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10.1186/s13578-017-0152-8 http://scihub22266oqcxt.onion/10.1186/s13578-017-0152-8 C5436453!5436453!28529687     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Biosci 2017 ; 7 (ä): ä Nephropedia Template TP {{tp|p=28529687|t=2017. Histone demethylases UTX and JMJD3 are required for NKT cell development in mice |pdf=|usr=}}{{28529687}} gab.com Text Histone demethylases UTX and JMJD3 are required for NKT cell development in mice JO: Cell Biosci http://www.kidney.de/pget.php?&tw=1&pmid=28529687 #FOAvip Background: Natural killer (NK)T cells and conventional T cells share phenotypic characteristic however they differ in transcription factor requirements and functional properties. The role of histone modifying enzymes in conventional T cell development has been extensively studied, little is known about the function of enzymes regulating histone methylation in NKT cells. Results: We show that conditional deletion of histone demethylases UTX and JMJD3 by CD4-Cre leads to near complete loss of liver NKT cells, while conventional T cells are less affected. Loss of NKT cells is cell intrinsic and not due to an insufficient selection environment. The absence of NKT cells in UTX/JMJD3-deficient mice protects mice from concanavalin A?induced liver injury, a model of NKT?mediated hepatitis. GO?analysis of RNA-seq data indicates that cell cycle genes are downregulated in UTX/JMJD3-deleted NKT progenitors, and suggest that failed expansion may account for some of the cellular deficiency. The phenotype appears to be demethylase?dependent, because UTY, a homolog of UTX that lacks catalytic function, is not sufficient to restore their development and removal of H3K27me3 by deletion of EZH2 partially rescues the defect. Conclusions: NKT cell development and gene expression is sensitive to proper regulation of H3K27 methylation. The H3K27me3 demethylase enzymes, in particular UTX, promote NKT cell development, and are required for effective NKT function. Electronic supplementary material: The online version of this article (doi:10.1186/s13578-017-0152-8) contains supplementary material, which is available to authorized users. Twit Text FOAVip Histone demethylases UTX and JMJD3 are required for NKT cell development in mice ????Cell Biosci http://www.kidney.de/pget.php?&tw=1&pmid=28529687 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28529687 #FOAvip English Wikipedia <ref>{{Cite pmid|28529687}}</ref> Histone demethylases UTX and JMJD3 are required for NKT cell development in mice #MMPMID28529687 Northrup D; Yagi R; Cui K; Proctor WR; Wang C; Placek K; Pohl LR; Wang R; Ge K; Zhu J; Zhao K Cell Biosci 2017[]; 7 (ä): ä PMID28529687show ga Background: Natural killer (NK)T cells and conventional T cells share phenotypic characteristic however they differ in transcription factor requirements and functional properties. The role of histone modifying enzymes in conventional T cell development has been extensively studied, little is known about the function of enzymes regulating histone methylation in NKT cells. Results: We show that conditional deletion of histone demethylases UTX and JMJD3 by CD4-Cre leads to near complete loss of liver NKT cells, while conventional T cells are less affected. Loss of NKT cells is cell intrinsic and not due to an insufficient selection environment. The absence of NKT cells in UTX/JMJD3-deficient mice protects mice from concanavalin A?induced liver injury, a model of NKT?mediated hepatitis. GO?analysis of RNA-seq data indicates that cell cycle genes are downregulated in UTX/JMJD3-deleted NKT progenitors, and suggest that failed expansion may account for some of the cellular deficiency. The phenotype appears to be demethylase?dependent, because UTY, a homolog of UTX that lacks catalytic function, is not sufficient to restore their development and removal of H3K27me3 by deletion of EZH2 partially rescues the defect. Conclusions: NKT cell development and gene expression is sensitive to proper regulation of H3K27 methylation. The H3K27me3 demethylase enzymes, in particular UTX, promote NKT cell development, and are required for effective NKT function. Electronic supplementary material: The online version of this article (doi:10.1186/s13578-017-0152-8) contains supplementary material, which is available to authorized users. äHistone demethylases UTX and JMJD3 are required for NKT cell developme(epmc).pdf DeepDyve Pubget Overpricing