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10.1074/jbc.M116.719997 http://scihub22266oqcxt.onion/10.1074/jbc.M116.719997 C4882437!4882437!27072130     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biol+Chem 2016 ; 291 (22): 11689-97 Nephropedia Template TP {{tp|p=27072130|t=2016. Tumor Suppressor Folliculin Regulates mTORC1 through Primary Cilia* |pdf=|usr=}}{{27072130}} gab.com Text Tumor Suppressor Folliculin Regulates mTORC1 through Primary Cilia* JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27072130 #FOAvip Folliculin (FLCN) is the tumor suppressor associated with Birt-Hogg-Dubé (BHD) syndrome that predisposes patients to incident of hamartomas and cysts in multiple organs. Its inactivation causes deregulation in the mammalian target of rapamycin complex 1 (mTORC1) signaling pathway. However, the underlying mechanism is poorly defined. In this study, we show that FLCN is a ciliary protein that functions through primary cilia to regulate mTORC1. In response to flow stress, FLCN associates with LKB1 and recruits the kinase to primary cilia for activation of AMPK resided at basal bodies, which causes mTORC1 down-regulation. In cells depleted of FLCN, LKB1 fails to accumulate in primary cilia and AMPK at the basal bodies remains inactive, thus nullifying the inhibitory effect of flow stress on mTORC1 activity. Our results demonstrate that FLCN is part of a flow sensory mechanism that regulates mTORC1 through primary cilia. Twit Text FOAVip Tumor Suppressor Folliculin Regulates mTORC1 through Primary Cilia* ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27072130 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27072130 #FOAvip English Wikipedia <ref>{{Cite pmid|27072130}}</ref> Tumor Suppressor Folliculin Regulates mTORC1 through Primary Cilia* #MMPMID27072130 Zhong M; Zhao X; Li J; Yuan W; Yan G; Tong M; Guo S; Zhu Y; Jiang Y; Liu Y; Jiang Y J Biol Chem 2016[May]; 291 (22): 11689-97 PMID27072130show ga Folliculin (FLCN) is the tumor suppressor associated with Birt-Hogg-Dubé (BHD) syndrome that predisposes patients to incident of hamartomas and cysts in multiple organs. Its inactivation causes deregulation in the mammalian target of rapamycin complex 1 (mTORC1) signaling pathway. However, the underlying mechanism is poorly defined. In this study, we show that FLCN is a ciliary protein that functions through primary cilia to regulate mTORC1. In response to flow stress, FLCN associates with LKB1 and recruits the kinase to primary cilia for activation of AMPK resided at basal bodies, which causes mTORC1 down-regulation. In cells depleted of FLCN, LKB1 fails to accumulate in primary cilia and AMPK at the basal bodies remains inactive, thus nullifying the inhibitory effect of flow stress on mTORC1 activity. Our results demonstrate that FLCN is part of a flow sensory mechanism that regulates mTORC1 through primary cilia. äTumor Suppressor Folliculin Regulates mTORC1 through Primary Cilia* (epmc).pdf DeepDyve Pubget Overpricing