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10.1038/onc.2017.16 http://scihub22266oqcxt.onion/10.1038/onc.2017.16 C5509478!5509478!28319059     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28319059&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 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 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 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\28319059.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Oncogene 2017 ; 36 (28): 4060-71 Nephropedia Template TP {{tp|p=28319059|t=2017. CAMK2? in Intestinal Epithelial Cells Modulates Colitis-Associated Colorectal Carcinogenesis via Enhancing STAT3 Activation |pdf=|usr=}}{{28319059}} gab.com Text CAMK2 in Intestinal Epithelial Cells Modulates Colitis-Associated Colorectal Carcinogenesis via Enhancing STAT3 Activation JO: Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=28319059 #FOAvip Inflammation is one of the major risk factors for cancer. Here, we show that calcium/calmodulin-dependent protein kinase II gamma (CAMK2?) in intestinal epithelial cells (IECs) modulates inflammatory signals and promotes colitis-associated cancer (CAC) in mice. We have identified CAMK2? as a downstream target of colitis-induced WNT5a signaling. Furthermore, we have shown that CAMK2? protects against intestine tissue injury by increasing IEC survival and proliferation. CAMK2? knockout mice displayed reduced CAC. Furthermore, we used bone marrow transplantation to reveal that CAMK2? in IECs, but not immune cells, was crucial for its effect on CAC. Consistently, transgenic over-expression of CAMK2? in IECs accelerated CAC development. Mechanistically, CAMK2? in IECs enhanced epithelial STAT3 activation to promote survival and proliferation of colonic epithelial cells during CAC development. These results thus identify a new molecular mechanism mediated by CAMK2? in IECs during CAC development, thereby providing a potential new therapeutic target for CAC. Twit Text FOAVip CAMK2 in Intestinal Epithelial Cells Modulates Colitis-Associated Colorectal Carcinogenesis via Enhancing STAT3 Activation ????Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=28319059 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28319059 #FOAvip English Wikipedia <ref>{{Cite pmid|28319059}}</ref> CAMK2? in Intestinal Epithelial Cells Modulates Colitis-Associated Colorectal Carcinogenesis via Enhancing STAT3 Activation #MMPMID28319059 Ma X; Meng Z; Jin L; Xiao Z; Wang X; Tsark WM; Ding L; Gu Y; Zhang J; Kim B; He M; Gan X; Shively JE; Yu H; Xu R; Huang W Oncogene 2017[Jul]; 36 (28): 4060-71 PMID28319059show ga Inflammation is one of the major risk factors for cancer. Here, we show that calcium/calmodulin-dependent protein kinase II gamma (CAMK2?) in intestinal epithelial cells (IECs) modulates inflammatory signals and promotes colitis-associated cancer (CAC) in mice. We have identified CAMK2? as a downstream target of colitis-induced WNT5a signaling. Furthermore, we have shown that CAMK2? protects against intestine tissue injury by increasing IEC survival and proliferation. CAMK2? knockout mice displayed reduced CAC. Furthermore, we used bone marrow transplantation to reveal that CAMK2? in IECs, but not immune cells, was crucial for its effect on CAC. Consistently, transgenic over-expression of CAMK2? in IECs accelerated CAC development. Mechanistically, CAMK2? in IECs enhanced epithelial STAT3 activation to promote survival and proliferation of colonic epithelial cells during CAC development. These results thus identify a new molecular mechanism mediated by CAMK2? in IECs during CAC development, thereby providing a potential new therapeutic target for CAC. äCAMK2? in Intestinal Epithelial Cells Modulates Colitis-Associated Col(epmc).pdf DeepDyve Pubget Overpricing