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10.1158/1535-7163.MCT-15-0017 http://scihub22266oqcxt.onion/10.1158/1535-7163.MCT-15-0017 C4560959!4560959!26141949     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cancer+Ther 2015 ; 14 (9): 2090-102 Nephropedia Template TP {{tp|p=26141949|t=2015. CDK1-mediated SIRT3 Activation Enhances Mitochondrial Function and Tumor Radioresistance |pdf=|usr=}}{{26141949}} gab.com Text CDK1-mediated SIRT3 Activation Enhances Mitochondrial Function and Tumor Radioresistance JO: Mol Cancer Ther http://www.kidney.de/pget.php?&tw=1&pmid=26141949 #FOAvip The tumor adaptive resistance to therapeutic radiation remains to be a barrier for further improvement of local cancer control. SIRT3, a member of the sirtuin family of NAD+-dependent protein deacetylases in mitochondria, promotes metabolic homeostasis through regulation of mitochondrial protein deacetylation and plays a key role in prevention of cell aging. Here, we demonstrate that SIRT3 expression is induced in an array of radiation-treated human tumor cells and their corresponding xenograft tumors including colon cancer HCT-116, glioblastoma U87 and breast cancer MDA-MB231 cells. The SIRT3 transcriptional activation is due to SIRT3 promoter activation controlled by the stress transcription factor NF-?B. Post-transcriptionally, the SIRT3 enzymatic activity is further enhanced via Thr150/Ser159 phosphorylation by Cyclin B1/CDK1, which is also induced by radiation and relocated to mitochondria together with SIRT3. Cells expressing the Thr150Ala/Ser159Ala mutant SIRT3 show a reduction in the mitochondrial protein lysine deacetylation, ??m, MnSOD activity and mitochondrial ATP generation. The clonogenicity of Thr150Ala/Ser159Ala mutant transfectants is lower and significantly decreased under radiation. Tumors harboring the Thr150Ala/Ser159Ala mutant SIRT3 show inhibited growth and sensitivity to in vivo local irradiation. These results demonstrate that enhanced SIRT3 transcription and post-translational modifications in mitochondria contribute to the adaptive radioresistance in tumor cells. The CDK1-mediated SIRT3 phosphorylation is a potential effective target to sensitize tumor cells to radiotherapy. Twit Text FOAVip CDK1-mediated SIRT3 Activation Enhances Mitochondrial Function and Tumor Radioresistance ????Mol Cancer Ther http://www.kidney.de/pget.php?&tw=1&pmid=26141949 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26141949 #FOAvip English Wikipedia <ref>{{Cite pmid|26141949}}</ref> CDK1-mediated SIRT3 Activation Enhances Mitochondrial Function and Tumor Radioresistance #MMPMID26141949 Liu R; Fan M; Candas D; Qin L; Zhang X; Eldridge A; Zou JX; Zhang T; Juma S; Jin C; Li RF; Perks J; Sun LQ; Vaughan AT; Hai CX; Gius DR; Li JJ Mol Cancer Ther 2015[Sep]; 14 (9): 2090-102 PMID26141949show ga The tumor adaptive resistance to therapeutic radiation remains to be a barrier for further improvement of local cancer control. SIRT3, a member of the sirtuin family of NAD+-dependent protein deacetylases in mitochondria, promotes metabolic homeostasis through regulation of mitochondrial protein deacetylation and plays a key role in prevention of cell aging. Here, we demonstrate that SIRT3 expression is induced in an array of radiation-treated human tumor cells and their corresponding xenograft tumors including colon cancer HCT-116, glioblastoma U87 and breast cancer MDA-MB231 cells. The SIRT3 transcriptional activation is due to SIRT3 promoter activation controlled by the stress transcription factor NF-?B. Post-transcriptionally, the SIRT3 enzymatic activity is further enhanced via Thr150/Ser159 phosphorylation by Cyclin B1/CDK1, which is also induced by radiation and relocated to mitochondria together with SIRT3. Cells expressing the Thr150Ala/Ser159Ala mutant SIRT3 show a reduction in the mitochondrial protein lysine deacetylation, ??m, MnSOD activity and mitochondrial ATP generation. The clonogenicity of Thr150Ala/Ser159Ala mutant transfectants is lower and significantly decreased under radiation. Tumors harboring the Thr150Ala/Ser159Ala mutant SIRT3 show inhibited growth and sensitivity to in vivo local irradiation. These results demonstrate that enhanced SIRT3 transcription and post-translational modifications in mitochondria contribute to the adaptive radioresistance in tumor cells. The CDK1-mediated SIRT3 phosphorylation is a potential effective target to sensitize tumor cells to radiotherapy. äCDK1-mediated SIRT3 Activation Enhances Mitochondrial Function and Tum(epmc).pdf DeepDyve Pubget Overpricing