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10.1038/s41598-017-11806-9 http://scihub22266oqcxt.onion/10.1038/s41598-017-11806-9 C5603518!5603518!28924147     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2017 ; 7 (ä): ä Nephropedia Template TP {{tp|p=28924147|t=2017. Tumor suppression via inhibition of SWI/SNF complex-dependent NF-?B activation |pdf=|usr=}}{{28924147}} gab.com Text Tumor suppression via inhibition of SWI/SNF complex-dependent NF- B activation JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28924147 #FOAvip The transcription factor NF-?B is constitutively activated in many epithelial tumors but few NF-?B inhibitors are suitable for cancer therapy because of its broad biological effects. We previously reported that the d4-family proteins (DPF1, DPF2, DPF3a/b) function as adaptor proteins linking NF-?B with the SWI/SNF complex. Here, using epithelial tumor cell lines, A549 and HeLaS3, we demonstrate that exogenous expression of the highly-conserved N-terminal 84-amino acid region (designated ?CT1?) of either DPF2 or DPF3a/b has stronger inhibitory effects on anchorage-independent growth than the single knockdown of any d4-family protein. This indicates that CT1 can function as an efficient dominant-negative mutant of the entire d4-family proteins. By in situ proximity ligation assay, CT1 was found to retain full adaptor function, indicating that the C-terminal region of d4-family proteins lacking in CT1 would include essential domains for SWI/SNF-dependent NF-?B activation. Microarray analysis revealed that CT1 suppresses only a portion of the NF-?B target genes, including representative SWI/SNF-dependent genes. Among these genes, IL6 was shown to strongly contribute to anchorage-independent growth. Finally, exogenous CT1 expression efficiently suppressed tumor formation in a mouse xenograft model, suggesting that the d4-family proteins are promising cancer therapy targets. Twit Text FOAVip Tumor suppression via inhibition of SWI/SNF complex-dependent NF- B activation ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28924147 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28924147 #FOAvip English Wikipedia <ref>{{Cite pmid|28924147}}</ref> Tumor suppression via inhibition of SWI/SNF complex-dependent NF-?B activation #MMPMID28924147 Kobayashi K; Hiramatsu H; Nakamura S; Kobayashi K; Haraguchi T; Iba H Sci Rep 2017[]; 7 (ä): ä PMID28924147show ga The transcription factor NF-?B is constitutively activated in many epithelial tumors but few NF-?B inhibitors are suitable for cancer therapy because of its broad biological effects. We previously reported that the d4-family proteins (DPF1, DPF2, DPF3a/b) function as adaptor proteins linking NF-?B with the SWI/SNF complex. Here, using epithelial tumor cell lines, A549 and HeLaS3, we demonstrate that exogenous expression of the highly-conserved N-terminal 84-amino acid region (designated ?CT1?) of either DPF2 or DPF3a/b has stronger inhibitory effects on anchorage-independent growth than the single knockdown of any d4-family protein. This indicates that CT1 can function as an efficient dominant-negative mutant of the entire d4-family proteins. By in situ proximity ligation assay, CT1 was found to retain full adaptor function, indicating that the C-terminal region of d4-family proteins lacking in CT1 would include essential domains for SWI/SNF-dependent NF-?B activation. Microarray analysis revealed that CT1 suppresses only a portion of the NF-?B target genes, including representative SWI/SNF-dependent genes. Among these genes, IL6 was shown to strongly contribute to anchorage-independent growth. Finally, exogenous CT1 expression efficiently suppressed tumor formation in a mouse xenograft model, suggesting that the d4-family proteins are promising cancer therapy targets. äTumor suppression via inhibition of SWI/SNF complex-dependent NF-?B ac(epmc).pdf DeepDyve Pubget Overpricing