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10.1038/cddis.2016.14 http://scihub22266oqcxt.onion/10.1038/cddis.2016.14 C4823929!4823929 !27031960     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 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 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\27031960 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell+Death+Dis 2016 ; 7 (3 ): e2163 Nephropedia Template TP {{tp|p=27031960 |t=2016. Renal cell carcinoma escapes death by p53 depletion through transglutaminase 2-chaperoned autophagy |pdf=|usr=}}{{27031960 }} gab.com Text Renal cell carcinoma escapes death by p53 depletion through transglutaminase 2-chaperoned autophagy JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=27031960 #FOAvip In renal cell carcinoma, transglutaminase 2 (TGase 2) crosslinks p53 in autophagosomes, resulting in p53 depletion and the tumor's evasion of apoptosis. Inhibition of TGase 2 stabilizes p53 and induces tumor cells to enter apoptosis. This study explored the mechanism of TGase 2-dependent p53 degradation. We found that TGase 2 competes with human double minute 2 homolog (HDM2) for binding to p53; promotes autophagy-dependent p53 degradation in renal cell carcinoma (RCC) cell lines under starvation; and binds to p53 and p62 simultaneously without ubiquitin-dependent recognition of p62. The bound complex does not have crosslinking activity. A binding assay using a series of deletion mutants of p62, p53 and TGase 2 revealed that the PB1 (Phox and Bem1p-1) domain of p62 (residues 85-110) directly interacts with the ?-barrel domains of TGase 2 (residues 592-687), whereas the HDM2-binding domain (transactivation domain, residues 15-26) of p53 interacts with the N terminus of TGase 2 (residues 1-139). In addition to the increase in p53 stability due to TGase 2 inhibition, the administration of a DNA-damaging anti-cancer drug such as doxorubicin-induced apoptosis in RCC cell lines and synergistically reduced tumor volume in a xenograft model. Combination therapy with a TGase 2 inhibitor and a DNA-damaging agent may represent an effective therapeutic approach for treating RCC. Twit Text FOAVip Renal cell carcinoma escapes death by p53 depletion through transglutaminase 2-chaperoned autophagy ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=27031960 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27031960 #FOAvip English Wikipedia <ref>{{Cite pmid|27031960 }}</ref> Renal cell carcinoma escapes death by p53 depletion through transglutaminase 2-chaperoned autophagy #MMPMID27031960 Kang JH ; Lee JS ; Hong D ; Lee SH ; Kim N ; Lee WK ; Sung TW ; Gong YD ; Kim SY Cell Death Dis 2016[Mar]; 7 (3 ): e2163 PMID27031960 show ga In renal cell carcinoma, transglutaminase 2 (TGase 2) crosslinks p53 in autophagosomes, resulting in p53 depletion and the tumor's evasion of apoptosis. Inhibition of TGase 2 stabilizes p53 and induces tumor cells to enter apoptosis. This study explored the mechanism of TGase 2-dependent p53 degradation. We found that TGase 2 competes with human double minute 2 homolog (HDM2) for binding to p53; promotes autophagy-dependent p53 degradation in renal cell carcinoma (RCC) cell lines under starvation; and binds to p53 and p62 simultaneously without ubiquitin-dependent recognition of p62. The bound complex does not have crosslinking activity. A binding assay using a series of deletion mutants of p62, p53 and TGase 2 revealed that the PB1 (Phox and Bem1p-1) domain of p62 (residues 85-110) directly interacts with the ?-barrel domains of TGase 2 (residues 592-687), whereas the HDM2-binding domain (transactivation domain, residues 15-26) of p53 interacts with the N terminus of TGase 2 (residues 1-139). In addition to the increase in p53 stability due to TGase 2 inhibition, the administration of a DNA-damaging anti-cancer drug such as doxorubicin-induced apoptosis in RCC cell lines and synergistically reduced tumor volume in a xenograft model. Combination therapy with a TGase 2 inhibitor and a DNA-damaging agent may represent an effective therapeutic approach for treating RCC. |*Apoptosis/drug effects [MESH] |Animals [MESH] |Antibiotics, Antineoplastic/pharmacology/therapeutic use [MESH] |Autophagy/drug effects [MESH] |Carcinoma, Renal Cell/drug therapy/metabolism/pathology [MESH] |Cell Line, Tumor [MESH] |Chloroquine/pharmacology [MESH] |DNA Damage/drug effects [MESH] |Doxorubicin/pharmacology/therapeutic use [MESH] |Female [MESH] |GTP-Binding Proteins/antagonists & inhibitors/genetics/*metabolism [MESH] |Humans [MESH] |Kidney Neoplasms/drug therapy/metabolism/pathology [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mice, Nude [MESH] |Phosphorylation/drug effects [MESH] |Protein Binding [MESH] |Protein Glutamine gamma Glutamyltransferase 2 [MESH] |Proto-Oncogene Proteins c-mdm2/antagonists & inhibitors/genetics/metabolism [MESH] |Pyrazines/pharmacology/therapeutic use [MESH] |RNA-Binding Proteins/chemistry/metabolism [MESH] |Transglutaminases/antagonists & inhibitors/genetics/*metabolism [MESH]Renal cell carcinoma escapes death by p53 depletion through transgluta(epmc).pdf DeepDyve Pubget Overpricing