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10.1038/onc.2017.394 http://scihub22266oqcxt.onion/10.1038/onc.2017.394 C5815498!5815498!29106388     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29106388.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Oncogene 2018 ; 37 (8): 982-92 Nephropedia Template TP {{tp|p=29106388|t=2018. Calcium signalling links MYC to NUAK1 |pdf=|usr=}}{{29106388}} gab.com Text Calcium signalling links MYC to NUAK1 JO: Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=29106388 #FOAvip NUAK1 is a member of the AMPK-related family of kinases. Recent evidence suggests that NUAK1 is an important regulator of cell adhesion and migration, cellular and organismal metabolism, and regulation of TAU stability. As such, NUAK1 may play key roles in multiple diseases ranging from neurodegeneration to diabetes and metastatic cancer. Previous work revealed a crucial role for NUAK1 in supporting viability of tumour cells specifically when MYC is overexpressed. This role is surprising, given that NUAK1 is activated by the tumour suppressor LKB1. Here we show that, in tumour cells lacking LKB1, NUAK1 activity is maintained by an alternative pathway involving calcium-dependent activation of PKC?. Calcium/PKC?-dependent activation of NUAK1 supports engagement of the AMPK-TORC1 metabolic checkpoint, thereby protecting tumour cells from MYC-driven cell death, and indeed, MYC selects for this pathway in part via transcriptional regulation of PKC? and ITPR. Our data point to a novel role for calcium in supporting tumour cell viability and clarify the synthetic lethal interaction between NUAK1 and MYC. Twit Text FOAVip Calcium signalling links MYC to NUAK1 ????Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=29106388 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29106388 #FOAvip English Wikipedia <ref>{{Cite pmid|29106388}}</ref> Calcium signalling links MYC to NUAK1 #MMPMID29106388 Monteverde T; Tait-Mulder J; Hedley A; Knight JR; Sansom OJ; Murphy DJ Oncogene 2018[Feb]; 37 (8): 982-92 PMID29106388show ga NUAK1 is a member of the AMPK-related family of kinases. Recent evidence suggests that NUAK1 is an important regulator of cell adhesion and migration, cellular and organismal metabolism, and regulation of TAU stability. As such, NUAK1 may play key roles in multiple diseases ranging from neurodegeneration to diabetes and metastatic cancer. Previous work revealed a crucial role for NUAK1 in supporting viability of tumour cells specifically when MYC is overexpressed. This role is surprising, given that NUAK1 is activated by the tumour suppressor LKB1. Here we show that, in tumour cells lacking LKB1, NUAK1 activity is maintained by an alternative pathway involving calcium-dependent activation of PKC?. Calcium/PKC?-dependent activation of NUAK1 supports engagement of the AMPK-TORC1 metabolic checkpoint, thereby protecting tumour cells from MYC-driven cell death, and indeed, MYC selects for this pathway in part via transcriptional regulation of PKC? and ITPR. Our data point to a novel role for calcium in supporting tumour cell viability and clarify the synthetic lethal interaction between NUAK1 and MYC. äCalcium signalling links MYC to NUAK1 (epmc).pdf DeepDyve Pubget Overpricing