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app swe  (Jackson Laboratory)

 
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    Jackson Laboratory app swe
    App Swe, supplied by Jackson Laboratory, 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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    Average 86 stars, based on 1 article reviews
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    RGS6 loss from DG NPCs does not alter the running patterns of control and <t>APP</t> <t>SWE</t> mice. (A) Schematic outlining CRISPR-Cas9 generation of RGS6 fl/fl mice. Rgs6 WT (top) and Rgs6 flox (bottom) alleles are depicted. E5, E6, E7 denote Rgs6 exons 5–7. PCR primers 1 and 2 (arrows) were used to amplify a DNA segment in the Rgs6 gene upstream of E5. (B) Schematics outlining the APP SWE transgene (top) and breeding cross to generate RGS6 fl/fl ; APP SWE mice (bottom). (C) PCR results confirming the generation of RGS6 fl/fl ; APP SWE mice. (D) Schematic outlining running wheel set up, mouse genotypes, and running groups. (E–G) Daily average running behavior patterns of 20-week-old RGS6 WT DG (dark grey closed circles/line), RGS6 KO DG (light grey border squares/line), RGS6 WT DG ; APP SWE (red closed circles/line), and RGS6 KO DG ; APP SWE (light red border squares/line) mice on free-running wheels over the course of 8 weeks during their dark cycle. Daily average time (E), distance traveled (F), and running speed (G) of mice during the dark cycle. Data are expressed as mean ± SEM. Two-way analysis of variance with Tukey’s post hoc adjustment was used to analyze the effects of and interaction between sex and genotype. No significant effects of genotype or sex were observed. (Fixed wheel: n = 8 RGS6 WT DG mice; n = 11 RGS6 KO DG mice; n = 10 RGS6 WT DG ; APP SWE mice; n = 12 RGS6 KO DG ; APP SWE mice. Free wheel: n = 7 RGS6 WT DG mice; n = 9 RGS6 KO DG mice; n = 10 RGS6 WT DG ; APP SWE mice; n = 15 RGS6 KO DG ; APP SWE mice). DG: Dentate gyrus; NPCs: neuronal progenitor cells; PCR: polymerase chain reaction; RGS6: regulator of G protein signaling 6.
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    RGS6 loss from DG NPCs does not alter the running patterns of control and <t>APP</t> <t>SWE</t> mice. (A) Schematic outlining CRISPR-Cas9 generation of RGS6 fl/fl mice. Rgs6 WT (top) and Rgs6 flox (bottom) alleles are depicted. E5, E6, E7 denote Rgs6 exons 5–7. PCR primers 1 and 2 (arrows) were used to amplify a DNA segment in the Rgs6 gene upstream of E5. (B) Schematics outlining the APP SWE transgene (top) and breeding cross to generate RGS6 fl/fl ; APP SWE mice (bottom). (C) PCR results confirming the generation of RGS6 fl/fl ; APP SWE mice. (D) Schematic outlining running wheel set up, mouse genotypes, and running groups. (E–G) Daily average running behavior patterns of 20-week-old RGS6 WT DG (dark grey closed circles/line), RGS6 KO DG (light grey border squares/line), RGS6 WT DG ; APP SWE (red closed circles/line), and RGS6 KO DG ; APP SWE (light red border squares/line) mice on free-running wheels over the course of 8 weeks during their dark cycle. Daily average time (E), distance traveled (F), and running speed (G) of mice during the dark cycle. Data are expressed as mean ± SEM. Two-way analysis of variance with Tukey’s post hoc adjustment was used to analyze the effects of and interaction between sex and genotype. No significant effects of genotype or sex were observed. (Fixed wheel: n = 8 RGS6 WT DG mice; n = 11 RGS6 KO DG mice; n = 10 RGS6 WT DG ; APP SWE mice; n = 12 RGS6 KO DG ; APP SWE mice. Free wheel: n = 7 RGS6 WT DG mice; n = 9 RGS6 KO DG mice; n = 10 RGS6 WT DG ; APP SWE mice; n = 15 RGS6 KO DG ; APP SWE mice). DG: Dentate gyrus; NPCs: neuronal progenitor cells; PCR: polymerase chain reaction; RGS6: regulator of G protein signaling 6.
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    RGS6 loss from DG NPCs does not alter the running patterns of control and APP SWE mice. (A) Schematic outlining CRISPR-Cas9 generation of RGS6 fl/fl mice. Rgs6 WT (top) and Rgs6 flox (bottom) alleles are depicted. E5, E6, E7 denote Rgs6 exons 5–7. PCR primers 1 and 2 (arrows) were used to amplify a DNA segment in the Rgs6 gene upstream of E5. (B) Schematics outlining the APP SWE transgene (top) and breeding cross to generate RGS6 fl/fl ; APP SWE mice (bottom). (C) PCR results confirming the generation of RGS6 fl/fl ; APP SWE mice. (D) Schematic outlining running wheel set up, mouse genotypes, and running groups. (E–G) Daily average running behavior patterns of 20-week-old RGS6 WT DG (dark grey closed circles/line), RGS6 KO DG (light grey border squares/line), RGS6 WT DG ; APP SWE (red closed circles/line), and RGS6 KO DG ; APP SWE (light red border squares/line) mice on free-running wheels over the course of 8 weeks during their dark cycle. Daily average time (E), distance traveled (F), and running speed (G) of mice during the dark cycle. Data are expressed as mean ± SEM. Two-way analysis of variance with Tukey’s post hoc adjustment was used to analyze the effects of and interaction between sex and genotype. No significant effects of genotype or sex were observed. (Fixed wheel: n = 8 RGS6 WT DG mice; n = 11 RGS6 KO DG mice; n = 10 RGS6 WT DG ; APP SWE mice; n = 12 RGS6 KO DG ; APP SWE mice. Free wheel: n = 7 RGS6 WT DG mice; n = 9 RGS6 KO DG mice; n = 10 RGS6 WT DG ; APP SWE mice; n = 15 RGS6 KO DG ; APP SWE mice). DG: Dentate gyrus; NPCs: neuronal progenitor cells; PCR: polymerase chain reaction; RGS6: regulator of G protein signaling 6.

    Journal: Neural Regeneration Research

    Article Title: Regulator of G protein signaling 6 mediates exercise-induced recovery of hippocampal neurogenesis, learning, and memory in a mouse model of Alzheimer’s disease

    doi: 10.4103/NRR.NRR-D-23-01993

    Figure Lengend Snippet: RGS6 loss from DG NPCs does not alter the running patterns of control and APP SWE mice. (A) Schematic outlining CRISPR-Cas9 generation of RGS6 fl/fl mice. Rgs6 WT (top) and Rgs6 flox (bottom) alleles are depicted. E5, E6, E7 denote Rgs6 exons 5–7. PCR primers 1 and 2 (arrows) were used to amplify a DNA segment in the Rgs6 gene upstream of E5. (B) Schematics outlining the APP SWE transgene (top) and breeding cross to generate RGS6 fl/fl ; APP SWE mice (bottom). (C) PCR results confirming the generation of RGS6 fl/fl ; APP SWE mice. (D) Schematic outlining running wheel set up, mouse genotypes, and running groups. (E–G) Daily average running behavior patterns of 20-week-old RGS6 WT DG (dark grey closed circles/line), RGS6 KO DG (light grey border squares/line), RGS6 WT DG ; APP SWE (red closed circles/line), and RGS6 KO DG ; APP SWE (light red border squares/line) mice on free-running wheels over the course of 8 weeks during their dark cycle. Daily average time (E), distance traveled (F), and running speed (G) of mice during the dark cycle. Data are expressed as mean ± SEM. Two-way analysis of variance with Tukey’s post hoc adjustment was used to analyze the effects of and interaction between sex and genotype. No significant effects of genotype or sex were observed. (Fixed wheel: n = 8 RGS6 WT DG mice; n = 11 RGS6 KO DG mice; n = 10 RGS6 WT DG ; APP SWE mice; n = 12 RGS6 KO DG ; APP SWE mice. Free wheel: n = 7 RGS6 WT DG mice; n = 9 RGS6 KO DG mice; n = 10 RGS6 WT DG ; APP SWE mice; n = 15 RGS6 KO DG ; APP SWE mice). DG: Dentate gyrus; NPCs: neuronal progenitor cells; PCR: polymerase chain reaction; RGS6: regulator of G protein signaling 6.

    Article Snippet: RGS6 fl/fl mice were bred with APP SWE mice (Taconic 1349, C57BL/6J background) to create mice to determine the impact of RGS6 loss in DG NPCs on neurogenesis in APP SWE mice.

    Techniques: Control, CRISPR, Polymerase Chain Reaction

    RGS6 in DG NPCs is required for running-induced cognitive improvements in APP SWE mice. (A) Schematic outlining experimental design. Mice were placed in cages containing either fixed (control) or free (running) wheels for 8 weeks. Mice underwent hippocampal-based learning and memory behavioral tasks after 4 weeks (Y-maze [B]) and 8 weeks (Y-maze [C] and contextual fear conditioning (CFC, [D]) of wheel treatment. (B, C) Multi-way analysis of variance with Tukey’s post hoc adjustment was used to analyze the effects of and interactions between genotype, sex, time, and wheel treatment after 4 (B) or 8 weeks (C) of wheel treatment. Top: % Spontaneous alternations— Significant effects of genotype ( F 3,154 = 16.261, P = 0.000) and wheel treatment ( F 1,154 = 52.906, P = 0.000), as well as their interaction ( F 3,154 = 19.638, P = 0.000) were observed. No significant effects of sex or time were observed. Bottom: % Time spent in novel arm— Significant effects of genotype ( F 3,154 = 30.835, P = 0.000) and wheel treatment ( F 1,154 = 22.496, P = 0.000), as well as their interaction ( F 3,154 = 7.652, P = 0.000) were observed. No significant effects of sex or time were observed. (D) Multi-way ANOVA with Tukey’s post hoc adjustment was used to analyze the effects of and interactions between genotype, sex, and wheel treatment. A significant effect of genotype ( F 3,55 = 6.217, P = 0.001) and its interaction with wheel treatment ( F 3,55 = 3.898, P = 0.013) were observed. No significant effects of sex or wheel treatment were observed. Data are expressed as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001. (Fixed wheel: n = 8 RGS6 WT DG mice; n = 11 RGS6 KO DG mice; n = 10 RGS6 WT DG ; APP SWE mice; n = 12 RGS6 KO DG ; APP SWE mice. Free wheel: n = 7 RGS6 WT DG mice; n = 9 RGS6 KO DG mice; n = 10 RGS6 WT DG ; APP SWE mice; n = 15 RGS6 KO DG ; APP SWE mice). DCX: Doublecortin; DG: dentate gyrus; GFP: green fluorescent protein; IHC: immunohistochemistry; NPCs: neuronal progenitor cells; RGS6: Regulator of G protein signaling 6.

    Journal: Neural Regeneration Research

    Article Title: Regulator of G protein signaling 6 mediates exercise-induced recovery of hippocampal neurogenesis, learning, and memory in a mouse model of Alzheimer’s disease

    doi: 10.4103/NRR.NRR-D-23-01993

    Figure Lengend Snippet: RGS6 in DG NPCs is required for running-induced cognitive improvements in APP SWE mice. (A) Schematic outlining experimental design. Mice were placed in cages containing either fixed (control) or free (running) wheels for 8 weeks. Mice underwent hippocampal-based learning and memory behavioral tasks after 4 weeks (Y-maze [B]) and 8 weeks (Y-maze [C] and contextual fear conditioning (CFC, [D]) of wheel treatment. (B, C) Multi-way analysis of variance with Tukey’s post hoc adjustment was used to analyze the effects of and interactions between genotype, sex, time, and wheel treatment after 4 (B) or 8 weeks (C) of wheel treatment. Top: % Spontaneous alternations— Significant effects of genotype ( F 3,154 = 16.261, P = 0.000) and wheel treatment ( F 1,154 = 52.906, P = 0.000), as well as their interaction ( F 3,154 = 19.638, P = 0.000) were observed. No significant effects of sex or time were observed. Bottom: % Time spent in novel arm— Significant effects of genotype ( F 3,154 = 30.835, P = 0.000) and wheel treatment ( F 1,154 = 22.496, P = 0.000), as well as their interaction ( F 3,154 = 7.652, P = 0.000) were observed. No significant effects of sex or time were observed. (D) Multi-way ANOVA with Tukey’s post hoc adjustment was used to analyze the effects of and interactions between genotype, sex, and wheel treatment. A significant effect of genotype ( F 3,55 = 6.217, P = 0.001) and its interaction with wheel treatment ( F 3,55 = 3.898, P = 0.013) were observed. No significant effects of sex or wheel treatment were observed. Data are expressed as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001. (Fixed wheel: n = 8 RGS6 WT DG mice; n = 11 RGS6 KO DG mice; n = 10 RGS6 WT DG ; APP SWE mice; n = 12 RGS6 KO DG ; APP SWE mice. Free wheel: n = 7 RGS6 WT DG mice; n = 9 RGS6 KO DG mice; n = 10 RGS6 WT DG ; APP SWE mice; n = 15 RGS6 KO DG ; APP SWE mice). DCX: Doublecortin; DG: dentate gyrus; GFP: green fluorescent protein; IHC: immunohistochemistry; NPCs: neuronal progenitor cells; RGS6: Regulator of G protein signaling 6.

    Article Snippet: RGS6 fl/fl mice were bred with APP SWE mice (Taconic 1349, C57BL/6J background) to create mice to determine the impact of RGS6 loss in DG NPCs on neurogenesis in APP SWE mice.

    Techniques: Control, Immunohistochemistry

    RGS6 in DG NPCs is required for basal AHN and running-induced AHN in APP SWE mice. (A) Schematic summarizing the process of AHN (top) and markers used at each stage (bottom). (B) Representative immunofluorescence images (20×, n = 8 RGS6 WT DG animals, n = 10 RGS6 KO DG animals) of neurogenesis markers (RV-eGFP or RV-Cre-eGFP, green; DCX, red) and DAPI (blue) in RGS6 WT DG and RGS6 KO DG sedentary and running mice from . Arrows highlight AHN in SGZ. Scale bar: 25 µm. (C) Representative immunofluorescence images (20×, n = 10/group) of neurogenesis markers (RV-eGFP or RV-Cre-eGFP, green; DCX, red) in RGS6 WT DG ; APP SWE and RGS6 KO DG ; APP SWE sedentary and running mice from . Scale bar: 25 µm. (D) Quantification of the number of GFP + DCX + neurons in RGS6 WT DG , RGS6 KO DG , RGS6 WT DG ; APP SWE , and RGS6 KO DG ; APP SWE mice. Multi-way analysis of variance with Tukey’s post hoc adjustment was used to analyze the effects of and interactions between genotype, wheel treatment, and sex. Significant effects of genotype ( F 3,68 = 157.885, P = 0.000), wheel treatment ( F 1,68 = 14.969, P = 0.000), and their interaction ( F 3,68 = 13.633, P = 0.000) were observed. Data are expressed as mean ± SEM. *** P < 0.001, **** P < 0.0001. AHN: Adult hippocampal neurogenesis; DAPI: 4′,6-diamidino-2-phenylindole; DCX: doublecortin; DG: dentate gyrus; GFP: green fluorescent protein; NPCs: neuronal progenitor cells; RGS6: Regulator of G protein signaling 6.

    Journal: Neural Regeneration Research

    Article Title: Regulator of G protein signaling 6 mediates exercise-induced recovery of hippocampal neurogenesis, learning, and memory in a mouse model of Alzheimer’s disease

    doi: 10.4103/NRR.NRR-D-23-01993

    Figure Lengend Snippet: RGS6 in DG NPCs is required for basal AHN and running-induced AHN in APP SWE mice. (A) Schematic summarizing the process of AHN (top) and markers used at each stage (bottom). (B) Representative immunofluorescence images (20×, n = 8 RGS6 WT DG animals, n = 10 RGS6 KO DG animals) of neurogenesis markers (RV-eGFP or RV-Cre-eGFP, green; DCX, red) and DAPI (blue) in RGS6 WT DG and RGS6 KO DG sedentary and running mice from . Arrows highlight AHN in SGZ. Scale bar: 25 µm. (C) Representative immunofluorescence images (20×, n = 10/group) of neurogenesis markers (RV-eGFP or RV-Cre-eGFP, green; DCX, red) in RGS6 WT DG ; APP SWE and RGS6 KO DG ; APP SWE sedentary and running mice from . Scale bar: 25 µm. (D) Quantification of the number of GFP + DCX + neurons in RGS6 WT DG , RGS6 KO DG , RGS6 WT DG ; APP SWE , and RGS6 KO DG ; APP SWE mice. Multi-way analysis of variance with Tukey’s post hoc adjustment was used to analyze the effects of and interactions between genotype, wheel treatment, and sex. Significant effects of genotype ( F 3,68 = 157.885, P = 0.000), wheel treatment ( F 1,68 = 14.969, P = 0.000), and their interaction ( F 3,68 = 13.633, P = 0.000) were observed. Data are expressed as mean ± SEM. *** P < 0.001, **** P < 0.0001. AHN: Adult hippocampal neurogenesis; DAPI: 4′,6-diamidino-2-phenylindole; DCX: doublecortin; DG: dentate gyrus; GFP: green fluorescent protein; NPCs: neuronal progenitor cells; RGS6: Regulator of G protein signaling 6.

    Article Snippet: RGS6 fl/fl mice were bred with APP SWE mice (Taconic 1349, C57BL/6J background) to create mice to determine the impact of RGS6 loss in DG NPCs on neurogenesis in APP SWE mice.

    Techniques: Immunofluorescence

    RGS6 in DG NPCs is required for basal AHN and running-induced AHN in APP SWE mice. (A) Representative immunofluorescence images (40×, n = 8 RGS6 WT DG animals, n = 10 RGS6 KO DG animals) analyzing RGS6 (red) co-expression with NeuN (green) and DAPI (blue) in RGS6 WT DG and RGS6 KO DG sedentary and running mice from . Scale bar: 40 µm. (B) Representative immunofluorescence images (40×, n = 10/group) analyzing RGS6 (red) co-expression with NeuN (green) and DAPI (blue) in RGS6 WT DG ; APP SWE and RGS6 KO DG ; APP SWE sedentary and running mice from . Scale bar: 40 µm. (C) Quantification of the number of RGS6 + NeuN + neurons in RGS6 WT DG , RGS6 KO DG , RGS6 WT DG ; APP SWE , and RGS6 KO DG ; APP SWE mice. Multi-way analysis of variance with Tukey’s post hoc adjustment was used to analyze the effects of and interactions between genotype, wheel treatment, and sex. Significant effects of genotype ( F 3,68 = 264.564, P = 0.000), wheel treatment ( F 1,68 = 12.290, P = 0.001), and their interaction ( F 3,68 = 12.621, P = 0.000) were observed. Data are expressed as mean ± SEM. *** P < 0.001, **** P < 0.0001. AHN: Adult hippocampal neurogenesis; DAPI: 4′,6-diamidino-2-phenylindole; DG: dentate gyrus; NeuN: neuronal nuclear antigen; NPCs: neuronal progenitor cells; RGS6: Regulator of G protein signaling 6.

    Journal: Neural Regeneration Research

    Article Title: Regulator of G protein signaling 6 mediates exercise-induced recovery of hippocampal neurogenesis, learning, and memory in a mouse model of Alzheimer’s disease

    doi: 10.4103/NRR.NRR-D-23-01993

    Figure Lengend Snippet: RGS6 in DG NPCs is required for basal AHN and running-induced AHN in APP SWE mice. (A) Representative immunofluorescence images (40×, n = 8 RGS6 WT DG animals, n = 10 RGS6 KO DG animals) analyzing RGS6 (red) co-expression with NeuN (green) and DAPI (blue) in RGS6 WT DG and RGS6 KO DG sedentary and running mice from . Scale bar: 40 µm. (B) Representative immunofluorescence images (40×, n = 10/group) analyzing RGS6 (red) co-expression with NeuN (green) and DAPI (blue) in RGS6 WT DG ; APP SWE and RGS6 KO DG ; APP SWE sedentary and running mice from . Scale bar: 40 µm. (C) Quantification of the number of RGS6 + NeuN + neurons in RGS6 WT DG , RGS6 KO DG , RGS6 WT DG ; APP SWE , and RGS6 KO DG ; APP SWE mice. Multi-way analysis of variance with Tukey’s post hoc adjustment was used to analyze the effects of and interactions between genotype, wheel treatment, and sex. Significant effects of genotype ( F 3,68 = 264.564, P = 0.000), wheel treatment ( F 1,68 = 12.290, P = 0.001), and their interaction ( F 3,68 = 12.621, P = 0.000) were observed. Data are expressed as mean ± SEM. *** P < 0.001, **** P < 0.0001. AHN: Adult hippocampal neurogenesis; DAPI: 4′,6-diamidino-2-phenylindole; DG: dentate gyrus; NeuN: neuronal nuclear antigen; NPCs: neuronal progenitor cells; RGS6: Regulator of G protein signaling 6.

    Article Snippet: RGS6 fl/fl mice were bred with APP SWE mice (Taconic 1349, C57BL/6J background) to create mice to determine the impact of RGS6 loss in DG NPCs on neurogenesis in APP SWE mice.

    Techniques: Immunofluorescence, Expressing

    Summary model of RGS6’s role in DG NPCs. Left: RGS6 DG NPC expression, stimulated by voluntary running exercise, promotes AHN to improve cognitive function in APP SWE mice. Right: RGS6 DG NPC loss leads to significant impairments in AHN, thus preventing the ability of voluntary running-mediated AHN to reverse cognitive dysfunction in APP SWE mice. AHN: Adult hippocampal neurogenesis; DG: dentate gyrus; NPCs: neuronal progenitor cells; RGS6: Regulator of G protein signaling 6.

    Journal: Neural Regeneration Research

    Article Title: Regulator of G protein signaling 6 mediates exercise-induced recovery of hippocampal neurogenesis, learning, and memory in a mouse model of Alzheimer’s disease

    doi: 10.4103/NRR.NRR-D-23-01993

    Figure Lengend Snippet: Summary model of RGS6’s role in DG NPCs. Left: RGS6 DG NPC expression, stimulated by voluntary running exercise, promotes AHN to improve cognitive function in APP SWE mice. Right: RGS6 DG NPC loss leads to significant impairments in AHN, thus preventing the ability of voluntary running-mediated AHN to reverse cognitive dysfunction in APP SWE mice. AHN: Adult hippocampal neurogenesis; DG: dentate gyrus; NPCs: neuronal progenitor cells; RGS6: Regulator of G protein signaling 6.

    Article Snippet: RGS6 fl/fl mice were bred with APP SWE mice (Taconic 1349, C57BL/6J background) to create mice to determine the impact of RGS6 loss in DG NPCs on neurogenesis in APP SWE mice.

    Techniques: Expressing