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10.1038/srep21810 http://scihub22266oqcxt.onion/10.1038/srep21810 C4766407!4766407 !26911452     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26911452 &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 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 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 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 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26911452 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Sci+Rep 2016 ; 6 (ä): 21810 Nephropedia Template TP {{tp|p=26911452 |t=2016. Specific regulation of PRMT1 expression by PIAS1 and RKIP in BEAS-2B epithelia cells and HFL-1 fibroblasts in lung inflammation |pdf=|usr=}}{{26911452 }} gab.com Text Specific regulation of PRMT1 expression by PIAS1 and RKIP in BEAS-2B epithelia cells and HFL-1 fibroblasts in lung inflammation JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26911452 #FOAvip Protein arginine methyltransferase 1 (PRMT1) catalyzes methylation of histones and other cellular proteins, and thus regulates gene transcription and protein activity. In antigen-induced pulmonary inflammation (AIPI) PRMT1 was up-regulated in the epithelium, while in chronic AIPI, increased PRMT1 shifted to fibroblasts. In this study we investigated the cell type specific regulatory mechanism of PRMT1. Epithelial cells and fibroblasts were stimulated with IL-4 or IL-1?. Gene and protein expression were determined by RT-qPCR, immunohistochemistry staining and Western blotting. Signaling pathway inhibitors, siRNAs and shRNA were used to determine the regulatory mechanism of PRMT1. The results showed that IL-4 up-regulated PRMT1 through STAT6 signaling in epithelial cells, while IL-1? regulated PRMT1 through NF-?B in fibroblasts. The NF-kB inhibitor protein RKIP was highly expressed in epithelial cells and blocked IL-1? induced PRMT1 up-regulation; while the STAT6 inhibitor protein PIAS1 was expressed in fibroblasts and suppressed IL-4 induced PRMT1 expression. Furthermore, IL-4 stimulated epithelial cells to release IL-1? which up-regulated PRMT1 expression in fibroblasts. In conclusion, the inhibitor proteins RKIP and PIAS1 regulated the cell type and signaling specific expression of PRMT1. Thus PRMT1 expression in structural lung cells in asthma can be considered as potential target for new therapeutic intervention. Twit Text FOAVip Specific regulation of PRMT1 expression by PIAS1 and RKIP in BEAS-2B epithelia cells and HFL-1 fibroblasts in lung inflammation ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26911452 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26911452 #FOAvip English Wikipedia <ref>{{Cite pmid|26911452 }}</ref> Specific regulation of PRMT1 expression by PIAS1 and RKIP in BEAS-2B epithelia cells and HFL-1 fibroblasts in lung inflammation #MMPMID26911452 Liu L ; Sun Q ; Bao R ; Roth M ; Zhong B ; Lan X ; Tian J ; He Q ; Li D ; Sun J ; Yang X ; Lu S Sci Rep 2016[Feb]; 6 (ä): 21810 PMID26911452 show ga Protein arginine methyltransferase 1 (PRMT1) catalyzes methylation of histones and other cellular proteins, and thus regulates gene transcription and protein activity. In antigen-induced pulmonary inflammation (AIPI) PRMT1 was up-regulated in the epithelium, while in chronic AIPI, increased PRMT1 shifted to fibroblasts. In this study we investigated the cell type specific regulatory mechanism of PRMT1. Epithelial cells and fibroblasts were stimulated with IL-4 or IL-1?. Gene and protein expression were determined by RT-qPCR, immunohistochemistry staining and Western blotting. Signaling pathway inhibitors, siRNAs and shRNA were used to determine the regulatory mechanism of PRMT1. The results showed that IL-4 up-regulated PRMT1 through STAT6 signaling in epithelial cells, while IL-1? regulated PRMT1 through NF-?B in fibroblasts. The NF-kB inhibitor protein RKIP was highly expressed in epithelial cells and blocked IL-1? induced PRMT1 up-regulation; while the STAT6 inhibitor protein PIAS1 was expressed in fibroblasts and suppressed IL-4 induced PRMT1 expression. Furthermore, IL-4 stimulated epithelial cells to release IL-1? which up-regulated PRMT1 expression in fibroblasts. In conclusion, the inhibitor proteins RKIP and PIAS1 regulated the cell type and signaling specific expression of PRMT1. Thus PRMT1 expression in structural lung cells in asthma can be considered as potential target for new therapeutic intervention. |A549 Cells [MESH] |Binding Sites [MESH] |Blotting, Western [MESH] |Cells, Cultured [MESH] |Cyclooxygenase 2/genetics/metabolism [MESH] |Epithelial Cells/cytology/metabolism [MESH] |Fibroblasts/cytology/metabolism [MESH] |Humans [MESH] |Immunoprecipitation [MESH] |Interleukin-1beta/genetics/metabolism/pharmacology [MESH] |Interleukin-4/genetics/metabolism/pharmacology [MESH] |Lung/metabolism/pathology [MESH] |Microscopy, Fluorescence [MESH] |NF-kappa B/antagonists & inhibitors/metabolism [MESH] |Phosphatidylethanolamine Binding Protein/antagonists & inhibitors/genetics/*metabolism [MESH] |Phosphorylation/drug effects [MESH] |Pneumonia/metabolism/pathology [MESH] |Promoter Regions, Genetic [MESH] |Protein Inhibitors of Activated STAT/antagonists & inhibitors/genetics/*metabolism [MESH] |Protein-Arginine N-Methyltransferases/antagonists & inhibitors/genetics/*metabolism [MESH] |RNA Interference [MESH] |RNA, Messenger/metabolism [MESH] |RNA, Small Interfering/metabolism [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Recombinant Proteins/biosynthesis/isolation & purification/pharmacology [MESH] |Repressor Proteins/antagonists & inhibitors/genetics/*metabolism [MESH] |STAT6 Transcription Factor/antagonists & inhibitors/genetics/metabolism [MESH] |Signal Transduction/drug effects [MESH] |Small Ubiquitin-Related Modifier Proteins/antagonists & inhibitors/genetics/*metabolism [MESH] |Up-Regulation/drug effects [MESH]Specific regulation of PRMT1 expression by PIAS1 and RKIP in BEAS-2B e(epmc).pdf DeepDyve Pubget Overpricing