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10.1016/j.brainres.2014.08.064 http://scihub22266oqcxt.onion/10.1016/j.brainres.2014.08.064 C4345149!4345149 !25192646     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 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\25192646 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Brain+Res 2015 ; 1619 (ä): 22-35 Nephropedia Template TP {{tp|p=25192646 |t=2015. Molecular mechanisms of scar-sourced axon growth inhibitors |pdf=|usr=}}{{25192646 }} gab.com Text Molecular mechanisms of scar-sourced axon growth inhibitors JO: Brain Res http://www.kidney.de/pget.php?&tw=1&pmid=25192646 #FOAvip Astrogliosis is a defense response of the CNS to minimize primary damage and to repair injured tissues, but it ultimately generates harmful effects by upregulating inhibitory molecules to suppress neuronal elongation and forming potent barriers to axon regeneration. Chondroitin sulfate proteoglycans (CSPGs) are highly expressed by reactive scars and are potent contributors to the non-permissive environment in mature CNS. Surmounting strong inhibition by CSPG-rich scar is an important therapeutic goal for achieving functional recovery after CNS injuries. Currently, enzymatic digestion of CSPGs with locally applied chondroitinase ABC is the main in vivo approach to overcome scar inhibition, but several disadvantages may prevent using this bacterial enzyme as a therapeutic option for patients. A better understanding of molecular mechanisms underlying CSPG function may facilitate development of new effective therapies to overcome scar-mediated inhibition. Previous studies support that CSPGs act by non-specifically hindering the binding of matrix molecules to their cell surface receptors through steric interactions, but two members of the leukocyte common antigen related (LAR) phosphatase subfamily, protein tyrosine phosphatase ? and LAR, are functional receptors that bind CSPGs with high affinity and mediate CSPG inhibition. CSPGs may also act by binding two receptors for myelin-associated growth inhibitors, Nogo receptors 1 and 3. Thus, CSPGs inhibit axon growth through multiple mechanisms, making them especially potent and difficult therapeutic targets. Identification of CSPG receptors is not only important for understanding the scar-mediated growth suppression, but also for developing novel and selective therapies to promote axon sprouting and/or regeneration after CNS injuries. This article is part of a Special Issue entitled SI: Spinal cord injury. Twit Text FOAVip Molecular mechanisms of scar-sourced axon growth inhibitors ????Brain Res http://www.kidney.de/pget.php?&tw=1&pmid=25192646 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25192646 #FOAvip English Wikipedia <ref>{{Cite pmid|25192646 }}</ref> Molecular mechanisms of scar-sourced axon growth inhibitors #MMPMID25192646 Ohtake Y ; Li S Brain Res 2015[Sep]; 1619 (ä): 22-35 PMID25192646 show ga Astrogliosis is a defense response of the CNS to minimize primary damage and to repair injured tissues, but it ultimately generates harmful effects by upregulating inhibitory molecules to suppress neuronal elongation and forming potent barriers to axon regeneration. Chondroitin sulfate proteoglycans (CSPGs) are highly expressed by reactive scars and are potent contributors to the non-permissive environment in mature CNS. Surmounting strong inhibition by CSPG-rich scar is an important therapeutic goal for achieving functional recovery after CNS injuries. Currently, enzymatic digestion of CSPGs with locally applied chondroitinase ABC is the main in vivo approach to overcome scar inhibition, but several disadvantages may prevent using this bacterial enzyme as a therapeutic option for patients. A better understanding of molecular mechanisms underlying CSPG function may facilitate development of new effective therapies to overcome scar-mediated inhibition. Previous studies support that CSPGs act by non-specifically hindering the binding of matrix molecules to their cell surface receptors through steric interactions, but two members of the leukocyte common antigen related (LAR) phosphatase subfamily, protein tyrosine phosphatase ? and LAR, are functional receptors that bind CSPGs with high affinity and mediate CSPG inhibition. CSPGs may also act by binding two receptors for myelin-associated growth inhibitors, Nogo receptors 1 and 3. Thus, CSPGs inhibit axon growth through multiple mechanisms, making them especially potent and difficult therapeutic targets. Identification of CSPG receptors is not only important for understanding the scar-mediated growth suppression, but also for developing novel and selective therapies to promote axon sprouting and/or regeneration after CNS injuries. This article is part of a Special Issue entitled SI: Spinal cord injury. |Animals [MESH] |Astrocytes/*metabolism [MESH] |Axons/drug effects/*metabolism/physiology [MESH] |Chondroitin ABC Lyase/administration & dosage [MESH] |Chondroitin Sulfate Proteoglycans/*metabolism [MESH] |Cicatrix/enzymology/*metabolism [MESH] |Gliosis/metabolism [MESH] |Growth Inhibitors/*metabolism [MESH] |Humans [MESH] |Nerve Regeneration/drug effects [MESH] |Receptor-Like Protein Tyrosine Phosphatases, Class 2/metabolism [MESH] |Receptors, Cell Surface/metabolism [MESH]Molecular mechanisms of scar-sourced axon growth inhibitors (epmc).pdf DeepDyve Pubget Overpricing