prk5 egfp tau wt Search Results


93
Addgene inc gfp tau
Gfp Tau, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/prk5+egfp+tau+wt/pRK5-EGFP-Tau+(Plasmid+%2346904)/bio_rxiv__456608-49-28-35
Average 93 stars, based on 1 article reviews
gfp tau - by Bioz Stars, 2026-09
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93
Addgene inc prk5 egfp tau p301l
Prk5 Egfp Tau P301l, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/prk5+egfp+tau+wt/pRK5-EGFP-Tau+P301L+(Plasmid+%2346908)/pmc08595217-37-86-85
Average 93 stars, based on 1 article reviews
prk5 egfp tau p301l - by Bioz Stars, 2026-09
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Addgene inc prk5 egfp tau e14
Pseudo-phosphorylated tau relocates the AIS down the axon in a process mediated by microtubules. Representative photomicrograph of A14- ( top ) and <t>E14-tau-EGFP</t> ( lower ) transfected hippocampal neurons stained for ankyrin G a 24 h and b 48 h after transfection. Arrows indicate the start, middle and end of the AIS as determined by quantitative analysis of the c , d axonal fluorescence profile. The dashed line indicates the normalized detection threshold. Quantification of ankyrin G labeling in neurons transfected with E14- ( blue ) and A14-tau ( black ) for e 24 h (start p = 0.48, middle p = 0.94, end p = 0.54; E14 n = 61, A14 n = 46) and f 48 h (start p = 0.0001, middle p = 0.0027, end p = 0.0017; E14 n = 47, A14 n = 62). AIS location of E14- and A14-tau-transfected neurons labeled for g βIV spectrin (start p = 0.0041, middle p = 0.0024, end p = 0.0084; E14 n = 55, A14 n = 52) and h Na V 1.6 (start p = 0.0042, middle p = 0.0045, end p = 0.0316; E14 n = 53, A14 n = 53). Using ankyrin G staining, the role of site-specific phosphorylation in AIS relocation was determined: i AT180 ( start p = 0.0138, middle p = 0.44, end p = 0.76; AT180E n = 53, AT180A n = 52), j 12E8 (start p = 0.0183, middle p = 0.0352, end p = 0.09; 12E8E n = 54, 12E8A n = 51), and k PFH1 (start p = 0.34, middle p = 0.56, end p = 0.75; PHF1E n = 50, PHF1A n = 38). l Treatment with 0.1 µM taxol ( magenta ) prevents AIS relocation (start, ANOVA, F = 8.05, p = 0.0005; middle, ANOVA, F = 4.057, p = 0.0191; end, ANOVA, F = 6.614, p = 0.0017; E14 n = 57, A14 n = 54, E14+ taxol n = 51). m Microtubule destabilization with 0.05 µM nocodazole ( green ) relocates the AIS ( gray , control, start: p = 0.0169, middle: p = 0.0297, end: p = 0.0856; nocodazole n = 54, control n = 55). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p ≤ 0.0001. Data presented as mean ± SEM. Scale bar 5 µm. Statistical comparisons were made using an unpaired two-tailed Student’s t test or a one-way ANOVA with a Sidak’s post hoc test
Prk5 Egfp Tau E14, supplied by Addgene inc, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/prk5+egfp+tau+wt/pRK5-EGFP-Tau+E14+(Plasmid+%2346907)/pmc05389999-64-47-51
Average 91 stars, based on 1 article reviews
prk5 egfp tau e14 - by Bioz Stars, 2026-09
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93
Addgene inc tau plasmid
Pseudo-phosphorylated tau relocates the AIS down the axon in a process mediated by microtubules. Representative photomicrograph of A14- ( top ) and <t>E14-tau-EGFP</t> ( lower ) transfected hippocampal neurons stained for ankyrin G a 24 h and b 48 h after transfection. Arrows indicate the start, middle and end of the AIS as determined by quantitative analysis of the c , d axonal fluorescence profile. The dashed line indicates the normalized detection threshold. Quantification of ankyrin G labeling in neurons transfected with E14- ( blue ) and A14-tau ( black ) for e 24 h (start p = 0.48, middle p = 0.94, end p = 0.54; E14 n = 61, A14 n = 46) and f 48 h (start p = 0.0001, middle p = 0.0027, end p = 0.0017; E14 n = 47, A14 n = 62). AIS location of E14- and A14-tau-transfected neurons labeled for g βIV spectrin (start p = 0.0041, middle p = 0.0024, end p = 0.0084; E14 n = 55, A14 n = 52) and h Na V 1.6 (start p = 0.0042, middle p = 0.0045, end p = 0.0316; E14 n = 53, A14 n = 53). Using ankyrin G staining, the role of site-specific phosphorylation in AIS relocation was determined: i AT180 ( start p = 0.0138, middle p = 0.44, end p = 0.76; AT180E n = 53, AT180A n = 52), j 12E8 (start p = 0.0183, middle p = 0.0352, end p = 0.09; 12E8E n = 54, 12E8A n = 51), and k PFH1 (start p = 0.34, middle p = 0.56, end p = 0.75; PHF1E n = 50, PHF1A n = 38). l Treatment with 0.1 µM taxol ( magenta ) prevents AIS relocation (start, ANOVA, F = 8.05, p = 0.0005; middle, ANOVA, F = 4.057, p = 0.0191; end, ANOVA, F = 6.614, p = 0.0017; E14 n = 57, A14 n = 54, E14+ taxol n = 51). m Microtubule destabilization with 0.05 µM nocodazole ( green ) relocates the AIS ( gray , control, start: p = 0.0169, middle: p = 0.0297, end: p = 0.0856; nocodazole n = 54, control n = 55). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p ≤ 0.0001. Data presented as mean ± SEM. Scale bar 5 µm. Statistical comparisons were made using an unpaired two-tailed Student’s t test or a one-way ANOVA with a Sidak’s post hoc test
Tau Plasmid, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/prk5+egfp+tau+wt/pRK5-EGFP-Tau+E14+P301L+(Plasmid+%2346909)/pmc12238675-70-16-21
Average 93 stars, based on 1 article reviews
tau plasmid - by Bioz Stars, 2026-09
93/100 stars
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Addgene inc prk5 egfp tau ap
Pseudo-phosphorylated tau relocates the AIS down the axon in a process mediated by microtubules. Representative photomicrograph of A14- ( top ) and <t>E14-tau-EGFP</t> ( lower ) transfected hippocampal neurons stained for ankyrin G a 24 h and b 48 h after transfection. Arrows indicate the start, middle and end of the AIS as determined by quantitative analysis of the c , d axonal fluorescence profile. The dashed line indicates the normalized detection threshold. Quantification of ankyrin G labeling in neurons transfected with E14- ( blue ) and A14-tau ( black ) for e 24 h (start p = 0.48, middle p = 0.94, end p = 0.54; E14 n = 61, A14 n = 46) and f 48 h (start p = 0.0001, middle p = 0.0027, end p = 0.0017; E14 n = 47, A14 n = 62). AIS location of E14- and A14-tau-transfected neurons labeled for g βIV spectrin (start p = 0.0041, middle p = 0.0024, end p = 0.0084; E14 n = 55, A14 n = 52) and h Na V 1.6 (start p = 0.0042, middle p = 0.0045, end p = 0.0316; E14 n = 53, A14 n = 53). Using ankyrin G staining, the role of site-specific phosphorylation in AIS relocation was determined: i AT180 ( start p = 0.0138, middle p = 0.44, end p = 0.76; AT180E n = 53, AT180A n = 52), j 12E8 (start p = 0.0183, middle p = 0.0352, end p = 0.09; 12E8E n = 54, 12E8A n = 51), and k PFH1 (start p = 0.34, middle p = 0.56, end p = 0.75; PHF1E n = 50, PHF1A n = 38). l Treatment with 0.1 µM taxol ( magenta ) prevents AIS relocation (start, ANOVA, F = 8.05, p = 0.0005; middle, ANOVA, F = 4.057, p = 0.0191; end, ANOVA, F = 6.614, p = 0.0017; E14 n = 57, A14 n = 54, E14+ taxol n = 51). m Microtubule destabilization with 0.05 µM nocodazole ( green ) relocates the AIS ( gray , control, start: p = 0.0169, middle: p = 0.0297, end: p = 0.0856; nocodazole n = 54, control n = 55). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p ≤ 0.0001. Data presented as mean ± SEM. Scale bar 5 µm. Statistical comparisons were made using an unpaired two-tailed Student’s t test or a one-way ANOVA with a Sidak’s post hoc test
Prk5 Egfp Tau Ap, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/prk5+egfp+tau+wt/pRK5-EGFP-Tau+AP+(Plasmid+%2346905)/pmc05389999-64-56-60
Average 93 stars, based on 1 article reviews
prk5 egfp tau ap - by Bioz Stars, 2026-09
93/100 stars
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93
Addgene inc app plasmid
Pseudo-phosphorylated tau relocates the AIS down the axon in a process mediated by microtubules. Representative photomicrograph of A14- ( top ) and <t>E14-tau-EGFP</t> ( lower ) transfected hippocampal neurons stained for ankyrin G a 24 h and b 48 h after transfection. Arrows indicate the start, middle and end of the AIS as determined by quantitative analysis of the c , d axonal fluorescence profile. The dashed line indicates the normalized detection threshold. Quantification of ankyrin G labeling in neurons transfected with E14- ( blue ) and A14-tau ( black ) for e 24 h (start p = 0.48, middle p = 0.94, end p = 0.54; E14 n = 61, A14 n = 46) and f 48 h (start p = 0.0001, middle p = 0.0027, end p = 0.0017; E14 n = 47, A14 n = 62). AIS location of E14- and A14-tau-transfected neurons labeled for g βIV spectrin (start p = 0.0041, middle p = 0.0024, end p = 0.0084; E14 n = 55, A14 n = 52) and h Na V 1.6 (start p = 0.0042, middle p = 0.0045, end p = 0.0316; E14 n = 53, A14 n = 53). Using ankyrin G staining, the role of site-specific phosphorylation in AIS relocation was determined: i AT180 ( start p = 0.0138, middle p = 0.44, end p = 0.76; AT180E n = 53, AT180A n = 52), j 12E8 (start p = 0.0183, middle p = 0.0352, end p = 0.09; 12E8E n = 54, 12E8A n = 51), and k PFH1 (start p = 0.34, middle p = 0.56, end p = 0.75; PHF1E n = 50, PHF1A n = 38). l Treatment with 0.1 µM taxol ( magenta ) prevents AIS relocation (start, ANOVA, F = 8.05, p = 0.0005; middle, ANOVA, F = 4.057, p = 0.0191; end, ANOVA, F = 6.614, p = 0.0017; E14 n = 57, A14 n = 54, E14+ taxol n = 51). m Microtubule destabilization with 0.05 µM nocodazole ( green ) relocates the AIS ( gray , control, start: p = 0.0169, middle: p = 0.0297, end: p = 0.0856; nocodazole n = 54, control n = 55). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p ≤ 0.0001. Data presented as mean ± SEM. Scale bar 5 µm. Statistical comparisons were made using an unpaired two-tailed Student’s t test or a one-way ANOVA with a Sidak’s post hoc test
App Plasmid, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/prk5+egfp+tau+wt/pCAX+APP+Swe%2FInd+(Plasmid+%2330145)/pm40629914-52-9-20
Average 93 stars, based on 1 article reviews
app plasmid - by Bioz Stars, 2026-09
93/100 stars
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90
Promega pbit1.1-n[tk/lgbit]
Pseudo-phosphorylated tau relocates the AIS down the axon in a process mediated by microtubules. Representative photomicrograph of A14- ( top ) and <t>E14-tau-EGFP</t> ( lower ) transfected hippocampal neurons stained for ankyrin G a 24 h and b 48 h after transfection. Arrows indicate the start, middle and end of the AIS as determined by quantitative analysis of the c , d axonal fluorescence profile. The dashed line indicates the normalized detection threshold. Quantification of ankyrin G labeling in neurons transfected with E14- ( blue ) and A14-tau ( black ) for e 24 h (start p = 0.48, middle p = 0.94, end p = 0.54; E14 n = 61, A14 n = 46) and f 48 h (start p = 0.0001, middle p = 0.0027, end p = 0.0017; E14 n = 47, A14 n = 62). AIS location of E14- and A14-tau-transfected neurons labeled for g βIV spectrin (start p = 0.0041, middle p = 0.0024, end p = 0.0084; E14 n = 55, A14 n = 52) and h Na V 1.6 (start p = 0.0042, middle p = 0.0045, end p = 0.0316; E14 n = 53, A14 n = 53). Using ankyrin G staining, the role of site-specific phosphorylation in AIS relocation was determined: i AT180 ( start p = 0.0138, middle p = 0.44, end p = 0.76; AT180E n = 53, AT180A n = 52), j 12E8 (start p = 0.0183, middle p = 0.0352, end p = 0.09; 12E8E n = 54, 12E8A n = 51), and k PFH1 (start p = 0.34, middle p = 0.56, end p = 0.75; PHF1E n = 50, PHF1A n = 38). l Treatment with 0.1 µM taxol ( magenta ) prevents AIS relocation (start, ANOVA, F = 8.05, p = 0.0005; middle, ANOVA, F = 4.057, p = 0.0191; end, ANOVA, F = 6.614, p = 0.0017; E14 n = 57, A14 n = 54, E14+ taxol n = 51). m Microtubule destabilization with 0.05 µM nocodazole ( green ) relocates the AIS ( gray , control, start: p = 0.0169, middle: p = 0.0297, end: p = 0.0856; nocodazole n = 54, control n = 55). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p ≤ 0.0001. Data presented as mean ± SEM. Scale bar 5 µm. Statistical comparisons were made using an unpaired two-tailed Student’s t test or a one-way ANOVA with a Sidak’s post hoc test
Pbit1.1 N[Tk/Lgbit], supplied by Promega, 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/product/prk5+egfp+tau+wt/pbit1+1+plasmids/pmc10277490-115-58-59
Average 90 stars, based on 1 article reviews
pbit1.1-n[tk/lgbit] - by Bioz Stars, 2026-09
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93
Addgene inc egfp pcdna3 3 egfp
Pseudo-phosphorylated tau relocates the AIS down the axon in a process mediated by microtubules. Representative photomicrograph of A14- ( top ) and <t>E14-tau-EGFP</t> ( lower ) transfected hippocampal neurons stained for ankyrin G a 24 h and b 48 h after transfection. Arrows indicate the start, middle and end of the AIS as determined by quantitative analysis of the c , d axonal fluorescence profile. The dashed line indicates the normalized detection threshold. Quantification of ankyrin G labeling in neurons transfected with E14- ( blue ) and A14-tau ( black ) for e 24 h (start p = 0.48, middle p = 0.94, end p = 0.54; E14 n = 61, A14 n = 46) and f 48 h (start p = 0.0001, middle p = 0.0027, end p = 0.0017; E14 n = 47, A14 n = 62). AIS location of E14- and A14-tau-transfected neurons labeled for g βIV spectrin (start p = 0.0041, middle p = 0.0024, end p = 0.0084; E14 n = 55, A14 n = 52) and h Na V 1.6 (start p = 0.0042, middle p = 0.0045, end p = 0.0316; E14 n = 53, A14 n = 53). Using ankyrin G staining, the role of site-specific phosphorylation in AIS relocation was determined: i AT180 ( start p = 0.0138, middle p = 0.44, end p = 0.76; AT180E n = 53, AT180A n = 52), j 12E8 (start p = 0.0183, middle p = 0.0352, end p = 0.09; 12E8E n = 54, 12E8A n = 51), and k PFH1 (start p = 0.34, middle p = 0.56, end p = 0.75; PHF1E n = 50, PHF1A n = 38). l Treatment with 0.1 µM taxol ( magenta ) prevents AIS relocation (start, ANOVA, F = 8.05, p = 0.0005; middle, ANOVA, F = 4.057, p = 0.0191; end, ANOVA, F = 6.614, p = 0.0017; E14 n = 57, A14 n = 54, E14+ taxol n = 51). m Microtubule destabilization with 0.05 µM nocodazole ( green ) relocates the AIS ( gray , control, start: p = 0.0169, middle: p = 0.0297, end: p = 0.0856; nocodazole n = 54, control n = 55). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p ≤ 0.0001. Data presented as mean ± SEM. Scale bar 5 µm. Statistical comparisons were made using an unpaired two-tailed Student’s t test or a one-way ANOVA with a Sidak’s post hoc test
Egfp Pcdna3 3 Egfp, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/prk5+egfp+tau+wt/pcDNA3%2E3_eGFP+(Plasmid+%2326822)/pm39753133-2005-22-20
Average 93 stars, based on 1 article reviews
egfp pcdna3 3 egfp - by Bioz Stars, 2026-09
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99
New England Biolabs gibson assembly cloning kit
Pseudo-phosphorylated tau relocates the AIS down the axon in a process mediated by microtubules. Representative photomicrograph of A14- ( top ) and <t>E14-tau-EGFP</t> ( lower ) transfected hippocampal neurons stained for ankyrin G a 24 h and b 48 h after transfection. Arrows indicate the start, middle and end of the AIS as determined by quantitative analysis of the c , d axonal fluorescence profile. The dashed line indicates the normalized detection threshold. Quantification of ankyrin G labeling in neurons transfected with E14- ( blue ) and A14-tau ( black ) for e 24 h (start p = 0.48, middle p = 0.94, end p = 0.54; E14 n = 61, A14 n = 46) and f 48 h (start p = 0.0001, middle p = 0.0027, end p = 0.0017; E14 n = 47, A14 n = 62). AIS location of E14- and A14-tau-transfected neurons labeled for g βIV spectrin (start p = 0.0041, middle p = 0.0024, end p = 0.0084; E14 n = 55, A14 n = 52) and h Na V 1.6 (start p = 0.0042, middle p = 0.0045, end p = 0.0316; E14 n = 53, A14 n = 53). Using ankyrin G staining, the role of site-specific phosphorylation in AIS relocation was determined: i AT180 ( start p = 0.0138, middle p = 0.44, end p = 0.76; AT180E n = 53, AT180A n = 52), j 12E8 (start p = 0.0183, middle p = 0.0352, end p = 0.09; 12E8E n = 54, 12E8A n = 51), and k PFH1 (start p = 0.34, middle p = 0.56, end p = 0.75; PHF1E n = 50, PHF1A n = 38). l Treatment with 0.1 µM taxol ( magenta ) prevents AIS relocation (start, ANOVA, F = 8.05, p = 0.0005; middle, ANOVA, F = 4.057, p = 0.0191; end, ANOVA, F = 6.614, p = 0.0017; E14 n = 57, A14 n = 54, E14+ taxol n = 51). m Microtubule destabilization with 0.05 µM nocodazole ( green ) relocates the AIS ( gray , control, start: p = 0.0169, middle: p = 0.0297, end: p = 0.0856; nocodazole n = 54, control n = 55). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p ≤ 0.0001. Data presented as mean ± SEM. Scale bar 5 µm. Statistical comparisons were made using an unpaired two-tailed Student’s t test or a one-way ANOVA with a Sidak’s post hoc test
Gibson Assembly Cloning Kit, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/prk5+egfp+tau+wt/Gibson+Assembly+Cloning+Kit/custom%40e5510%4028091722
Average 99 stars, based on 1 article reviews
gibson assembly cloning kit - by Bioz Stars, 2026-09
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Promega fugene hd transfection reagent
Pseudo-phosphorylated tau relocates the AIS down the axon in a process mediated by microtubules. Representative photomicrograph of A14- ( top ) and <t>E14-tau-EGFP</t> ( lower ) transfected hippocampal neurons stained for ankyrin G a 24 h and b 48 h after transfection. Arrows indicate the start, middle and end of the AIS as determined by quantitative analysis of the c , d axonal fluorescence profile. The dashed line indicates the normalized detection threshold. Quantification of ankyrin G labeling in neurons transfected with E14- ( blue ) and A14-tau ( black ) for e 24 h (start p = 0.48, middle p = 0.94, end p = 0.54; E14 n = 61, A14 n = 46) and f 48 h (start p = 0.0001, middle p = 0.0027, end p = 0.0017; E14 n = 47, A14 n = 62). AIS location of E14- and A14-tau-transfected neurons labeled for g βIV spectrin (start p = 0.0041, middle p = 0.0024, end p = 0.0084; E14 n = 55, A14 n = 52) and h Na V 1.6 (start p = 0.0042, middle p = 0.0045, end p = 0.0316; E14 n = 53, A14 n = 53). Using ankyrin G staining, the role of site-specific phosphorylation in AIS relocation was determined: i AT180 ( start p = 0.0138, middle p = 0.44, end p = 0.76; AT180E n = 53, AT180A n = 52), j 12E8 (start p = 0.0183, middle p = 0.0352, end p = 0.09; 12E8E n = 54, 12E8A n = 51), and k PFH1 (start p = 0.34, middle p = 0.56, end p = 0.75; PHF1E n = 50, PHF1A n = 38). l Treatment with 0.1 µM taxol ( magenta ) prevents AIS relocation (start, ANOVA, F = 8.05, p = 0.0005; middle, ANOVA, F = 4.057, p = 0.0191; end, ANOVA, F = 6.614, p = 0.0017; E14 n = 57, A14 n = 54, E14+ taxol n = 51). m Microtubule destabilization with 0.05 µM nocodazole ( green ) relocates the AIS ( gray , control, start: p = 0.0169, middle: p = 0.0297, end: p = 0.0856; nocodazole n = 54, control n = 55). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p ≤ 0.0001. Data presented as mean ± SEM. Scale bar 5 µm. Statistical comparisons were made using an unpaired two-tailed Student’s t test or a one-way ANOVA with a Sidak’s post hoc test
Fugene Hd Transfection Reagent, supplied by Promega, 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/product/prk5+egfp+tau+wt/fugene+hd/10__2147_slash_ijn__s258311-57-0-7
Average 90 stars, based on 1 article reviews
fugene hd transfection reagent - by Bioz Stars, 2026-09
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Addgene inc plasmids pegfp n1 app
Pseudo-phosphorylated tau relocates the AIS down the axon in a process mediated by microtubules. Representative photomicrograph of A14- ( top ) and <t>E14-tau-EGFP</t> ( lower ) transfected hippocampal neurons stained for ankyrin G a 24 h and b 48 h after transfection. Arrows indicate the start, middle and end of the AIS as determined by quantitative analysis of the c , d axonal fluorescence profile. The dashed line indicates the normalized detection threshold. Quantification of ankyrin G labeling in neurons transfected with E14- ( blue ) and A14-tau ( black ) for e 24 h (start p = 0.48, middle p = 0.94, end p = 0.54; E14 n = 61, A14 n = 46) and f 48 h (start p = 0.0001, middle p = 0.0027, end p = 0.0017; E14 n = 47, A14 n = 62). AIS location of E14- and A14-tau-transfected neurons labeled for g βIV spectrin (start p = 0.0041, middle p = 0.0024, end p = 0.0084; E14 n = 55, A14 n = 52) and h Na V 1.6 (start p = 0.0042, middle p = 0.0045, end p = 0.0316; E14 n = 53, A14 n = 53). Using ankyrin G staining, the role of site-specific phosphorylation in AIS relocation was determined: i AT180 ( start p = 0.0138, middle p = 0.44, end p = 0.76; AT180E n = 53, AT180A n = 52), j 12E8 (start p = 0.0183, middle p = 0.0352, end p = 0.09; 12E8E n = 54, 12E8A n = 51), and k PFH1 (start p = 0.34, middle p = 0.56, end p = 0.75; PHF1E n = 50, PHF1A n = 38). l Treatment with 0.1 µM taxol ( magenta ) prevents AIS relocation (start, ANOVA, F = 8.05, p = 0.0005; middle, ANOVA, F = 4.057, p = 0.0191; end, ANOVA, F = 6.614, p = 0.0017; E14 n = 57, A14 n = 54, E14+ taxol n = 51). m Microtubule destabilization with 0.05 µM nocodazole ( green ) relocates the AIS ( gray , control, start: p = 0.0169, middle: p = 0.0297, end: p = 0.0856; nocodazole n = 54, control n = 55). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p ≤ 0.0001. Data presented as mean ± SEM. Scale bar 5 µm. Statistical comparisons were made using an unpaired two-tailed Student’s t test or a one-way ANOVA with a Sidak’s post hoc test
Plasmids Pegfp N1 App, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/prk5+egfp+tau+wt/pEGFP-n1-APP+(Plasmid+%2369924)/pmc12664514-63-1-12
Average 93 stars, based on 1 article reviews
plasmids pegfp n1 app - by Bioz Stars, 2026-09
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95
Addgene inc pll3 7
Pseudo-phosphorylated tau relocates the AIS down the axon in a process mediated by microtubules. Representative photomicrograph of A14- ( top ) and <t>E14-tau-EGFP</t> ( lower ) transfected hippocampal neurons stained for ankyrin G a 24 h and b 48 h after transfection. Arrows indicate the start, middle and end of the AIS as determined by quantitative analysis of the c , d axonal fluorescence profile. The dashed line indicates the normalized detection threshold. Quantification of ankyrin G labeling in neurons transfected with E14- ( blue ) and A14-tau ( black ) for e 24 h (start p = 0.48, middle p = 0.94, end p = 0.54; E14 n = 61, A14 n = 46) and f 48 h (start p = 0.0001, middle p = 0.0027, end p = 0.0017; E14 n = 47, A14 n = 62). AIS location of E14- and A14-tau-transfected neurons labeled for g βIV spectrin (start p = 0.0041, middle p = 0.0024, end p = 0.0084; E14 n = 55, A14 n = 52) and h Na V 1.6 (start p = 0.0042, middle p = 0.0045, end p = 0.0316; E14 n = 53, A14 n = 53). Using ankyrin G staining, the role of site-specific phosphorylation in AIS relocation was determined: i AT180 ( start p = 0.0138, middle p = 0.44, end p = 0.76; AT180E n = 53, AT180A n = 52), j 12E8 (start p = 0.0183, middle p = 0.0352, end p = 0.09; 12E8E n = 54, 12E8A n = 51), and k PFH1 (start p = 0.34, middle p = 0.56, end p = 0.75; PHF1E n = 50, PHF1A n = 38). l Treatment with 0.1 µM taxol ( magenta ) prevents AIS relocation (start, ANOVA, F = 8.05, p = 0.0005; middle, ANOVA, F = 4.057, p = 0.0191; end, ANOVA, F = 6.614, p = 0.0017; E14 n = 57, A14 n = 54, E14+ taxol n = 51). m Microtubule destabilization with 0.05 µM nocodazole ( green ) relocates the AIS ( gray , control, start: p = 0.0169, middle: p = 0.0297, end: p = 0.0856; nocodazole n = 54, control n = 55). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p ≤ 0.0001. Data presented as mean ± SEM. Scale bar 5 µm. Statistical comparisons were made using an unpaired two-tailed Student’s t test or a one-way ANOVA with a Sidak’s post hoc test
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Pseudo-phosphorylated tau relocates the AIS down the axon in a process mediated by microtubules. Representative photomicrograph of A14- ( top ) and E14-tau-EGFP ( lower ) transfected hippocampal neurons stained for ankyrin G a 24 h and b 48 h after transfection. Arrows indicate the start, middle and end of the AIS as determined by quantitative analysis of the c , d axonal fluorescence profile. The dashed line indicates the normalized detection threshold. Quantification of ankyrin G labeling in neurons transfected with E14- ( blue ) and A14-tau ( black ) for e 24 h (start p = 0.48, middle p = 0.94, end p = 0.54; E14 n = 61, A14 n = 46) and f 48 h (start p = 0.0001, middle p = 0.0027, end p = 0.0017; E14 n = 47, A14 n = 62). AIS location of E14- and A14-tau-transfected neurons labeled for g βIV spectrin (start p = 0.0041, middle p = 0.0024, end p = 0.0084; E14 n = 55, A14 n = 52) and h Na V 1.6 (start p = 0.0042, middle p = 0.0045, end p = 0.0316; E14 n = 53, A14 n = 53). Using ankyrin G staining, the role of site-specific phosphorylation in AIS relocation was determined: i AT180 ( start p = 0.0138, middle p = 0.44, end p = 0.76; AT180E n = 53, AT180A n = 52), j 12E8 (start p = 0.0183, middle p = 0.0352, end p = 0.09; 12E8E n = 54, 12E8A n = 51), and k PFH1 (start p = 0.34, middle p = 0.56, end p = 0.75; PHF1E n = 50, PHF1A n = 38). l Treatment with 0.1 µM taxol ( magenta ) prevents AIS relocation (start, ANOVA, F = 8.05, p = 0.0005; middle, ANOVA, F = 4.057, p = 0.0191; end, ANOVA, F = 6.614, p = 0.0017; E14 n = 57, A14 n = 54, E14+ taxol n = 51). m Microtubule destabilization with 0.05 µM nocodazole ( green ) relocates the AIS ( gray , control, start: p = 0.0169, middle: p = 0.0297, end: p = 0.0856; nocodazole n = 54, control n = 55). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p ≤ 0.0001. Data presented as mean ± SEM. Scale bar 5 µm. Statistical comparisons were made using an unpaired two-tailed Student’s t test or a one-way ANOVA with a Sidak’s post hoc test

Journal: Acta Neuropathologica

Article Title: Hyperphosphorylated tau causes reduced hippocampal CA1 excitability by relocating the axon initial segment

doi: 10.1007/s00401-017-1674-1

Figure Lengend Snippet: Pseudo-phosphorylated tau relocates the AIS down the axon in a process mediated by microtubules. Representative photomicrograph of A14- ( top ) and E14-tau-EGFP ( lower ) transfected hippocampal neurons stained for ankyrin G a 24 h and b 48 h after transfection. Arrows indicate the start, middle and end of the AIS as determined by quantitative analysis of the c , d axonal fluorescence profile. The dashed line indicates the normalized detection threshold. Quantification of ankyrin G labeling in neurons transfected with E14- ( blue ) and A14-tau ( black ) for e 24 h (start p = 0.48, middle p = 0.94, end p = 0.54; E14 n = 61, A14 n = 46) and f 48 h (start p = 0.0001, middle p = 0.0027, end p = 0.0017; E14 n = 47, A14 n = 62). AIS location of E14- and A14-tau-transfected neurons labeled for g βIV spectrin (start p = 0.0041, middle p = 0.0024, end p = 0.0084; E14 n = 55, A14 n = 52) and h Na V 1.6 (start p = 0.0042, middle p = 0.0045, end p = 0.0316; E14 n = 53, A14 n = 53). Using ankyrin G staining, the role of site-specific phosphorylation in AIS relocation was determined: i AT180 ( start p = 0.0138, middle p = 0.44, end p = 0.76; AT180E n = 53, AT180A n = 52), j 12E8 (start p = 0.0183, middle p = 0.0352, end p = 0.09; 12E8E n = 54, 12E8A n = 51), and k PFH1 (start p = 0.34, middle p = 0.56, end p = 0.75; PHF1E n = 50, PHF1A n = 38). l Treatment with 0.1 µM taxol ( magenta ) prevents AIS relocation (start, ANOVA, F = 8.05, p = 0.0005; middle, ANOVA, F = 4.057, p = 0.0191; end, ANOVA, F = 6.614, p = 0.0017; E14 n = 57, A14 n = 54, E14+ taxol n = 51). m Microtubule destabilization with 0.05 µM nocodazole ( green ) relocates the AIS ( gray , control, start: p = 0.0169, middle: p = 0.0297, end: p = 0.0856; nocodazole n = 54, control n = 55). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p ≤ 0.0001. Data presented as mean ± SEM. Scale bar 5 µm. Statistical comparisons were made using an unpaired two-tailed Student’s t test or a one-way ANOVA with a Sidak’s post hoc test

Article Snippet: Two mutant Tau-EGFP constructs termed E14 and A14 (all 14 serine or threonine residues T111, T153, T175, T181, S199, S202, T205, T212, T217, T231, S235, S396, S404, and S422 mutated to glutamic acid (E14) or alanine (A14), respectively) were generated by subcloning the mutant Tau fragment from pRK5-EGFP-Tau E14 (0N4R Tau, Addgene plasmid # 46907) or pRK5-EGFP-Tau AP (0N4R Tau, Addgene plasmid # 46905) into the wild-type Tau-EGFP backbone, using the Gibson assembly method (NEB E5510S).

Techniques: Transfection, Staining, Fluorescence, Labeling, Phospho-proteomics, Control, Two Tailed Test

Pseudo-phosphorylated tau reduces AP firing in a similar manner to that observed in tau transgenic mouse models. Representative traces of APs fired by a A14- ( black ), b E14-transfected ( blue ) neurons and c E14-transfected neurons treated with 0.1 µM taxol ( magenta ) following injection of a −60, 0, rheobase and 320 pA current step. d Representative traces of the initial AP fired for A14, E14 and E14+ taxol neurons. Pooled data demonstrating the AP firing, including e input–output relationships (ANOVA, F = 4.084, p = 0.0274; E14 n = 12, A14 n = 11, E14+ taxol n = 10), f AP threshold (ANOVA, F = 2.439, p = 0.10), g AP amplitude (ANOVA, F = 4.152, p = 0.0256), and h rheobase (ANOVA, F = 2.4, p = 0.11). * p < 0.05. Data are presented as mean ± SEM and individual data points. Statistical comparisons were made using a one-way ANOVA with a Sidak’s post hoc test between all three groups

Journal: Acta Neuropathologica

Article Title: Hyperphosphorylated tau causes reduced hippocampal CA1 excitability by relocating the axon initial segment

doi: 10.1007/s00401-017-1674-1

Figure Lengend Snippet: Pseudo-phosphorylated tau reduces AP firing in a similar manner to that observed in tau transgenic mouse models. Representative traces of APs fired by a A14- ( black ), b E14-transfected ( blue ) neurons and c E14-transfected neurons treated with 0.1 µM taxol ( magenta ) following injection of a −60, 0, rheobase and 320 pA current step. d Representative traces of the initial AP fired for A14, E14 and E14+ taxol neurons. Pooled data demonstrating the AP firing, including e input–output relationships (ANOVA, F = 4.084, p = 0.0274; E14 n = 12, A14 n = 11, E14+ taxol n = 10), f AP threshold (ANOVA, F = 2.439, p = 0.10), g AP amplitude (ANOVA, F = 4.152, p = 0.0256), and h rheobase (ANOVA, F = 2.4, p = 0.11). * p < 0.05. Data are presented as mean ± SEM and individual data points. Statistical comparisons were made using a one-way ANOVA with a Sidak’s post hoc test between all three groups

Article Snippet: Two mutant Tau-EGFP constructs termed E14 and A14 (all 14 serine or threonine residues T111, T153, T175, T181, S199, S202, T205, T212, T217, T231, S235, S396, S404, and S422 mutated to glutamic acid (E14) or alanine (A14), respectively) were generated by subcloning the mutant Tau fragment from pRK5-EGFP-Tau E14 (0N4R Tau, Addgene plasmid # 46907) or pRK5-EGFP-Tau AP (0N4R Tau, Addgene plasmid # 46905) into the wild-type Tau-EGFP backbone, using the Gibson assembly method (NEB E5510S).

Techniques: Transgenic Assay, Transfection, Injection