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10.1016/j.neuroscience.2015.02.049 http://scihub22266oqcxt.onion/10.1016/j.neuroscience.2015.02.049 C5384639!5384639!25743255     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Neuroscience 2015 ; 294 (ä): 101-8 Nephropedia Template TP {{tp|p=25743255|t=2015. ACTIVATION OF THE WNT/?-CATENIN SIGNALING CASCADE AFTER TRAUMATIC NERVE INJURY |pdf=|usr=}}{{25743255}} gab.com Text ACTIVATION OF THE WNT/ -CATENIN SIGNALING CASCADE AFTER TRAUMATIC NERVE INJURY JO: Neuroscience http://www.kidney.de/pget.php?&tw=1&pmid=25743255 #FOAvip Recent data have shown that preservation of the neuromuscular junction (NMJ) after traumatic nerve injury helps to improve functional recovery with surgical repair via matrix metalloproteinase-3 (MMP3) blockade. As such, we sought to explore additional pathways that may augment this response. Wnt3a has been shown to inhibit acetylcholine receptor (AChR) clustering via ?-catenin-dependent signaling in the development of the NMJ. Therefore, we hypothesized that Wnt3a and ?-catenin are associated with NMJ destabilization following traumatic denervation. A critical size nerve defect was created by excising a 10-mm segment of the sciatic nerve in mice. Denervated muscles were then harvested at multiple time points for immunofluorescence staining, quantitative real-time PCR, and western blot analysis for Wnt3a and ?-catenin levels. Moreover, a novel Wnt/?-catenin transgenic reporter mouse line was utilized to support our hypothesis of Wnt activation after traumatic nerve injury. The expression of Wnt3a mRNA was significantly increased by 2 weeks post-injury and remained upregulated for 2 months. Additionally, ?-catenin was activated at 2 months post-injury relative to controls. Correspondingly, immunohistochemical analysis of denervated transgenic mouse line TCF/Lef:H2B-GFP muscles demonstrated that the number of GFP-positive cells was increased at the motor endplate band. These collective data support that post-synaptic AChRs destabilize after denervation by a process that involves the Wnt/?-catenin pathway. As such, this pathway serves as a potential therapeutic target to prevent the motor endplate degeneration that occurs following traumatic nerve injury. Twit Text FOAVip ACTIVATION OF THE WNT/ -CATENIN SIGNALING CASCADE AFTER TRAUMATIC NERVE INJURY ????Neuroscience http://www.kidney.de/pget.php?&tw=1&pmid=25743255 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25743255 #FOAvip English Wikipedia <ref>{{Cite pmid|25743255}}</ref> ACTIVATION OF THE WNT/?-CATENIN SIGNALING CASCADE AFTER TRAUMATIC NERVE INJURY #MMPMID25743255 KURIMOTO S; JUNG J; TAPADIA M; LENGFELD J; AGALLIU D; WATERMAN M; MOZAFFAR T; GUPTA R Neuroscience 2015[May]; 294 (ä): 101-8 PMID25743255show ga Recent data have shown that preservation of the neuromuscular junction (NMJ) after traumatic nerve injury helps to improve functional recovery with surgical repair via matrix metalloproteinase-3 (MMP3) blockade. As such, we sought to explore additional pathways that may augment this response. Wnt3a has been shown to inhibit acetylcholine receptor (AChR) clustering via ?-catenin-dependent signaling in the development of the NMJ. Therefore, we hypothesized that Wnt3a and ?-catenin are associated with NMJ destabilization following traumatic denervation. A critical size nerve defect was created by excising a 10-mm segment of the sciatic nerve in mice. Denervated muscles were then harvested at multiple time points for immunofluorescence staining, quantitative real-time PCR, and western blot analysis for Wnt3a and ?-catenin levels. Moreover, a novel Wnt/?-catenin transgenic reporter mouse line was utilized to support our hypothesis of Wnt activation after traumatic nerve injury. The expression of Wnt3a mRNA was significantly increased by 2 weeks post-injury and remained upregulated for 2 months. Additionally, ?-catenin was activated at 2 months post-injury relative to controls. Correspondingly, immunohistochemical analysis of denervated transgenic mouse line TCF/Lef:H2B-GFP muscles demonstrated that the number of GFP-positive cells was increased at the motor endplate band. These collective data support that post-synaptic AChRs destabilize after denervation by a process that involves the Wnt/?-catenin pathway. As such, this pathway serves as a potential therapeutic target to prevent the motor endplate degeneration that occurs following traumatic nerve injury. äACTIVATION OF THE WNT/?-CATENIN SIGNALING CASCADE AFTER TRAUMATIC NERV(epmc).pdf DeepDyve Pubget Overpricing