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10.3389/fphys.2017.00682 http://scihub22266oqcxt.onion/10.3389/fphys.2017.00682 C5596098!5596098 !28943853     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28943853 &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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28943853 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Physiol 2017 ; 8 (ä): 682 Nephropedia Template TP {{tp|p=28943853 |t=2017. Arginase-II Deficiency Extends Lifespan in Mice |pdf=|usr=}}{{28943853 }} gab.com Text Arginase-II Deficiency Extends Lifespan in Mice JO: Front Physiol http://www.kidney.de/pget.php?&tw=1&pmid=28943853 #FOAvip The mitochondrial arginase type II (Arg-II) has been shown to interact with ribosomal protein S6 kinase 1 (S6K1) and mitochondrial p66(Shc) and to promote cell senescence, apoptosis and inflammation under pathological conditions. However, the impact of Arg-II on organismal lifespan is not known. In this study, we demonstrate a significant lifespan extension in mice with Arg-II gene deficiency (Arg-II(-/-)) as compared to wild type (WT) control animals. This effect is more pronounced in the females than in the males. The gender difference is associated with higher Arg-II expression levels in the females than in the males in skin and heart at both young and old age. Ablation of Arg-II gene significantly reduces the aging marker p16(INK4a) levels in these tissues of old female mice, whereas in the male mice this effect of Arg-II deficiency is weaker. In line with this observation, age-associated increases in S6K1 signaling and p66(Shc) levels in heart are significantly attenuated in the female Arg-II(-/-) mice. In the male mice, only p66(Shc) but not S6K1 signaling is reduced. In summary, our study demonstrates that Arg-II may play an important role in the acceleration of aging in mice. Genetic disruption of Arg-II in mouse extends lifespan predominantly in females, which relates to inhibition of S6K1, p66(Shc), and p16(INK4a). Thus, Arg-II may represent a promising target to decelerate aging process and extend lifespan as well as to treat age-related diseases. Twit Text FOAVip Arginase-II Deficiency Extends Lifespan in Mice ????Front Physiol http://www.kidney.de/pget.php?&tw=1&pmid=28943853 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28943853 #FOAvip English Wikipedia <ref>{{Cite pmid|28943853 }}</ref> Arginase-II Deficiency Extends Lifespan in Mice #MMPMID28943853 Xiong Y ; Yepuri G ; Montani JP ; Ming XF ; Yang Z Front Physiol 2017[]; 8 (ä): 682 PMID28943853 show ga The mitochondrial arginase type II (Arg-II) has been shown to interact with ribosomal protein S6 kinase 1 (S6K1) and mitochondrial p66(Shc) and to promote cell senescence, apoptosis and inflammation under pathological conditions. However, the impact of Arg-II on organismal lifespan is not known. In this study, we demonstrate a significant lifespan extension in mice with Arg-II gene deficiency (Arg-II(-/-)) as compared to wild type (WT) control animals. This effect is more pronounced in the females than in the males. The gender difference is associated with higher Arg-II expression levels in the females than in the males in skin and heart at both young and old age. Ablation of Arg-II gene significantly reduces the aging marker p16(INK4a) levels in these tissues of old female mice, whereas in the male mice this effect of Arg-II deficiency is weaker. In line with this observation, age-associated increases in S6K1 signaling and p66(Shc) levels in heart are significantly attenuated in the female Arg-II(-/-) mice. In the male mice, only p66(Shc) but not S6K1 signaling is reduced. In summary, our study demonstrates that Arg-II may play an important role in the acceleration of aging in mice. Genetic disruption of Arg-II in mouse extends lifespan predominantly in females, which relates to inhibition of S6K1, p66(Shc), and p16(INK4a). Thus, Arg-II may represent a promising target to decelerate aging process and extend lifespan as well as to treat age-related diseases. äArginase-II Deficiency Extends Lifespan in Mice (epmc).pdf DeepDyve Pubget Overpricing