dmso treatment Search Results


dmso  (Merck & Co)
90
Merck & Co dmso
JQ1 but not HDACi can increase splicing in the absence and presence of Tat. HEK293T cells were co-transfected with the pLTR.gp140/EGFP.Rev∆38/DsRed splicing reporter together with a plasmid expressing Rev, in the absence ( a , b ) or presence ( c , d ) of 100 ng of pTat101 (AD8)-Flag expression plasmid and then treated with a panel of LRAs or <t>DMSO</t> diluent control (n = 5). EGFP (unspliced) and DsRed (spliced) expression were measured using flow cytometry. Comparisons of each condition to DMSO were made using 2-way ANOVA test. Only statistically significant comparisons are shown *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. The black lines represent the mean ± SEM. <t>DMSO</t> <t>(1:5000),</t> VOR = vorinostat (0.5 μM), PAN = panobinostat (30 nM), JQ1 (+) (1 μM), CTN = chaetocin (30 nM), DIS = disulfiram (500 nM), or PMA/PHA = phorbol myristate acetate/phytohaemagglutinin (10 nM PMA, 10 μg/mL PHA)
Dmso, supplied by Merck & Co, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/dmso/product/Merck & Co
Average 90 stars, based on 1 article reviews
dmso - by Bioz Stars, 2026-04
90/100 stars
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dimethylsulfoxide (dmso  (Merck & Co)
90
Merck & Co dimethylsulfoxide (dmso
JQ1 but not HDACi can increase splicing in the absence and presence of Tat. HEK293T cells were co-transfected with the pLTR.gp140/EGFP.Rev∆38/DsRed splicing reporter together with a plasmid expressing Rev, in the absence ( a , b ) or presence ( c , d ) of 100 ng of pTat101 (AD8)-Flag expression plasmid and then treated with a panel of LRAs or <t>DMSO</t> diluent control (n = 5). EGFP (unspliced) and DsRed (spliced) expression were measured using flow cytometry. Comparisons of each condition to DMSO were made using 2-way ANOVA test. Only statistically significant comparisons are shown *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. The black lines represent the mean ± SEM. <t>DMSO</t> <t>(1:5000),</t> VOR = vorinostat (0.5 μM), PAN = panobinostat (30 nM), JQ1 (+) (1 μM), CTN = chaetocin (30 nM), DIS = disulfiram (500 nM), or PMA/PHA = phorbol myristate acetate/phytohaemagglutinin (10 nM PMA, 10 μg/mL PHA)
Dimethylsulfoxide (Dmso, supplied by Merck & Co, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/dimethylsulfoxide (dmso/product/Merck & Co
Average 90 stars, based on 1 article reviews
dimethylsulfoxide (dmso - by Bioz Stars, 2026-04
90/100 stars
  Buy from Supplier

Image Search Results


JQ1 but not HDACi can increase splicing in the absence and presence of Tat. HEK293T cells were co-transfected with the pLTR.gp140/EGFP.Rev∆38/DsRed splicing reporter together with a plasmid expressing Rev, in the absence ( a , b ) or presence ( c , d ) of 100 ng of pTat101 (AD8)-Flag expression plasmid and then treated with a panel of LRAs or DMSO diluent control (n = 5). EGFP (unspliced) and DsRed (spliced) expression were measured using flow cytometry. Comparisons of each condition to DMSO were made using 2-way ANOVA test. Only statistically significant comparisons are shown *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. The black lines represent the mean ± SEM. DMSO (1:5000), VOR = vorinostat (0.5 μM), PAN = panobinostat (30 nM), JQ1 (+) (1 μM), CTN = chaetocin (30 nM), DIS = disulfiram (500 nM), or PMA/PHA = phorbol myristate acetate/phytohaemagglutinin (10 nM PMA, 10 μg/mL PHA)

Journal: Retrovirology

Article Title: HIV latency reversing agents act through Tat post translational modifications

doi: 10.1186/s12977-018-0421-6

Figure Lengend Snippet: JQ1 but not HDACi can increase splicing in the absence and presence of Tat. HEK293T cells were co-transfected with the pLTR.gp140/EGFP.Rev∆38/DsRed splicing reporter together with a plasmid expressing Rev, in the absence ( a , b ) or presence ( c , d ) of 100 ng of pTat101 (AD8)-Flag expression plasmid and then treated with a panel of LRAs or DMSO diluent control (n = 5). EGFP (unspliced) and DsRed (spliced) expression were measured using flow cytometry. Comparisons of each condition to DMSO were made using 2-way ANOVA test. Only statistically significant comparisons are shown *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. The black lines represent the mean ± SEM. DMSO (1:5000), VOR = vorinostat (0.5 μM), PAN = panobinostat (30 nM), JQ1 (+) (1 μM), CTN = chaetocin (30 nM), DIS = disulfiram (500 nM), or PMA/PHA = phorbol myristate acetate/phytohaemagglutinin (10 nM PMA, 10 μg/mL PHA)

Article Snippet: Cells were incubated for 5 h prior to treatment with DMSO (1:5000, #67-68-S Merck), vorinostat (0.5 μM, #10009929 Cayman Chemical or #S1047 Selleck Chemicals), panobinostat (30 nM, #P180500 TRC or #S1030 Selleck Chemicals), JQ1 (+) (1 μM, #11187 Cayman Chemical or #S7110 Selleck Chemicals), JQ1 (−) (1 μM, #11232 Cayman Chemical), chaetocin (30 nM, #C9492 Sigma), disulfiram (500 nM, #D3374 LKT or #S1680 Selleck Chemicals), or PMA/PHA (10 nM PMA, #16561-29-8 Sigma-Aldrich/10 μg/mL PHA, #HA15/R30852701 Remel).

Techniques: Transfection, Plasmid Preparation, Expressing, Flow Cytometry

JQ1 consistently rescued HIV D4A7 splicing. HEK293T cells were transfected with the pLTR.gp140/EGFP.Rev∆38/DsRed splicing reporter without ( a ) or with 100 ng of pTat101 (AD8)-Flag that was either wild-type (shown in Fig. ) or had the specific mutations: b K28A, c K50A, d K50/51A, e K71A or f R53A. Transfected cells were then treated with a panel of LRAs for 48 h, harvested and DsRed expression was quantified using flow cytometry. The fold change in the proportion of spliced product [DsRed/(DsRed + EGFP) × 100] in the no Tat or Tat mutants relative to WT Tat+ DMSO is represented. Comparisons of each condition to DMSO were made using the 2-way ANOVA test. Only statistically significant comparisons are shown *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. The black lines represent the mean ± SEM. DMSO (1:5000), VOR = vorinostat (0.5 μM), PAN = panobinostat (30 nM), JQ1 (+) (1 μM), CTN = chaetocin (30 nM), DIS = disulfiram (500 nM), or PMA/PHA = phorbol myristate acetate/phytohaemagglutinin (10 nM PMA, 10 μg/mL PHA)

Journal: Retrovirology

Article Title: HIV latency reversing agents act through Tat post translational modifications

doi: 10.1186/s12977-018-0421-6

Figure Lengend Snippet: JQ1 consistently rescued HIV D4A7 splicing. HEK293T cells were transfected with the pLTR.gp140/EGFP.Rev∆38/DsRed splicing reporter without ( a ) or with 100 ng of pTat101 (AD8)-Flag that was either wild-type (shown in Fig. ) or had the specific mutations: b K28A, c K50A, d K50/51A, e K71A or f R53A. Transfected cells were then treated with a panel of LRAs for 48 h, harvested and DsRed expression was quantified using flow cytometry. The fold change in the proportion of spliced product [DsRed/(DsRed + EGFP) × 100] in the no Tat or Tat mutants relative to WT Tat+ DMSO is represented. Comparisons of each condition to DMSO were made using the 2-way ANOVA test. Only statistically significant comparisons are shown *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. The black lines represent the mean ± SEM. DMSO (1:5000), VOR = vorinostat (0.5 μM), PAN = panobinostat (30 nM), JQ1 (+) (1 μM), CTN = chaetocin (30 nM), DIS = disulfiram (500 nM), or PMA/PHA = phorbol myristate acetate/phytohaemagglutinin (10 nM PMA, 10 μg/mL PHA)

Article Snippet: Cells were incubated for 5 h prior to treatment with DMSO (1:5000, #67-68-S Merck), vorinostat (0.5 μM, #10009929 Cayman Chemical or #S1047 Selleck Chemicals), panobinostat (30 nM, #P180500 TRC or #S1030 Selleck Chemicals), JQ1 (+) (1 μM, #11187 Cayman Chemical or #S7110 Selleck Chemicals), JQ1 (−) (1 μM, #11232 Cayman Chemical), chaetocin (30 nM, #C9492 Sigma), disulfiram (500 nM, #D3374 LKT or #S1680 Selleck Chemicals), or PMA/PHA (10 nM PMA, #16561-29-8 Sigma-Aldrich/10 μg/mL PHA, #HA15/R30852701 Remel).

Techniques: Transfection, Expressing, Flow Cytometry

JQ1 can rescue the splicing activity lost by Tat mutants. HEK293T cells were transfected with the pLTR.gp140/EGFP.Rev∆38/DsRed splicing reporter and 100 ng of pTat101 (AD8) WT or with specific mutations (K28A, K50A, K50/51A, K71A and R53A). Cells were treated with DMSO (D, 1:5000) or JQ1 (J, 1 μM), harvested at 48 h and DsRed and EGFP expression quantified using flow cytometry. a Data were represented as the proportion of spliced product [DsRed/(DsRed + EGFP) × 100] relative to WT Tat+ DMSO. Comparisons between DMSO and JQ1 for either no Tat, WT Tat or each mutant Tat were made using multiple paired T tests. b The difference between JQ1 and DMSO in the proportion of spliced product [DsRed/(DsRed + EGFP) × 100] was calculated for each Tat mutant, no Tat or WT Tat, and then compared to the difference with WT Tat101. Only statistically significant comparisons are shown *p < 0.05; **p < 0.01; ***p < 0.001. The black lines represent the mean ± SEM (n = 5)

Journal: Retrovirology

Article Title: HIV latency reversing agents act through Tat post translational modifications

doi: 10.1186/s12977-018-0421-6

Figure Lengend Snippet: JQ1 can rescue the splicing activity lost by Tat mutants. HEK293T cells were transfected with the pLTR.gp140/EGFP.Rev∆38/DsRed splicing reporter and 100 ng of pTat101 (AD8) WT or with specific mutations (K28A, K50A, K50/51A, K71A and R53A). Cells were treated with DMSO (D, 1:5000) or JQ1 (J, 1 μM), harvested at 48 h and DsRed and EGFP expression quantified using flow cytometry. a Data were represented as the proportion of spliced product [DsRed/(DsRed + EGFP) × 100] relative to WT Tat+ DMSO. Comparisons between DMSO and JQ1 for either no Tat, WT Tat or each mutant Tat were made using multiple paired T tests. b The difference between JQ1 and DMSO in the proportion of spliced product [DsRed/(DsRed + EGFP) × 100] was calculated for each Tat mutant, no Tat or WT Tat, and then compared to the difference with WT Tat101. Only statistically significant comparisons are shown *p < 0.05; **p < 0.01; ***p < 0.001. The black lines represent the mean ± SEM (n = 5)

Article Snippet: Cells were incubated for 5 h prior to treatment with DMSO (1:5000, #67-68-S Merck), vorinostat (0.5 μM, #10009929 Cayman Chemical or #S1047 Selleck Chemicals), panobinostat (30 nM, #P180500 TRC or #S1030 Selleck Chemicals), JQ1 (+) (1 μM, #11187 Cayman Chemical or #S7110 Selleck Chemicals), JQ1 (−) (1 μM, #11232 Cayman Chemical), chaetocin (30 nM, #C9492 Sigma), disulfiram (500 nM, #D3374 LKT or #S1680 Selleck Chemicals), or PMA/PHA (10 nM PMA, #16561-29-8 Sigma-Aldrich/10 μg/mL PHA, #HA15/R30852701 Remel).

Techniques: Activity Assay, Transfection, Expressing, Flow Cytometry, Mutagenesis

BRD4 mediates HIV D4-A7 RNA splicing. HEK293T cells were co-transfected with the pLTR.gp140/EGFP.Rev∆38/DsRed splicing reporter, 20 ng of pRev and 100 ng of pTat101 (AD8) without (wild-type, WT) or with specific mutations (K28A, K50A, K50/51A, K71A and R53A) then treated with DMSO, 1 μM JQ1 (+) or JQ1 (−). Cells were harvested at 48 h, EGFP and DsRed expression was quantified by flow cytometry. a The flow cytometry gating strategy used to identify % EGFP and % DsRed positive cells in a representative result from n = 3 independent experiments, each conducted in triplicate. b The mean percentage of spliced product DsRed/(DsRed + EGFP) from the 3 independent experiments is shown. Comparisons of each condition to JQ1 (+) were made using Friedman nonparametric test. Only statistically significant comparisons are shown *p < 0.05; **p < 0.01

Journal: Retrovirology

Article Title: HIV latency reversing agents act through Tat post translational modifications

doi: 10.1186/s12977-018-0421-6

Figure Lengend Snippet: BRD4 mediates HIV D4-A7 RNA splicing. HEK293T cells were co-transfected with the pLTR.gp140/EGFP.Rev∆38/DsRed splicing reporter, 20 ng of pRev and 100 ng of pTat101 (AD8) without (wild-type, WT) or with specific mutations (K28A, K50A, K50/51A, K71A and R53A) then treated with DMSO, 1 μM JQ1 (+) or JQ1 (−). Cells were harvested at 48 h, EGFP and DsRed expression was quantified by flow cytometry. a The flow cytometry gating strategy used to identify % EGFP and % DsRed positive cells in a representative result from n = 3 independent experiments, each conducted in triplicate. b The mean percentage of spliced product DsRed/(DsRed + EGFP) from the 3 independent experiments is shown. Comparisons of each condition to JQ1 (+) were made using Friedman nonparametric test. Only statistically significant comparisons are shown *p < 0.05; **p < 0.01

Article Snippet: Cells were incubated for 5 h prior to treatment with DMSO (1:5000, #67-68-S Merck), vorinostat (0.5 μM, #10009929 Cayman Chemical or #S1047 Selleck Chemicals), panobinostat (30 nM, #P180500 TRC or #S1030 Selleck Chemicals), JQ1 (+) (1 μM, #11187 Cayman Chemical or #S7110 Selleck Chemicals), JQ1 (−) (1 μM, #11232 Cayman Chemical), chaetocin (30 nM, #C9492 Sigma), disulfiram (500 nM, #D3374 LKT or #S1680 Selleck Chemicals), or PMA/PHA (10 nM PMA, #16561-29-8 Sigma-Aldrich/10 μg/mL PHA, #HA15/R30852701 Remel).

Techniques: Transfection, Expressing, Flow Cytometry