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10.1172/JCI89935 http://scihub22266oqcxt.onion/10.1172/JCI89935 C5490751!5490751!28530645     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest ä ; 127 (7): 2555-68 Nephropedia Template TP {{tp|p=28530645|t=ä. MYC-dependent oxidative metabolism regulates osteoclastogenesis via nuclear receptor ERR? |pdf=|usr=}}{{28530645}} gab.com Text MYC-dependent oxidative metabolism regulates osteoclastogenesis via nuclear receptor ERR JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28530645 #FOAvip Osteoporosis is a metabolic bone disorder associated with compromised bone strength and an increased risk of fracture. Inhibition of the differentiation of bone-resorbing osteoclasts is an effective strategy for the treatment of osteoporosis. Prior work by our laboratory and others has shown that MYC promotes osteoclastogenesis in vitro, but the underlying mechanisms are not well understood. In addition, the in vivo importance of osteoclast-expressed MYC in physiological and pathological bone loss is not known. Here, we have demonstrated that deletion of Myc in osteoclasts increases bone mass and protects mice from ovariectomy-induced (OVX-induced) osteoporosis. Transcriptomic analysis revealed that MYC drives metabolic reprogramming during osteoclast differentiation and functions as a metabolic switch to an oxidative state. We identified a role for MYC action in the transcriptional induction of estrogen receptor?related receptor ? (ERR?), a nuclear receptor that cooperates with the transcription factor nuclear factor of activated T cells, c1 (NFATc1) to drive osteoclastogenesis. Accordingly, pharmacological inhibition of ERR? attenuated OVX-induced bone loss in mice. Our findings highlight a MYC/ERR? pathway that contributes to physiological and pathological bone loss by integrating the MYC/ERR? axis to drive metabolic reprogramming during osteoclast differentiation. Twit Text FOAVip MYC-dependent oxidative metabolism regulates osteoclastogenesis via nuclear receptor ERR ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28530645 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28530645 #FOAvip English Wikipedia <ref>{{Cite pmid|28530645}}</ref> MYC-dependent oxidative metabolism regulates osteoclastogenesis via nuclear receptor ERR? #MMPMID28530645 Bae S; Lee MJ; Mun SH; Giannopoulou EG; Yong-Gonzalez V; Cross JR; Murata K; Gigučre V; van der Meulen M; Park-Min KH J Clin Invest ä[]; 127 (7): 2555-68 PMID28530645show ga Osteoporosis is a metabolic bone disorder associated with compromised bone strength and an increased risk of fracture. Inhibition of the differentiation of bone-resorbing osteoclasts is an effective strategy for the treatment of osteoporosis. Prior work by our laboratory and others has shown that MYC promotes osteoclastogenesis in vitro, but the underlying mechanisms are not well understood. In addition, the in vivo importance of osteoclast-expressed MYC in physiological and pathological bone loss is not known. Here, we have demonstrated that deletion of Myc in osteoclasts increases bone mass and protects mice from ovariectomy-induced (OVX-induced) osteoporosis. Transcriptomic analysis revealed that MYC drives metabolic reprogramming during osteoclast differentiation and functions as a metabolic switch to an oxidative state. We identified a role for MYC action in the transcriptional induction of estrogen receptor?related receptor ? (ERR?), a nuclear receptor that cooperates with the transcription factor nuclear factor of activated T cells, c1 (NFATc1) to drive osteoclastogenesis. Accordingly, pharmacological inhibition of ERR? attenuated OVX-induced bone loss in mice. Our findings highlight a MYC/ERR? pathway that contributes to physiological and pathological bone loss by integrating the MYC/ERR? axis to drive metabolic reprogramming during osteoclast differentiation. äMYC-dependent oxidative metabolism regulates osteoclastogenesis via nu(epmc).pdf DeepDyve Pubget Overpricing