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10.1073/pnas.1711477115 http://scihub22266oqcxt.onion/10.1073/pnas.1711477115 C5798328!5798328!29339491     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Proc+Natl+Acad+Sci+U+S+A 2018 ; 115 (5): 1015-20 Nephropedia Template TP {{tp|p=29339491|t=2018. Kinase-independent function of E-type cyclins in liver cancer |pdf=|usr=}}{{29339491}} gab.com Text Kinase-independent function of E-type cyclins in liver cancer JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=29339491 #FOAvip Amplification of the cyclin E genes and overexpression of cyclin E proteins is very frequent in several human tumor types. In particular, overexpression of E cyclins was implicated in the pathogenesis of liver cancers. According to the current cell division models, E cyclins drive tumor cell proliferation by activating its kinase partner, the cyclin-dependent kinase 2 (CDK2). In this study, we demonstrate that E cyclins are dispensable for adult mouse physiology, but essential for liver cancer progression. Surprisingly, we found that the function of E cyclins in liver tumorigenesis is kinase independent. Our study suggests that agents targeting E cyclins would be efficacious in liver cancer treatment, as they would halt proliferation of tumor cells while sparing normal tissues. Twit Text FOAVip Kinase-independent function of E-type cyclins in liver cancer ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=29339491 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29339491 #FOAvip English Wikipedia <ref>{{Cite pmid|29339491}}</ref> Kinase-independent function of E-type cyclins in liver cancer #MMPMID29339491 Geng Y; Michowski W; Chick JM; Wang YE; Jecrois ME; Sweeney KE; Liu L; Han RC; Ke N; Zagozdzon A; Sicinska E; Bronson RT; Gygi SP; Sicinski P Proc Natl Acad Sci U S A 2018[Jan]; 115 (5): 1015-20 PMID29339491show ga Amplification of the cyclin E genes and overexpression of cyclin E proteins is very frequent in several human tumor types. In particular, overexpression of E cyclins was implicated in the pathogenesis of liver cancers. According to the current cell division models, E cyclins drive tumor cell proliferation by activating its kinase partner, the cyclin-dependent kinase 2 (CDK2). In this study, we demonstrate that E cyclins are dispensable for adult mouse physiology, but essential for liver cancer progression. Surprisingly, we found that the function of E cyclins in liver tumorigenesis is kinase independent. Our study suggests that agents targeting E cyclins would be efficacious in liver cancer treatment, as they would halt proliferation of tumor cells while sparing normal tissues. äKinase-independent function of E-type cyclins in liver cancer (epmc).pdf DeepDyve Pubget Overpricing