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10.4137/JEN.S33122 http://scihub22266oqcxt.onion/10.4137/JEN.S33122 C4807884!4807884!27042141     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 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\27042141.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Exp+Neurosci 2016 ; 10 (ä): 39-49 Nephropedia Template TP {{tp|p=27042141|t=2016. Molecular Mechanisms of Neurodegeneration in Spinal Muscular Atrophy |pdf=|usr=}}{{27042141}} gab.com Text Molecular Mechanisms of Neurodegeneration in Spinal Muscular Atrophy JO: J Exp Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=27042141 #FOAvip Spinal muscular atrophy (SMA) is an autosomal recessive motor neuron disease with a high incidence and is the most common genetic cause of infant mortality. SMA is primarily characterized by degeneration of the spinal motor neurons that leads to skeletal muscle atrophy followed by symmetric limb paralysis, respiratory failure, and death. In humans, mutation of the Survival Motor Neuron 1 (SMN1) gene shifts the load of expression of SMN protein to the SMN2 gene that produces low levels of full-length SMN protein because of alternative splicing, which are sufficient for embryonic development and survival but result in SMA. The molecular mechanisms of the (a) regulation of SMN gene expression and (b) degeneration of motor neurons caused by low levels of SMN are unclear. However, some progress has been made in recent years that have provided new insights into understanding of the cellular and molecular basis of SMA pathogenesis. In this review, we have briefly summarized recent advances toward understanding of the molecular mechanisms of regulation of SMN levels and signaling mechanisms that mediate neurodegeneration in SMA. Twit Text FOAVip Molecular Mechanisms of Neurodegeneration in Spinal Muscular Atrophy ????J Exp Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=27042141 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27042141 #FOAvip English Wikipedia <ref>{{Cite pmid|27042141}}</ref> Molecular Mechanisms of Neurodegeneration in Spinal Muscular Atrophy #MMPMID27042141 Ahmad S; Bhatia K; Kannan A; Gangwani L J Exp Neurosci 2016[]; 10 (ä): 39-49 PMID27042141show ga Spinal muscular atrophy (SMA) is an autosomal recessive motor neuron disease with a high incidence and is the most common genetic cause of infant mortality. SMA is primarily characterized by degeneration of the spinal motor neurons that leads to skeletal muscle atrophy followed by symmetric limb paralysis, respiratory failure, and death. In humans, mutation of the Survival Motor Neuron 1 (SMN1) gene shifts the load of expression of SMN protein to the SMN2 gene that produces low levels of full-length SMN protein because of alternative splicing, which are sufficient for embryonic development and survival but result in SMA. The molecular mechanisms of the (a) regulation of SMN gene expression and (b) degeneration of motor neurons caused by low levels of SMN are unclear. However, some progress has been made in recent years that have provided new insights into understanding of the cellular and molecular basis of SMA pathogenesis. In this review, we have briefly summarized recent advances toward understanding of the molecular mechanisms of regulation of SMN levels and signaling mechanisms that mediate neurodegeneration in SMA. äMolecular Mechanisms of Neurodegeneration in Spinal Muscular Atrophy (epmc).pdf DeepDyve Pubget Overpricing