Charles Allerson
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View article: Utilization of a novel siRNA platform technology to target APOE in the brain for the treatment of Alzheimer’s Disease
Utilization of a novel siRNA platform technology to target APOE in the brain for the treatment of Alzheimer’s Disease Open
Background The greatest genetic risk factor for late‐onset Alzheimer’s disease (AD) is Apolipoprotein E (APOE)*ε4. Preclinical studies have demonstrated that genetic ablation or reduction of APOE4 mRNA in amyloid and tauopathy mouse models…
View article: Supplementary Figure 2 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Figure 2 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Figure 2. Anti-miR-21 treatment causes limited caspase 3/7 activation in non-transformed cell lines. Caspase 3/7 activation after treatment of SKHep1, IMR-90, and WI-38 cells with MM control or anti-miR-21 for 72 hours. (Mean…
View article: Supplementary Figure 1 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Figure 1 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Figure 1. miR-21 mimic suppresses expression of ANKRD46, DDAH1 and RECK. SKHep1 cells were transfected with miR-21 or negative mimic. RNA was isolated and expression of ANKRD46, DDAH1 and RECK was assessed by qPCR. (Mean, {pl…
View article: Supplementary Figure 4 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Figure 4 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Figure 4. Pathway analysis of gene expression changes following anti-miR-21 treatment. SKHep1 cells treated with anti-miR-21 were subjected to microarray gene expression analysis. Changes in cellular processes (top) and pathw…
View article: Supplementary Table 1 and Table 2 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Table 1 and Table 2 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Tables 1 and 2. Supplementary Table 1: Fold de-repression of miR-21 target genes after anti-miR-21 treatment. Supplementary Table 2: Taqman Primer and Probes
View article: Supplementary Figure 3 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Figure 3 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Figure 3. HMBG1 and LDH are induced upon miR-21 inhibition. SKHep1, HepG2 and Hep3B cells were treated with anti-miR-21 or MM control and extracellular HMBG1 and LDH activity was quantified. (Mean, {plus minus} SEM, n=3)
View article: Supplementary Figure 1 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Figure 1 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Figure 1. miR-21 mimic suppresses expression of ANKRD46, DDAH1 and RECK. SKHep1 cells were transfected with miR-21 or negative mimic. RNA was isolated and expression of ANKRD46, DDAH1 and RECK was assessed by qPCR. (Mean, {pl…
View article: Supplementary Table 1 and Table 2 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Table 1 and Table 2 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Tables 1 and 2. Supplementary Table 1: Fold de-repression of miR-21 target genes after anti-miR-21 treatment. Supplementary Table 2: Taqman Primer and Probes
View article: Supplementary Figure Legends from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Figure Legends from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Figure Legends. Figure legends for Supplementary Figures 1, 2, 3, and 4.
View article: Supplementary Data 1 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Data 1 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Data 1. Excel sheet with fold change in gene expression following anti-miR-21 treatment.
View article: Data from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Data from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Hepatocellular carcinoma (HCC) remains a significant clinical challenge with few therapeutic options available to cancer patients. MicroRNA 21-5p (miR-21) has been shown to be upregulated in HCC, but the contribution of this oncomiR to the…
View article: Supplementary Figure 2 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Figure 2 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Figure 2. Anti-miR-21 treatment causes limited caspase 3/7 activation in non-transformed cell lines. Caspase 3/7 activation after treatment of SKHep1, IMR-90, and WI-38 cells with MM control or anti-miR-21 for 72 hours. (Mean…
View article: Supplementary Figure 3 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Figure 3 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Figure 3. HMBG1 and LDH are induced upon miR-21 inhibition. SKHep1, HepG2 and Hep3B cells were treated with anti-miR-21 or MM control and extracellular HMBG1 and LDH activity was quantified. (Mean, {plus minus} SEM, n=3)
View article: Supplementary Figure 4 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Figure 4 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Figure 4. Pathway analysis of gene expression changes following anti-miR-21 treatment. SKHep1 cells treated with anti-miR-21 were subjected to microarray gene expression analysis. Changes in cellular processes (top) and pathw…
View article: Supplementary Data 1 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Data 1 from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Data 1. Excel sheet with fold change in gene expression following anti-miR-21 treatment.
View article: Data from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Data from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Hepatocellular carcinoma (HCC) remains a significant clinical challenge with few therapeutic options available to cancer patients. MicroRNA 21-5p (miR-21) has been shown to be upregulated in HCC, but the contribution of this oncomiR to the…
View article: Supplementary Figure Legends from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation
Supplementary Figure Legends from Anti–miR-21 Suppresses Hepatocellular Carcinoma Growth via Broad Transcriptional Network Deregulation Open
Supplementary Figure Legends. Figure legends for Supplementary Figures 1, 2, 3, and 4.
View article: Discovery and preclinical evaluation of anti-miR-17 oligonucleotide RGLS4326 for the treatment of polycystic kidney disease
Discovery and preclinical evaluation of anti-miR-17 oligonucleotide RGLS4326 for the treatment of polycystic kidney disease Open
Autosomal dominant polycystic kidney disease (ADPKD), caused by mutations in either PKD1 or PKD2 genes, is one of the most common human monogenetic disorders and the leading genetic cause of end-stage renal disease. Unfortunately, treatmen…