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10.1152/ajpcell.00022.2015 http://scihub22266oqcxt.onion/10.1152/ajpcell.00022.2015 C4556895!4556895 !26108661     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26108661 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26108661 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Am+J+Physiol+Cell+Physiol 2015 ; 309 (5 ): C296-307 Nephropedia Template TP {{tp|p=26108661 |t=2015. Endothelial cell tumor growth is Ape/ref-1 dependent |pdf=|usr=}}{{26108661 }} gab.com Text Endothelial cell tumor growth is Ape/ref-1 dependent JO: Am J Physiol Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26108661 #FOAvip Tumor-forming endothelial cells have highly elevated levels of Nox-4 that release H2O2 into the nucleus, which is generally not compatible with cell survival. We sought to identify compensatory mechanisms that enable tumor-forming endothelial cells to survive and proliferate under these conditions. Ape-1/ref-1 (Apex-1) is a multifunctional protein that promotes DNA binding of redox-sensitive transcription factors, such as AP-1, and repairs oxidative DNA damage. A validated mouse endothelial cell (EOMA) tumor model was used to demonstrate that Nox-4-derived H2O2 causes DNA oxidation that induces Apex-1 expression. Apex-1 functions as a chaperone to keep transcription factors in a reduced state. In EOMA cells Apex-1 enables AP-1 binding to the monocyte chemoattractant protein-1 (mcp-1) promoter and expression of that protein is required for endothelial cell tumor formation. Intraperitoneal injection of the small molecule inhibitor E3330, which specifically targets Apex-1 redox-sensitive functions, resulted in a 50% decrease in tumor volume compared with mice injected with vehicle control (n = 6 per group), indicating that endothelial cell tumor proliferation is dependent on Apex-1 expression. These are the first reported results to establish Nox-4 induction of Apex-1 as a mechanism promoting endothelial cell tumor formation. Twit Text FOAVip Endothelial cell tumor growth is Ape/ref-1 dependent ????Am J Physiol Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26108661 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26108661 #FOAvip English Wikipedia <ref>{{Cite pmid|26108661 }}</ref> Endothelial cell tumor growth is Ape/ref-1 dependent #MMPMID26108661 Biswas A ; Khanna S ; Roy S ; Pan X ; Sen CK ; Gordillo GM Am J Physiol Cell Physiol 2015[Sep]; 309 (5 ): C296-307 PMID26108661 show ga Tumor-forming endothelial cells have highly elevated levels of Nox-4 that release H2O2 into the nucleus, which is generally not compatible with cell survival. We sought to identify compensatory mechanisms that enable tumor-forming endothelial cells to survive and proliferate under these conditions. Ape-1/ref-1 (Apex-1) is a multifunctional protein that promotes DNA binding of redox-sensitive transcription factors, such as AP-1, and repairs oxidative DNA damage. A validated mouse endothelial cell (EOMA) tumor model was used to demonstrate that Nox-4-derived H2O2 causes DNA oxidation that induces Apex-1 expression. Apex-1 functions as a chaperone to keep transcription factors in a reduced state. In EOMA cells Apex-1 enables AP-1 binding to the monocyte chemoattractant protein-1 (mcp-1) promoter and expression of that protein is required for endothelial cell tumor formation. Intraperitoneal injection of the small molecule inhibitor E3330, which specifically targets Apex-1 redox-sensitive functions, resulted in a 50% decrease in tumor volume compared with mice injected with vehicle control (n = 6 per group), indicating that endothelial cell tumor proliferation is dependent on Apex-1 expression. These are the first reported results to establish Nox-4 induction of Apex-1 as a mechanism promoting endothelial cell tumor formation. |*Cell Proliferation/drug effects [MESH] |Animals [MESH] |Benzoquinones/administration & dosage [MESH] |Cell Survival/drug effects/physiology [MESH] |DNA-(Apurinic or Apyrimidinic Site) Lyase/antagonists & inhibitors/*biosynthesis [MESH] |Endothelial Cells/drug effects/*metabolism/pathology [MESH] |Female [MESH] |Mice [MESH] |Mice, 129 Strain [MESH] |Neoplasms/drug therapy/*metabolism/*pathology [MESH]Endothelial cell tumor growth is Ape/ref-1 dependent (epmc).pdf DeepDyve Pubget Overpricing