Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.3389/fimmu.2018.00549 http://scihub22266oqcxt.onion/10.3389/fimmu.2018.00549 C5879148!5879148 !29632530     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29632530 &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 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 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\29632530 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Immunol 2018 ; 9 (ä): 549 Nephropedia Template TP {{tp|p=29632530 |t=2018. Ezh2 Regulates Activation-Induced CD8(+) T Cell Cycle Progression via Repressing Cdkn2a and Cdkn1c Expression |pdf=|usr=}}{{29632530 }} gab.com Text Ezh2 Regulates Activation-Induced CD8(+) T Cell Cycle Progression via Repressing Cdkn2a and Cdkn1c Expression JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29632530 #FOAvip Transition from resting to cell cycle in response to antigenic stimulation is an essential step for naïve CD8(+) T cells to differentiate to effector and memory cells. Leaving the resting state requires dramatic changes of chromatin status in the key cell cycle inhibitors but the details of these concerted events are not fully elucidated. Here, we showed that Ezh2, an enzymatic component of polycomb repressive complex 2 (PRC2) catalyzing the trimethylation of lysine 27 on histone 3 (H3K27me3), regulates activation induced naïve CD8(+) T cells proliferation and apoptosis. Upon deletion of Ezh2 during thymocyte development (Ezh2(fl/fl)Cd4Cre(+) mice), naive CD8(+) T cells displayed impaired proliferation and increased apoptosis in response to antigen stimulation. However, naive CD8(+) T cells only had impaired proliferation but no increase in apoptosis when Ezh2 was deleted after activation (Ezh2(fl/fl)GzmBCre(+) mice), suggesting cell cycle and apoptosis are temporally separable events controlled by Ezh2. We then showed that deletion of Ezh2 resulted in the increase in expression of cyclin-dependent kinase inhibitors Cdkn2a (p16 and Arf) and Cdkn1c (p57) in activated naïve CD8(+) T cells as the consequence of reduced levels of H3K27me3 at these two gene loci. Finally, with real time imaging, we observed prolonged cell division times of naïve CD8(+) T cells in the absence of Ezh2 post in vitro stimulation. Together, these findings reveal that repression of Cdkn1c and Cdkn2a by Ezh2 plays a critical role in execution of activation-induced CD8(+) T cell proliferation. Twit Text FOAVip Ezh2 Regulates Activation-Induced CD8(+) T Cell Cycle Progression via Repressing Cdkn2a and Cdkn1c Expression ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29632530 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29632530 #FOAvip English Wikipedia <ref>{{Cite pmid|29632530 }}</ref> Ezh2 Regulates Activation-Induced CD8(+) T Cell Cycle Progression via Repressing Cdkn2a and Cdkn1c Expression #MMPMID29632530 Chen G ; Subedi K ; Chakraborty S ; Sharov A ; Lu J ; Kim J ; Mi X ; Wersto R ; Sung MH ; Weng NP Front Immunol 2018[]; 9 (ä): 549 PMID29632530 show ga Transition from resting to cell cycle in response to antigenic stimulation is an essential step for naïve CD8(+) T cells to differentiate to effector and memory cells. Leaving the resting state requires dramatic changes of chromatin status in the key cell cycle inhibitors but the details of these concerted events are not fully elucidated. Here, we showed that Ezh2, an enzymatic component of polycomb repressive complex 2 (PRC2) catalyzing the trimethylation of lysine 27 on histone 3 (H3K27me3), regulates activation induced naïve CD8(+) T cells proliferation and apoptosis. Upon deletion of Ezh2 during thymocyte development (Ezh2(fl/fl)Cd4Cre(+) mice), naive CD8(+) T cells displayed impaired proliferation and increased apoptosis in response to antigen stimulation. However, naive CD8(+) T cells only had impaired proliferation but no increase in apoptosis when Ezh2 was deleted after activation (Ezh2(fl/fl)GzmBCre(+) mice), suggesting cell cycle and apoptosis are temporally separable events controlled by Ezh2. We then showed that deletion of Ezh2 resulted in the increase in expression of cyclin-dependent kinase inhibitors Cdkn2a (p16 and Arf) and Cdkn1c (p57) in activated naïve CD8(+) T cells as the consequence of reduced levels of H3K27me3 at these two gene loci. Finally, with real time imaging, we observed prolonged cell division times of naïve CD8(+) T cells in the absence of Ezh2 post in vitro stimulation. Together, these findings reveal that repression of Cdkn1c and Cdkn2a by Ezh2 plays a critical role in execution of activation-induced CD8(+) T cell proliferation. |Animals [MESH] |Antigens/immunology [MESH] |Apoptosis [MESH] |CD8-Positive T-Lymphocytes/*physiology [MESH] |Cell Cycle/*physiology [MESH] |Cell Proliferation [MESH] |Cyclin-Dependent Kinase Inhibitor p16/*physiology [MESH] |Cyclin-Dependent Kinase Inhibitor p57/*physiology [MESH] |Enhancer of Zeste Homolog 2 Protein/*physiology [MESH] |Listeria monocytogenes [MESH] |Listeriosis/immunology [MESH] |Mice, Knockout [MESH]Ezh2 Regulates Activation-Induced CD8(+) T Cell Cycle Progression via (epmc).pdf DeepDyve Pubget Overpricing