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10.15252/emmm.201607180 http://scihub22266oqcxt.onion/10.15252/emmm.201607180 C5577530!5577530!28539478     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28539478&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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+Mol+Med 2017 ; 9 (7): 933-49 Nephropedia Template TP {{tp|p=28539478|t=2017. A novel epigenetic AML1?ETO/THAP10/miR?383 mini?circuitry contributes to t(8;21) leukaemogenesis |pdf=|usr=}}{{28539478}} gab.com Text A novel epigenetic AML1 ETO/THAP10/miR 383 mini circuitry contributes to t(8;21) leukaemogenesis JO: EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=28539478 #FOAvip DNA methylation patterns are frequently deregulated in t(8;21) acute myeloid leukaemia (AML), but little is known of the mechanisms by which specific gene sets become aberrantly methylated. Here, we found that the promoter DNA methylation signature of t(8;21)+ AML blasts differs from that of t(8;21)? AMLs. This study demonstrated that a novel hypermethylated zinc finger?containing protein, THAP10, is a target gene and can be epigenetically suppressed by AML1?ETO at the transcriptional level in t(8;21) AML. Our findings also show that THAP10 is a bona fide target of miR?383 that can be epigenetically activated by the AML1?ETO recruiting co?activator p300. In this study, we demonstrated that epigenetic suppression of THAP10 is the mechanistic link between AML1?ETO fusion proteins and tyrosine kinase cascades. In addition, we showed that THAP10 is a nuclear protein that inhibits myeloid proliferation and promotes differentiation both in vitro and in vivo. Altogether, our results revealed an unexpected and important epigenetic mini?circuit of AML1?ETO/THAP10/miR?383 in t(8;21) AML, in which epigenetic suppression of THAP10 predicts a poor clinical outcome and represents a novel therapeutic target. Twit Text FOAVip A novel epigenetic AML1 ETO/THAP10/miR 383 mini circuitry contributes to t(8;21) leukaemogenesis ????EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=28539478 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28539478 #FOAvip English Wikipedia <ref>{{Cite pmid|28539478}}</ref> A novel epigenetic AML1?ETO/THAP10/miR?383 mini?circuitry contributes to t(8;21) leukaemogenesis #MMPMID28539478 Li Y; Ning Q; Shi J; Chen Y; Jiang M; Gao L; Huang W; Jing Y; Huang S; Liu A; Hu Z; Liu D; Wang L; Nervi C; Dai Y; Zhang MQ; Yu L EMBO Mol Med 2017[Jul]; 9 (7): 933-49 PMID28539478show ga DNA methylation patterns are frequently deregulated in t(8;21) acute myeloid leukaemia (AML), but little is known of the mechanisms by which specific gene sets become aberrantly methylated. Here, we found that the promoter DNA methylation signature of t(8;21)+ AML blasts differs from that of t(8;21)? AMLs. This study demonstrated that a novel hypermethylated zinc finger?containing protein, THAP10, is a target gene and can be epigenetically suppressed by AML1?ETO at the transcriptional level in t(8;21) AML. Our findings also show that THAP10 is a bona fide target of miR?383 that can be epigenetically activated by the AML1?ETO recruiting co?activator p300. In this study, we demonstrated that epigenetic suppression of THAP10 is the mechanistic link between AML1?ETO fusion proteins and tyrosine kinase cascades. In addition, we showed that THAP10 is a nuclear protein that inhibits myeloid proliferation and promotes differentiation both in vitro and in vivo. Altogether, our results revealed an unexpected and important epigenetic mini?circuit of AML1?ETO/THAP10/miR?383 in t(8;21) AML, in which epigenetic suppression of THAP10 predicts a poor clinical outcome and represents a novel therapeutic target. äA novel epigenetic AML1?ETO/THAP10/miR?383 mini?circuitry contributes (epmc).pdf DeepDyve Pubget Overpricing