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10.1126/science.aah6893 http://scihub22266oqcxt.onion/10.1126/science.aah6893 C5485411!5485411!28336670     free     free     free Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Science 2017 ; 355 (6331): 1324-30 Nephropedia Template TP {{tp|p=28336670|t=2017. PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D |pdf=|usr=}}{{28336670}} gab.com Text PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D JO: Science http://www.kidney.de/pget.php?&tw=1&pmid=28336670 #FOAvip Activating mutations in PIK3CA, the gene encoding phosphoinositide-(3)-kinase ? (PI3K?), are frequently found in estrogen receptor (ER)?positive breast cancer. PI3K? inhibitors, now in late-stage clinical development, elicit a robust compensatory increase in ER-dependent transcription that limits therapeutic efficacy. We investigated the chromatin-based mechanisms leading to the activation of ER upon PI3K? inhibition. We found that PI3K? inhibition mediates an open chromatin state at the ER target loci in breast cancer models and clinical samples. KMT2D, a histone H3 lysine 4 methyltransferase, is required for FOXA1, PBX1, and ER recruitment and activation. AKT binds and phosphorylates KMT2D, attenuating methyltransferase activity and ER function, whereas PI3K? inhibition enhances KMT2D activity. These findings uncover a mechanism that controls the activation of ER by the posttranslational modification of epigenetic regulators, providing a rationale for epigenetic therapy in ER-positive breast cancer. Twit Text FOAVip PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D ????Science http://www.kidney.de/pget.php?&tw=1&pmid=28336670 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28336670 #FOAvip English Wikipedia <ref>{{Cite pmid|28336670}}</ref> PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D #MMPMID28336670 Toska E; Osmanbeyoglu HU; Castel P; Chan C; Hendrickson RC; Elkabets M; Dickler MN; Scaltriti M; Leslie CS; Armstrong SA; Baselga J Science 2017[Mar]; 355 (6331): 1324-30 PMID28336670show ga Activating mutations in PIK3CA, the gene encoding phosphoinositide-(3)-kinase ? (PI3K?), are frequently found in estrogen receptor (ER)?positive breast cancer. PI3K? inhibitors, now in late-stage clinical development, elicit a robust compensatory increase in ER-dependent transcription that limits therapeutic efficacy. We investigated the chromatin-based mechanisms leading to the activation of ER upon PI3K? inhibition. We found that PI3K? inhibition mediates an open chromatin state at the ER target loci in breast cancer models and clinical samples. KMT2D, a histone H3 lysine 4 methyltransferase, is required for FOXA1, PBX1, and ER recruitment and activation. AKT binds and phosphorylates KMT2D, attenuating methyltransferase activity and ER function, whereas PI3K? inhibition enhances KMT2D activity. These findings uncover a mechanism that controls the activation of ER by the posttranslational modification of epigenetic regulators, providing a rationale for epigenetic therapy in ER-positive breast cancer. äPI3K pathway regulates ER-dependent transcription in breast cancer thr(epmc).pdf DeepDyve Pubget Overpricing