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10.1007/s11060-013-1112-8 http://scihub22266oqcxt.onion/10.1007/s11060-013-1112-8 C3679321!3679321!23525947     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Neurooncol 2013 ; 113 (2): 195-205 Nephropedia Template TP {{tp|p=23525947|t=2013. Mutant Tristetraprolin: a Potent Inhibitor of Malignant Glioma Cell Growth |pdf=|usr=}}{{23525947}} gab.com Text Mutant Tristetraprolin: a Potent Inhibitor of Malignant Glioma Cell Growth JO: J Neurooncol http://www.kidney.de/pget.php?&tw=1&pmid=23525947 #FOAvip Malignant gliomas rely on the production of certain critical growth factors including VEGF, interleukin (IL)-6 and IL-8, to fuel rapid tumor growth, angiogenesis, and treatment resistance. Post-transcriptional regulation through adenine and uridine-rich elements (ARE) of the 3? untranslated region (UTR) is one mechanism for upregulating these and other growth factors. In glioma cells, we have shown that the post-transcriptional machinery is optimized for growth factor upregulation secondary to overexpression of the mRNA stabilizer, HuR. The negative regulator, tristetraprolin (TTP), on the other hand, may be suppressed because of extensive phosphorylation. Here we test that possibility by analyzing the phenotypic effects of a mutated form of TTP (mt-TTP) in which 8 phosphoserine residues were converted to alanines. We observed a significantly enhanced negative effect on growth factor expression in glioma cells at the post-transcriptional and transcriptional levels. The protein became stabilized and displayed significantly increased antiproliferative effects compared to wild-type TTP. Macroautophagy was induced with both forms of TTP, but inhibition of autophagy did not affect cell viability. We conclude that glioma cells suppress TTP function through phosphorylation of critical serine residues which in turn contributes to growth factor upregulation and tumor progression. Twit Text FOAVip Mutant Tristetraprolin: a Potent Inhibitor of Malignant Glioma Cell Growth ????J Neurooncol http://www.kidney.de/pget.php?&tw=1&pmid=23525947 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23525947 #FOAvip English Wikipedia <ref>{{Cite pmid|23525947}}</ref> Mutant Tristetraprolin: a Potent Inhibitor of Malignant Glioma Cell Growth #MMPMID23525947 Suswam EA; Shacka JJ; Walker K; Lu L; Li X; Si Y; Zhang X; Zheng L; Nabors LB; Cao H; King PH J Neurooncol 2013[Jun]; 113 (2): 195-205 PMID23525947show ga Malignant gliomas rely on the production of certain critical growth factors including VEGF, interleukin (IL)-6 and IL-8, to fuel rapid tumor growth, angiogenesis, and treatment resistance. Post-transcriptional regulation through adenine and uridine-rich elements (ARE) of the 3? untranslated region (UTR) is one mechanism for upregulating these and other growth factors. In glioma cells, we have shown that the post-transcriptional machinery is optimized for growth factor upregulation secondary to overexpression of the mRNA stabilizer, HuR. The negative regulator, tristetraprolin (TTP), on the other hand, may be suppressed because of extensive phosphorylation. Here we test that possibility by analyzing the phenotypic effects of a mutated form of TTP (mt-TTP) in which 8 phosphoserine residues were converted to alanines. We observed a significantly enhanced negative effect on growth factor expression in glioma cells at the post-transcriptional and transcriptional levels. The protein became stabilized and displayed significantly increased antiproliferative effects compared to wild-type TTP. Macroautophagy was induced with both forms of TTP, but inhibition of autophagy did not affect cell viability. We conclude that glioma cells suppress TTP function through phosphorylation of critical serine residues which in turn contributes to growth factor upregulation and tumor progression. äMutant Tristetraprolin: a Potent Inhibitor of Malignant Glioma Cell Gr(epmc).pdf DeepDyve Pubget Overpricing