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10.1080/21541248.2016.1224287 http://scihub22266oqcxt.onion/10.1080/21541248.2016.1224287 C5927483!5927483 !27532209     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27532209 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Small+GTPases 2018 ; 9 (3 ): 274-282 Nephropedia Template TP {{tp|p=27532209 |t=2018. Myc requires RhoA/SRF to reprogram glutamine metabolism |pdf=|usr=}}{{27532209 }} gab.com Text Myc requires RhoA/SRF to reprogram glutamine metabolism JO: Small GTPases http://www.kidney.de/pget.php?&tw=1&pmid=27532209 #FOAvip RhoA regulates actin cytoskeleton but recent evidence suggest a role for this conserved Rho GTPase also in other cellular processes, including transcriptional control of cell proliferation and survival. Interestingy, loss of RhoA is synthetic lethal with oncogenic Myc, a master transcription factor that turns on anabolic metabolism to promote cell growth in many cancers. We show evidence indicating that the synthetic lethal interaction between RhoA loss and Myc arises from deficiency in glutamine utilization, resulting from impaired co-regulation of glutaminase expression and anaplerosis by Myc and RhoA - serum response factor (SRF) pathway. The results suggest metabolic coordination between Myc and RhoA/SRF in sustaining cancer cell viability and indicate RhoA/SRF as a potential vulnerability in cancer cells for therapeutic targeting. Twit Text FOAVip Myc requires RhoA/SRF to reprogram glutamine metabolism ????Small GTPases http://www.kidney.de/pget.php?&tw=1&pmid=27532209 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27532209 #FOAvip English Wikipedia <ref>{{Cite pmid|27532209 }}</ref> Myc requires RhoA/SRF to reprogram glutamine metabolism #MMPMID27532209 Haikala HM ; Marques E ; Turunen M ; Klefström J Small GTPases 2018[May]; 9 (3 ): 274-282 PMID27532209 show ga RhoA regulates actin cytoskeleton but recent evidence suggest a role for this conserved Rho GTPase also in other cellular processes, including transcriptional control of cell proliferation and survival. Interestingy, loss of RhoA is synthetic lethal with oncogenic Myc, a master transcription factor that turns on anabolic metabolism to promote cell growth in many cancers. We show evidence indicating that the synthetic lethal interaction between RhoA loss and Myc arises from deficiency in glutamine utilization, resulting from impaired co-regulation of glutaminase expression and anaplerosis by Myc and RhoA - serum response factor (SRF) pathway. The results suggest metabolic coordination between Myc and RhoA/SRF in sustaining cancer cell viability and indicate RhoA/SRF as a potential vulnerability in cancer cells for therapeutic targeting. |Cell Line, Tumor [MESH] |Glutamine/*metabolism [MESH] |Humans [MESH] |Proto-Oncogene Proteins c-myc/*metabolism [MESH] |Serum Response Factor/*metabolism [MESH]Myc requires RhoA/SRF to reprogram glutamine metabolism (epmc).pdf DeepDyve Pubget Overpricing