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10.1038/ncomms12730 http://scihub22266oqcxt.onion/10.1038/ncomms12730 C5023956!5023956!27601261     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 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2016 ; 7 (ä): ä Nephropedia Template TP {{tp|p=27601261|t=2016. NK cell development requires Tsc1-dependent negative regulation of IL-15-triggered mTORC1 activation |pdf=|usr=}}{{27601261}} gab.com Text NK cell development requires Tsc1-dependent negative regulation of IL-15-triggered mTORC1 activation JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=27601261 #FOAvip Activation of metabolic signalling by IL-15 is required for natural killer (NK) cell development. Here we show that Tsc1, a repressor of mTOR, is dispensable for the terminal maturation, survival and function of NK cells but is critical to restrict exhaustive proliferation of immature NK cells and activation downstream of IL-15 during NK cell development. Tsc1 is expressed in immature NK cells and is upregulated by IL-15. Haematopoietic-specific deletion of Tsc1 causes a marked decrease in the number of NK cells and compromises rejection of ?missing-self' haematopoietic tumours and allogeneic bone marrow. The residual Tsc1-null NK cells display activated, pro-apoptotic phenotype and elevated mTORC1 activity. Deletion of Raptor, a component of mTORC1, largely reverses these defects. Tsc1-deficient NK cells express increased levels of T-bet and downregulate Eomes and CD122, a subunit of IL-15 receptor. These results reveal a role for Tsc1-dependent inhibition of mTORC1 activation during immature NK cell development. Twit Text FOAVip NK cell development requires Tsc1-dependent negative regulation of IL-15-triggered mTORC1 activation ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=27601261 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27601261 #FOAvip English Wikipedia <ref>{{Cite pmid|27601261}}</ref> NK cell development requires Tsc1-dependent negative regulation of IL-15-triggered mTORC1 activation #MMPMID27601261 Yang M; Chen S; Du J; He J; Wang Y; Li Z; Liu G; Peng W; Zeng X; Li D; Xu P; Guo W; Chang Z; Wang S; Tian Z; Dong Z Nat Commun 2016[]; 7 (ä): ä PMID27601261show ga Activation of metabolic signalling by IL-15 is required for natural killer (NK) cell development. Here we show that Tsc1, a repressor of mTOR, is dispensable for the terminal maturation, survival and function of NK cells but is critical to restrict exhaustive proliferation of immature NK cells and activation downstream of IL-15 during NK cell development. Tsc1 is expressed in immature NK cells and is upregulated by IL-15. Haematopoietic-specific deletion of Tsc1 causes a marked decrease in the number of NK cells and compromises rejection of ?missing-self' haematopoietic tumours and allogeneic bone marrow. The residual Tsc1-null NK cells display activated, pro-apoptotic phenotype and elevated mTORC1 activity. Deletion of Raptor, a component of mTORC1, largely reverses these defects. Tsc1-deficient NK cells express increased levels of T-bet and downregulate Eomes and CD122, a subunit of IL-15 receptor. These results reveal a role for Tsc1-dependent inhibition of mTORC1 activation during immature NK cell development. äNK cell development requires Tsc1-dependent negative regulation of IL-(epmc).pdf DeepDyve Pubget Overpricing