s129a plasmids Search Results


s129a plasmids  (Addgene inc)
86
Addgene inc s129a plasmids
Fig. 7 Synaptic plasticity is impaired in S129AKI mouse. a–f Generation of the <t>S129A</t> knock-in mutation in mice. a Genomic structure of the mouse SNCA gene. Exons are depicted after transcript variant SNCA-201 (ENSMUST00000114268.5), with coding and non-coding regions shown as filled or open boxes, respectively. Exon 5 is boxed with red dashed line. b A knock-in strategy using CRISPR-Cas9 and ssODN was employed to generate the S129A mutation in Exon 5 of the endogenous SNCA gene. Relative positions of sgRNA (orange horizontal line), ssODN (blue horizontal line), and the S129A mutation (red vertical line) are indicated. c–f ES cell clone screening and mouse genotyping. A 3-primer PCR strategy (primers indicated with black and red arrows) was designed to distinguish WT and mutant alleles (c, d). For genotyping, a common pair of primers (indicated with green arrows) was used for PCR followed by sequencing to distinguish different genotypes (c, e, f). g Total mouse brain homogenates from indicated genotypes. WB for total αS, pS129 (D1R1R) and GAPDH. h Input and out current curve from hippocampal slices (CA1 region) of indicated mouse genotypes. N = 3 animals each, n = 16 (WT) or 17 (S129AKI) individual slices. i Paired- pulse facilitation of WT and S129AKI hippocampal slices. Inter-stimulation intervals as indicated. N = 3 animals each, n = 16 (WT) or 17 (S129AKI) individual slices. Unpaired t-tests for 20, 40, 60, 100, 200, and 500 ms with Welch’s correction; two-tailed; mean ± SD; ns not significant; *p < 0.05; **p < 0.01. j Short-term plasticity assessed by multi-pulse events. Values normalized to first excitatory post synaptic current (EPSP). N = 3 animals each, n = 16 (WT) or 17 (S129AKI) individual slices. Unpaired t-tests for pulses 2, 3, 4, 5, 6, 7, and 8 with Welch’s correction; two-tailed; mean ± SD; ns not significant; *p < 0.05; **p < 0.01; ***p < 0.001. k, l Long Term Potentiation (LTP) of WT and S129AKI. LTP induced by standard 100 Hz stimulation. N = 3 animals each, n = 8 (WT) or 10 (S129AKI) individual slices. Unpaired t-tests for panel l (values at 60 min from K) with Welch’s correction; two-tailed; mean ± SD; **p < 0.01.
S129a Plasmids, supplied by Addgene inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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plasmids myc/mych-α-syn/myc-s129a ch884935  (Vigene Biosciences)
90
Vigene Biosciences plasmids myc/mych-α-syn/myc-s129a ch884935
Fig. 7 Synaptic plasticity is impaired in S129AKI mouse. a–f Generation of the <t>S129A</t> knock-in mutation in mice. a Genomic structure of the mouse SNCA gene. Exons are depicted after transcript variant SNCA-201 (ENSMUST00000114268.5), with coding and non-coding regions shown as filled or open boxes, respectively. Exon 5 is boxed with red dashed line. b A knock-in strategy using CRISPR-Cas9 and ssODN was employed to generate the S129A mutation in Exon 5 of the endogenous SNCA gene. Relative positions of sgRNA (orange horizontal line), ssODN (blue horizontal line), and the S129A mutation (red vertical line) are indicated. c–f ES cell clone screening and mouse genotyping. A 3-primer PCR strategy (primers indicated with black and red arrows) was designed to distinguish WT and mutant alleles (c, d). For genotyping, a common pair of primers (indicated with green arrows) was used for PCR followed by sequencing to distinguish different genotypes (c, e, f). g Total mouse brain homogenates from indicated genotypes. WB for total αS, pS129 (D1R1R) and GAPDH. h Input and out current curve from hippocampal slices (CA1 region) of indicated mouse genotypes. N = 3 animals each, n = 16 (WT) or 17 (S129AKI) individual slices. i Paired- pulse facilitation of WT and S129AKI hippocampal slices. Inter-stimulation intervals as indicated. N = 3 animals each, n = 16 (WT) or 17 (S129AKI) individual slices. Unpaired t-tests for 20, 40, 60, 100, 200, and 500 ms with Welch’s correction; two-tailed; mean ± SD; ns not significant; *p < 0.05; **p < 0.01. j Short-term plasticity assessed by multi-pulse events. Values normalized to first excitatory post synaptic current (EPSP). N = 3 animals each, n = 16 (WT) or 17 (S129AKI) individual slices. Unpaired t-tests for pulses 2, 3, 4, 5, 6, 7, and 8 with Welch’s correction; two-tailed; mean ± SD; ns not significant; *p < 0.05; **p < 0.01; ***p < 0.001. k, l Long Term Potentiation (LTP) of WT and S129AKI. LTP induced by standard 100 Hz stimulation. N = 3 animals each, n = 8 (WT) or 10 (S129AKI) individual slices. Unpaired t-tests for panel l (values at 60 min from K) with Welch’s correction; two-tailed; mean ± SD; **p < 0.01.
Plasmids Myc/Mych α Syn/Myc S129a Ch884935, supplied by Vigene Biosciences, 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/plasmids myc/mych-α-syn/myc-s129a ch884935/product/Vigene Biosciences
Average 90 stars, based on 1 article reviews
plasmids myc/mych-α-syn/myc-s129a ch884935 - by Bioz Stars, 2026-02
90/100 stars
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Image Search Results


Fig. 7 Synaptic plasticity is impaired in S129AKI mouse. a–f Generation of the S129A knock-in mutation in mice. a Genomic structure of the mouse SNCA gene. Exons are depicted after transcript variant SNCA-201 (ENSMUST00000114268.5), with coding and non-coding regions shown as filled or open boxes, respectively. Exon 5 is boxed with red dashed line. b A knock-in strategy using CRISPR-Cas9 and ssODN was employed to generate the S129A mutation in Exon 5 of the endogenous SNCA gene. Relative positions of sgRNA (orange horizontal line), ssODN (blue horizontal line), and the S129A mutation (red vertical line) are indicated. c–f ES cell clone screening and mouse genotyping. A 3-primer PCR strategy (primers indicated with black and red arrows) was designed to distinguish WT and mutant alleles (c, d). For genotyping, a common pair of primers (indicated with green arrows) was used for PCR followed by sequencing to distinguish different genotypes (c, e, f). g Total mouse brain homogenates from indicated genotypes. WB for total αS, pS129 (D1R1R) and GAPDH. h Input and out current curve from hippocampal slices (CA1 region) of indicated mouse genotypes. N = 3 animals each, n = 16 (WT) or 17 (S129AKI) individual slices. i Paired- pulse facilitation of WT and S129AKI hippocampal slices. Inter-stimulation intervals as indicated. N = 3 animals each, n = 16 (WT) or 17 (S129AKI) individual slices. Unpaired t-tests for 20, 40, 60, 100, 200, and 500 ms with Welch’s correction; two-tailed; mean ± SD; ns not significant; *p < 0.05; **p < 0.01. j Short-term plasticity assessed by multi-pulse events. Values normalized to first excitatory post synaptic current (EPSP). N = 3 animals each, n = 16 (WT) or 17 (S129AKI) individual slices. Unpaired t-tests for pulses 2, 3, 4, 5, 6, 7, and 8 with Welch’s correction; two-tailed; mean ± SD; ns not significant; *p < 0.05; **p < 0.01; ***p < 0.001. k, l Long Term Potentiation (LTP) of WT and S129AKI. LTP induced by standard 100 Hz stimulation. N = 3 animals each, n = 8 (WT) or 10 (S129AKI) individual slices. Unpaired t-tests for panel l (values at 60 min from K) with Welch’s correction; two-tailed; mean ± SD; **p < 0.01.

Journal: NPJ Parkinson's disease

Article Title: Dynamic physiological α-synuclein S129 phosphorylation is driven by neuronal activity.

doi: 10.1038/s41531-023-00444-w

Figure Lengend Snippet: Fig. 7 Synaptic plasticity is impaired in S129AKI mouse. a–f Generation of the S129A knock-in mutation in mice. a Genomic structure of the mouse SNCA gene. Exons are depicted after transcript variant SNCA-201 (ENSMUST00000114268.5), with coding and non-coding regions shown as filled or open boxes, respectively. Exon 5 is boxed with red dashed line. b A knock-in strategy using CRISPR-Cas9 and ssODN was employed to generate the S129A mutation in Exon 5 of the endogenous SNCA gene. Relative positions of sgRNA (orange horizontal line), ssODN (blue horizontal line), and the S129A mutation (red vertical line) are indicated. c–f ES cell clone screening and mouse genotyping. A 3-primer PCR strategy (primers indicated with black and red arrows) was designed to distinguish WT and mutant alleles (c, d). For genotyping, a common pair of primers (indicated with green arrows) was used for PCR followed by sequencing to distinguish different genotypes (c, e, f). g Total mouse brain homogenates from indicated genotypes. WB for total αS, pS129 (D1R1R) and GAPDH. h Input and out current curve from hippocampal slices (CA1 region) of indicated mouse genotypes. N = 3 animals each, n = 16 (WT) or 17 (S129AKI) individual slices. i Paired- pulse facilitation of WT and S129AKI hippocampal slices. Inter-stimulation intervals as indicated. N = 3 animals each, n = 16 (WT) or 17 (S129AKI) individual slices. Unpaired t-tests for 20, 40, 60, 100, 200, and 500 ms with Welch’s correction; two-tailed; mean ± SD; ns not significant; *p < 0.05; **p < 0.01. j Short-term plasticity assessed by multi-pulse events. Values normalized to first excitatory post synaptic current (EPSP). N = 3 animals each, n = 16 (WT) or 17 (S129AKI) individual slices. Unpaired t-tests for pulses 2, 3, 4, 5, 6, 7, and 8 with Welch’s correction; two-tailed; mean ± SD; ns not significant; *p < 0.05; **p < 0.01; ***p < 0.001. k, l Long Term Potentiation (LTP) of WT and S129AKI. LTP induced by standard 100 Hz stimulation. N = 3 animals each, n = 8 (WT) or 10 (S129AKI) individual slices. Unpaired t-tests for panel l (values at 60 min from K) with Welch’s correction; two-tailed; mean ± SD; **p < 0.01.

Article Snippet: Briefly, 293-T cells were transfected with αS WT or S129A plasmids along with pMD2.G and psPAX2 (packaging plasmids: Addgene #12259 and #12260, respectively).

Techniques: Knock-In, Mutagenesis, Variant Assay, CRISPR, Sequencing, Two Tailed Test