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Synaptic Systems anti-gfp chicken polyclonal #132006
a GFP immunofluorescence confirmed the transduction of AAV-shCtr and AAV-shRTP801 in 9-week-old WT and R6/1 mice striatal cells. A secondary control was performed without the incubation of primary <t>antibody</t> <t>(anti-GFP).</t> Scale bar 450 μm. b Striatal lysates of WT and R6/1 injected with AAV-shCtr ( n = 6 WT and n = 6 R6/1) or AAV-shRTP801 ( n = 6 WT and n = 7 R6/1) were subjected to WB. Membranes were probed against RTP801, GFP, and actin as a loading control. Graph show the densitometric quantification of RTP801 signal. Data are shown as a mean ± SEM and were analyzed with two-way ANOVA followed by Bonferroni’s multiple comparisons test for post hoc analyses (* P < 0.05 vs. WT AAV-shCtr # P < 0.05 vs. R6/1 AAV-shCtr). c Five weeks after adeno-associated transduction, motor learning was assessed in the same animals by the accelerating rotarod ( n = 8 WT-shCtr, n = 8 WT shRTP801, n = 9 R6/1-shCtr, n = 9 R6/1-shRTP801). The graph shows the latency to fall as the mean of three trials tested each day. Values are expressed as mean ± SEM and were analyzed with two-way ANOVA followed by Bonferroni’s multiple comparisons test for post hoc analyses (* P < 0.05, ** P < 0.01, and *** P < 0.001 R6/1-shCtr vs. WT-shCtr and # P < 0.05 R6/1-shRTP801 vs. R6/1-shCtr).
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TransGen biotech co mouse anti-gfp mab
a GFP immunofluorescence confirmed the transduction of AAV-shCtr and AAV-shRTP801 in 9-week-old WT and R6/1 mice striatal cells. A secondary control was performed without the incubation of primary <t>antibody</t> <t>(anti-GFP).</t> Scale bar 450 μm. b Striatal lysates of WT and R6/1 injected with AAV-shCtr ( n = 6 WT and n = 6 R6/1) or AAV-shRTP801 ( n = 6 WT and n = 7 R6/1) were subjected to WB. Membranes were probed against RTP801, GFP, and actin as a loading control. Graph show the densitometric quantification of RTP801 signal. Data are shown as a mean ± SEM and were analyzed with two-way ANOVA followed by Bonferroni’s multiple comparisons test for post hoc analyses (* P < 0.05 vs. WT AAV-shCtr # P < 0.05 vs. R6/1 AAV-shCtr). c Five weeks after adeno-associated transduction, motor learning was assessed in the same animals by the accelerating rotarod ( n = 8 WT-shCtr, n = 8 WT shRTP801, n = 9 R6/1-shCtr, n = 9 R6/1-shRTP801). The graph shows the latency to fall as the mean of three trials tested each day. Values are expressed as mean ± SEM and were analyzed with two-way ANOVA followed by Bonferroni’s multiple comparisons test for post hoc analyses (* P < 0.05, ** P < 0.01, and *** P < 0.001 R6/1-shCtr vs. WT-shCtr and # P < 0.05 R6/1-shRTP801 vs. R6/1-shCtr).
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Image Search Results


a GFP immunofluorescence confirmed the transduction of AAV-shCtr and AAV-shRTP801 in 9-week-old WT and R6/1 mice striatal cells. A secondary control was performed without the incubation of primary antibody (anti-GFP). Scale bar 450 μm. b Striatal lysates of WT and R6/1 injected with AAV-shCtr ( n = 6 WT and n = 6 R6/1) or AAV-shRTP801 ( n = 6 WT and n = 7 R6/1) were subjected to WB. Membranes were probed against RTP801, GFP, and actin as a loading control. Graph show the densitometric quantification of RTP801 signal. Data are shown as a mean ± SEM and were analyzed with two-way ANOVA followed by Bonferroni’s multiple comparisons test for post hoc analyses (* P < 0.05 vs. WT AAV-shCtr # P < 0.05 vs. R6/1 AAV-shCtr). c Five weeks after adeno-associated transduction, motor learning was assessed in the same animals by the accelerating rotarod ( n = 8 WT-shCtr, n = 8 WT shRTP801, n = 9 R6/1-shCtr, n = 9 R6/1-shRTP801). The graph shows the latency to fall as the mean of three trials tested each day. Values are expressed as mean ± SEM and were analyzed with two-way ANOVA followed by Bonferroni’s multiple comparisons test for post hoc analyses (* P < 0.05, ** P < 0.01, and *** P < 0.001 R6/1-shCtr vs. WT-shCtr and # P < 0.05 R6/1-shRTP801 vs. R6/1-shCtr).

Journal: Cell Death & Disease

Article Title: Synaptic RTP801 contributes to motor-learning dysfunction in Huntington’s disease

doi: 10.1038/s41419-020-02775-5

Figure Lengend Snippet: a GFP immunofluorescence confirmed the transduction of AAV-shCtr and AAV-shRTP801 in 9-week-old WT and R6/1 mice striatal cells. A secondary control was performed without the incubation of primary antibody (anti-GFP). Scale bar 450 μm. b Striatal lysates of WT and R6/1 injected with AAV-shCtr ( n = 6 WT and n = 6 R6/1) or AAV-shRTP801 ( n = 6 WT and n = 7 R6/1) were subjected to WB. Membranes were probed against RTP801, GFP, and actin as a loading control. Graph show the densitometric quantification of RTP801 signal. Data are shown as a mean ± SEM and were analyzed with two-way ANOVA followed by Bonferroni’s multiple comparisons test for post hoc analyses (* P < 0.05 vs. WT AAV-shCtr # P < 0.05 vs. R6/1 AAV-shCtr). c Five weeks after adeno-associated transduction, motor learning was assessed in the same animals by the accelerating rotarod ( n = 8 WT-shCtr, n = 8 WT shRTP801, n = 9 R6/1-shCtr, n = 9 R6/1-shRTP801). The graph shows the latency to fall as the mean of three trials tested each day. Values are expressed as mean ± SEM and were analyzed with two-way ANOVA followed by Bonferroni’s multiple comparisons test for post hoc analyses (* P < 0.05, ** P < 0.01, and *** P < 0.001 R6/1-shCtr vs. WT-shCtr and # P < 0.05 R6/1-shRTP801 vs. R6/1-shCtr).

Article Snippet: After, slices were incubated overnight at 4 °C with the primary antibodies anti-GFP chicken polyclonal (Synaptic Systems, #132006) diluted 1:500 in SuperBlock-PBS 0.3% Triton X-100.

Techniques: Immunofluorescence, Transduction, Control, Incubation, Injection