dc.contributor.googleauthorYuk, Jae-Min-
dc.contributor.googleauthorKim, Soo Yeon-
dc.contributor.googleauthorKim, Tae Sung-
dc.contributor.googleauthorJin, Hyo Sun-
dc.contributor.googleauthorYang, Chul-Su-
dc.contributor.googleauthorJo, Eun-Kyeong-
dc.relation.code2015003628-
dc.sector.campusS-
dc.sector.daehakGRADUATE SCHOOL[S]-
dc.sector.departmentDEPARTMENT OF BIONANOTECHNOLOGY-
dc.identifier.pidchulsuyang-
Appears in Collections:
GRADUATE SCHOOL[S](대학원) > BIONANOTECHNOLOGY(바이오나노학과) > Articles
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