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10.1158/0008-5472.CAN-15-2391 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-15-2391 C5026615!5026615!27440725     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Res 2016 ; 76 (18): 5337-47 Nephropedia Template TP {{tp|p=27440725|t=2016. Jak1-STAT3 signals are essential effectors of the USP6/TRE17 oncogene in tumorigenesis |pdf=|usr=}}{{27440725}} gab.com Text Jak1-STAT3 signals are essential effectors of the USP6/TRE17 oncogene in tumorigenesis JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27440725 #FOAvip Bone and soft tissue tumors are relatively poorly understood, hampering the development of effective therapies. Here we report a critical effector pathway for the ubiquitin-specific protease 6(USP6)/TRE17, which is overexpressed upon chromosome translation in various human tumors, including aneurysmal bone cyst and the related benign lesion nodular fasciitis. Ectopic expression of USP6 is known to drive formation of tumors which recapitulate key features of ABC and NF, however, the identity of USP6's relevant substrates has been obscure. Here we report that the Jak1-STAT3 signaling pathway serves as an essential effector of USP6 in BSTT formation. We found that USP6 directly de-ubiquitinated Jak1, leading to its stabilization and activation of STAT3. The tumorigenic potential of USP6 was attenuated significantly by CRISPR-mediated deletion of Jak1 or STAT3, or by administration of a Jak family inhibitor. Analysis of primary clinical samples of NF confirmed the activation of a Jak1-STAT3 gene signature in vivo. Together, our studies highlight Jak1 as the first identified substrate for USP6, and they offer a mechanistic rationale for the clinical investigation of Jak and STAT3 inhibitors as therapeutics for the treatment of bone and soft tissue tumors along with other neoplasms driven by USP6 overexpression. Twit Text FOAVip Jak1-STAT3 signals are essential effectors of the USP6/TRE17 oncogene in tumorigenesis ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27440725 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27440725 #FOAvip English Wikipedia <ref>{{Cite pmid|27440725}}</ref> Jak1-STAT3 signals are essential effectors of the USP6/TRE17 oncogene in tumorigenesis #MMPMID27440725 Quick L; Young R; Henrich IC; Wang X; Asmann YW; Oliveira AM; Chou MM Cancer Res 2016[Sep]; 76 (18): 5337-47 PMID27440725show ga Bone and soft tissue tumors are relatively poorly understood, hampering the development of effective therapies. Here we report a critical effector pathway for the ubiquitin-specific protease 6(USP6)/TRE17, which is overexpressed upon chromosome translation in various human tumors, including aneurysmal bone cyst and the related benign lesion nodular fasciitis. Ectopic expression of USP6 is known to drive formation of tumors which recapitulate key features of ABC and NF, however, the identity of USP6's relevant substrates has been obscure. Here we report that the Jak1-STAT3 signaling pathway serves as an essential effector of USP6 in BSTT formation. We found that USP6 directly de-ubiquitinated Jak1, leading to its stabilization and activation of STAT3. The tumorigenic potential of USP6 was attenuated significantly by CRISPR-mediated deletion of Jak1 or STAT3, or by administration of a Jak family inhibitor. Analysis of primary clinical samples of NF confirmed the activation of a Jak1-STAT3 gene signature in vivo. Together, our studies highlight Jak1 as the first identified substrate for USP6, and they offer a mechanistic rationale for the clinical investigation of Jak and STAT3 inhibitors as therapeutics for the treatment of bone and soft tissue tumors along with other neoplasms driven by USP6 overexpression. äJak1-STAT3 signals are essential effectors of the USP6/TRE17 oncogene (epmc).pdf DeepDyve Pubget Overpricing