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10.18632/oncotarget.12866 http://scihub22266oqcxt.onion/10.18632/oncotarget.12866 C5363637!5363637!27793001     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2016 ; 7 (47): 77978-86 Nephropedia Template TP {{tp|p=27793001|t=2016. miR-135b-5p inhibits LPS-induced TNF? production via silencing AMPK phosphatase Ppm1e |pdf=|usr=}}{{27793001}} gab.com Text miR-135b-5p inhibits LPS-induced TNF production via silencing AMPK phosphatase Ppm1e JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27793001 #FOAvip AMPK activation in monocytes could suppress lipopolysaccharide (LPS)-induced tissue-damaging TNFa production. We are set to provoke AMPK activation via microRNA (?miRNA?) downregulating its phosphatase Ppm1e. In human U937 and THP-1 monocytes, forced expression of microRNA-135b-5p (?miR-135b-5p?) downregulated Ppm1e and activated AMPK signaling. Further, LPS-induced TNF? production in above cells was dramatically attenuated. Ppm1e shRNA knockdown in U937 cells also activated AMPK and inhibited TNF? production by LPS. AMPK activation is required for miR-135b-induced actions in monocytes, AMPK? shRNA knockdown or T172A dominant negative mutation almost abolished miR-135b-5p's suppression on LPS-induced TNF? production. Significantly, miR-135b-5p inhibited LPS-induced reactive oxygen species (ROS) production, NF?B activation and TNF? mRNA expression in human macrophages. AMPK? knockdown or mutation again abolished above actions by miR-135b-5p. We conclude that miR-135b-5p expression downregulates Ppm1e to activate AMPK signaling, which inhibits LPS-induced TNF? production via suppressing ROS production and NF?B activation. Twit Text FOAVip miR-135b-5p inhibits LPS-induced TNF production via silencing AMPK phosphatase Ppm1e ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27793001 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27793001 #FOAvip English Wikipedia <ref>{{Cite pmid|27793001}}</ref> miR-135b-5p inhibits LPS-induced TNF? production via silencing AMPK phosphatase Ppm1e #MMPMID27793001 Li P; Fan Jb; Gao Y; Zhang M; Zhang L; Yang N; Zhao X Oncotarget 2016[Nov]; 7 (47): 77978-86 PMID27793001show ga AMPK activation in monocytes could suppress lipopolysaccharide (LPS)-induced tissue-damaging TNFa production. We are set to provoke AMPK activation via microRNA (?miRNA?) downregulating its phosphatase Ppm1e. In human U937 and THP-1 monocytes, forced expression of microRNA-135b-5p (?miR-135b-5p?) downregulated Ppm1e and activated AMPK signaling. Further, LPS-induced TNF? production in above cells was dramatically attenuated. Ppm1e shRNA knockdown in U937 cells also activated AMPK and inhibited TNF? production by LPS. AMPK activation is required for miR-135b-induced actions in monocytes, AMPK? shRNA knockdown or T172A dominant negative mutation almost abolished miR-135b-5p's suppression on LPS-induced TNF? production. Significantly, miR-135b-5p inhibited LPS-induced reactive oxygen species (ROS) production, NF?B activation and TNF? mRNA expression in human macrophages. AMPK? knockdown or mutation again abolished above actions by miR-135b-5p. We conclude that miR-135b-5p expression downregulates Ppm1e to activate AMPK signaling, which inhibits LPS-induced TNF? production via suppressing ROS production and NF?B activation. ämiR-135b-5p inhibits LPS-induced TNF? production via silencing AMPK ph(epmc).pdf DeepDyve Pubget Overpricing