<p>Primary testis cells (A) and primary spinal cord neurons (B) of SMA mice were co-transfected with <i>SMN2</i> minigene plasmid and <i>Tra2-β1</i> overexpression plasmid, <i>ASF/SF2</i> overexpression plasmid or blank vector as control for 48 hours. Total RNA was isolated from transfected cells and then subjected to RT-PCR to amplify <i>SMN2</i> minigene FL and Δ7 mRNAs. The result showed that overexpression of Tra2-β1, but not ASF/SF2, remarkably increased <i>SMN2</i> exon 7 inclusion in both primary testis cells and primary spinal cord neurons of SMA mice. Error bars represent standard deviation. (*) <i>P</i> < 0.05, compared with the vector control.</p
RNA modalities are developing as a powerful means to re-direct pathogenic pre-mRNA splicing events. ...
AbstractSpinal muscular atrophy (SMA) is a neuromuscular disease caused by disruption of the surviva...
[[abstract]]The survival motor neuron gene is present in humans in a telomeric copy, SMN1, and sever...
<p>Primary testis cells of SMA mice were cultured for 72 hours and then transfected with Tra2-β1 siR...
Spinal muscular atrophy (SMA) is an inherited neuromuscular disease caused by deletion or mutation o...
<p>Various tissues of type 3 SMA mice were collected. (A) Total RNA was isolated and subjected to RT...
<p>(<b>A</b>) Western blot analysis of tissue from PND10–12 controls (1) and SMA mice with (2) or wi...
<p>(A) Proteins extracted from primary testis cells cultured for 2 hours and 96 hours were subjected...
Spinal muscular atrophy is caused by loss of the SMN1 gene and retention of SMN2. TheSMN2 copy numbe...
<p>(<b>A</b>) Semi-quantitative radiolabelled RT-PCR of endogenous <i>SMN2</i> mRNA following select...
<p>(<b>A</b>) Immunoblots of SMN and β-actin following knockdown of SR proteins in GM00232 type 1 SM...
<p>(<b>A</b>) Immunoblot of SMN and β-actin following knockdown of SRSF3 with siRNA in SMA patient-d...
Spinal muscular atrophy (SMA) is a neuromuscular disease caused by disruption of the survival motor ...
Spinal muscular atrophy is caused by loss of the SMN1 gene and retention of SMN2. The SMN2 copy numb...
<p>(<b>A</b>) RT-PCR analysis of tissue from an adult (PND32) double transgenic <i>(Nes-Cre;Smn<sup>...
RNA modalities are developing as a powerful means to re-direct pathogenic pre-mRNA splicing events. ...
AbstractSpinal muscular atrophy (SMA) is a neuromuscular disease caused by disruption of the surviva...
[[abstract]]The survival motor neuron gene is present in humans in a telomeric copy, SMN1, and sever...
<p>Primary testis cells of SMA mice were cultured for 72 hours and then transfected with Tra2-β1 siR...
Spinal muscular atrophy (SMA) is an inherited neuromuscular disease caused by deletion or mutation o...
<p>Various tissues of type 3 SMA mice were collected. (A) Total RNA was isolated and subjected to RT...
<p>(<b>A</b>) Western blot analysis of tissue from PND10–12 controls (1) and SMA mice with (2) or wi...
<p>(A) Proteins extracted from primary testis cells cultured for 2 hours and 96 hours were subjected...
Spinal muscular atrophy is caused by loss of the SMN1 gene and retention of SMN2. TheSMN2 copy numbe...
<p>(<b>A</b>) Semi-quantitative radiolabelled RT-PCR of endogenous <i>SMN2</i> mRNA following select...
<p>(<b>A</b>) Immunoblots of SMN and β-actin following knockdown of SR proteins in GM00232 type 1 SM...
<p>(<b>A</b>) Immunoblot of SMN and β-actin following knockdown of SRSF3 with siRNA in SMA patient-d...
Spinal muscular atrophy (SMA) is a neuromuscular disease caused by disruption of the survival motor ...
Spinal muscular atrophy is caused by loss of the SMN1 gene and retention of SMN2. The SMN2 copy numb...
<p>(<b>A</b>) RT-PCR analysis of tissue from an adult (PND32) double transgenic <i>(Nes-Cre;Smn<sup>...
RNA modalities are developing as a powerful means to re-direct pathogenic pre-mRNA splicing events. ...
AbstractSpinal muscular atrophy (SMA) is a neuromuscular disease caused by disruption of the surviva...
[[abstract]]The survival motor neuron gene is present in humans in a telomeric copy, SMN1, and sever...