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PRMT5 suppresses DR4-mediated CCL20 release via NF-κB pathway

PRMT5 suppresses DR4-mediated CCL20 release via NF-κB pathway
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摘要 Construct expression vectors of pCMV-DR4-HA and pCMV-PRMT5-Flag,and transfect them into HEK293 cells to identify the interaction between TRAIL-R1 and PRMT5 and the molecular mechanism underlying DR4-mediated inhibition of chemokine CCL20 release via TRAIL receptor 1(DR4).Inflammatory cytokine was detected by RT-PCR and ELISA after TRAIL-R1 and/or PRMT5 transfection,respectively.NF-κB activity was detected by Dual Luciferase Reporter Gene Assay.ERK1/2 phosphorylation was analyzed by Western blot.PRMT5 could inhibit DR4-activated NF-κB activity and ERK1/2 phosphorylation.PRMT5 could inhibit NF-κB activition,ERK1/2 phosphorylation as well as CCL20 secretion via binding with DR4 in HEK293 cell,suggesting that PRMT5 may involve in DR4 dependent immune regulation. Construct expression vectors of pCMV-DR4-HA and pCMV-PRMT5-Flag, and transfect them into HEK293 cells to identify the interaction between TRAIL-R1 and PRMT5 and the molecular mechanism underlying DR4-mediated inhibition of chemokine CCL20 release via TRAIL receptor 1 (DR4). Inflammatory cytokine was detected by RT-PCR and ELISA after TRAIL-R1 and/or PRMT5 transfection, respectively. NF-κB activity was detected by Dual Luciferase Reporter Gene Assay. ERK1/2 phosphorylation was analyzed by Western blot. PRMT5 could inhibit DR4-activated NF-κB activity and ERK1/2 phosphorylation. FRMT5 could inhibit NF-κB activition, ERK1/2 phosphorylation as well as CCL20 secretion via binding with DR4 in HEK293 cell, sug- gesting that PRMT5 may involve in DR4 dependent immune regulation.
出处 《Chinese Science Bulletin》 SCIE CAS 2012年第33期4351-4355,共5页
基金 supported by the National Natural Science Foundation of China (81001315 and 30972684) the National Basic Research Program of China (2007CB507404)
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