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14647 1 ap  (Proteintech)


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    Structured Review

    Proteintech 14647 1 ap
    14647 1 Ap, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/bin1/bio_rxiv__64898__2026__03__14__711835-404-12-13?v=Proteintech
    Average 93 stars, based on 19 article reviews
    14647 1 ap - by Bioz Stars, 2026-08
    93/100 stars

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    Loss of <t>Bin1</t> from PV neurons does not alter brain structure, survival, or body weight. A , Nissl stain of Ctrl and Bin1- pvKO mice. B , Survival curves of Ctrl and Bin1- pvKO mice split by sex (Mantel–Cox test, χ 2 = 1.330; p = 0.7221; df = 3; n = 63–71 mice per group). C , Body weight measurements of Ctrl and Bin1- pvKO mice across younger cohorts (3–10 months old), split by sex (two-way ANOVA; interaction, F (1,158) = 0.1807; p = 0.6713; sex, F (1,158) = 19.83; p < 0.0001; genotype, F (1,158) = 0.2965; p = 0.5868). D , Body weight measurements of Ctrl and Bin1- pvKO mice across aged cohorts (16–22 months old), split by sex (two-way ANOVA; interaction, F (1,110) = 2.447; p = 0.1206; sex, F (1,110) = 14.86; p = 0.0002; genotype, F (1,110) = 1.745; p = 0.1892; Fisher’s LSD, females, p = 0.0503; males, p = 0.8593; Ctrl, p < 0.0001; Bin1 -pvKO, p = 0.1256).
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    Loss of <t>Bin1</t> from PV neurons does not alter brain structure, survival, or body weight. A , Nissl stain of Ctrl and Bin1- pvKO mice. B , Survival curves of Ctrl and Bin1- pvKO mice split by sex (Mantel–Cox test, χ 2 = 1.330; p = 0.7221; df = 3; n = 63–71 mice per group). C , Body weight measurements of Ctrl and Bin1- pvKO mice across younger cohorts (3–10 months old), split by sex (two-way ANOVA; interaction, F (1,158) = 0.1807; p = 0.6713; sex, F (1,158) = 19.83; p < 0.0001; genotype, F (1,158) = 0.2965; p = 0.5868). D , Body weight measurements of Ctrl and Bin1- pvKO mice across aged cohorts (16–22 months old), split by sex (two-way ANOVA; interaction, F (1,110) = 2.447; p = 0.1206; sex, F (1,110) = 14.86; p = 0.0002; genotype, F (1,110) = 1.745; p = 0.1892; Fisher’s LSD, females, p = 0.0503; males, p = 0.8593; Ctrl, p < 0.0001; Bin1 -pvKO, p = 0.1256).
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    Loss of <t>Bin1</t> from PV neurons does not alter brain structure, survival, or body weight. A , Nissl stain of Ctrl and Bin1- pvKO mice. B , Survival curves of Ctrl and Bin1- pvKO mice split by sex (Mantel–Cox test, χ 2 = 1.330; p = 0.7221; df = 3; n = 63–71 mice per group). C , Body weight measurements of Ctrl and Bin1- pvKO mice across younger cohorts (3–10 months old), split by sex (two-way ANOVA; interaction, F (1,158) = 0.1807; p = 0.6713; sex, F (1,158) = 19.83; p < 0.0001; genotype, F (1,158) = 0.2965; p = 0.5868). D , Body weight measurements of Ctrl and Bin1- pvKO mice across aged cohorts (16–22 months old), split by sex (two-way ANOVA; interaction, F (1,110) = 2.447; p = 0.1206; sex, F (1,110) = 14.86; p = 0.0002; genotype, F (1,110) = 1.745; p = 0.1892; Fisher’s LSD, females, p = 0.0503; males, p = 0.8593; Ctrl, p < 0.0001; Bin1 -pvKO, p = 0.1256).
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    Loss of <t>Bin1</t> from PV neurons does not alter brain structure, survival, or body weight. A , Nissl stain of Ctrl and Bin1- pvKO mice. B , Survival curves of Ctrl and Bin1- pvKO mice split by sex (Mantel–Cox test, χ 2 = 1.330; p = 0.7221; df = 3; n = 63–71 mice per group). C , Body weight measurements of Ctrl and Bin1- pvKO mice across younger cohorts (3–10 months old), split by sex (two-way ANOVA; interaction, F (1,158) = 0.1807; p = 0.6713; sex, F (1,158) = 19.83; p < 0.0001; genotype, F (1,158) = 0.2965; p = 0.5868). D , Body weight measurements of Ctrl and Bin1- pvKO mice across aged cohorts (16–22 months old), split by sex (two-way ANOVA; interaction, F (1,110) = 2.447; p = 0.1206; sex, F (1,110) = 14.86; p = 0.0002; genotype, F (1,110) = 1.745; p = 0.1892; Fisher’s LSD, females, p = 0.0503; males, p = 0.8593; Ctrl, p < 0.0001; Bin1 -pvKO, p = 0.1256).
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    Image Search Results


    Loss of Bin1 from PV neurons does not alter brain structure, survival, or body weight. A , Nissl stain of Ctrl and Bin1- pvKO mice. B , Survival curves of Ctrl and Bin1- pvKO mice split by sex (Mantel–Cox test, χ 2 = 1.330; p = 0.7221; df = 3; n = 63–71 mice per group). C , Body weight measurements of Ctrl and Bin1- pvKO mice across younger cohorts (3–10 months old), split by sex (two-way ANOVA; interaction, F (1,158) = 0.1807; p = 0.6713; sex, F (1,158) = 19.83; p < 0.0001; genotype, F (1,158) = 0.2965; p = 0.5868). D , Body weight measurements of Ctrl and Bin1- pvKO mice across aged cohorts (16–22 months old), split by sex (two-way ANOVA; interaction, F (1,110) = 2.447; p = 0.1206; sex, F (1,110) = 14.86; p = 0.0002; genotype, F (1,110) = 1.745; p = 0.1892; Fisher’s LSD, females, p = 0.0503; males, p = 0.8593; Ctrl, p < 0.0001; Bin1 -pvKO, p = 0.1256).

    Journal: eNeuro

    Article Title: Parvalbumin Neuron–Targeted Loss of Alzheimer’s Disease Risk Gene BIN1 Is Insufficient to Drive Cognitive or Network Excitability Changes

    doi: 10.1523/ENEURO.0304-25.2026

    Figure Lengend Snippet: Loss of Bin1 from PV neurons does not alter brain structure, survival, or body weight. A , Nissl stain of Ctrl and Bin1- pvKO mice. B , Survival curves of Ctrl and Bin1- pvKO mice split by sex (Mantel–Cox test, χ 2 = 1.330; p = 0.7221; df = 3; n = 63–71 mice per group). C , Body weight measurements of Ctrl and Bin1- pvKO mice across younger cohorts (3–10 months old), split by sex (two-way ANOVA; interaction, F (1,158) = 0.1807; p = 0.6713; sex, F (1,158) = 19.83; p < 0.0001; genotype, F (1,158) = 0.2965; p = 0.5868). D , Body weight measurements of Ctrl and Bin1- pvKO mice across aged cohorts (16–22 months old), split by sex (two-way ANOVA; interaction, F (1,110) = 2.447; p = 0.1206; sex, F (1,110) = 14.86; p = 0.0002; genotype, F (1,110) = 1.745; p = 0.1892; Fisher’s LSD, females, p = 0.0503; males, p = 0.8593; Ctrl, p < 0.0001; Bin1 -pvKO, p = 0.1256).

    Article Snippet: Bin1 flox/flox mice were also crossed with Nestin-Cre mice (RRID:IMSR_JAX:00377) for knock-out validation ( ).

    Techniques: Staining

    Older Bin1 -pvKO mice show mildly decreased exploratory behavior. Behavioral screening of 16–20-month-old Bin1- pvKO mice showed a significant decrease in A , the number of arm entrances in the Y maze (unpaired t test, t (64) = 2.247; p = 0.0281; n = 31–35 per group; split by sex in Extended Data Figure 3-1 A , B ) distance traveled in the Y maze (unpaired t test, t (64) = 2.220; p = 0.0300; n = 31–35 per group; split by sex in Extended Data Fig. 3-1 B ), but not in C , distance traveled in the elevated plus maze (unpaired t test, t (26) = 1.130; p = 0.2688; n = 12–16 per group), or D , total distance traveled in the open field (two-way RM ANOVA; interaction effect, F (9,576) = 0.3908; p = 0.9397; genotype effect, F (1,64) = 0.5156; p = 0.4753; time effect, F (1.808,115.7) = 61.76; p < 0.0001; n = 31–35 per group). Bin1- pvKO mice do not show differences in E , the percentage of time spent in the open arms of the elevated plus maze (Mann–Whitney test, U = 506; p = 0.6435; n = 31–35 per group); F , amount of time spent in the center of the open-field maze (Mann–Whitney test, U = 541; p = 0.9872; n = 31–35 per group); G , spontaneous alternations in the Y maze (Mann–Whitney test, U = 452.5; p = 0.3432; n = 30–35 per group); or H , the percentage of time freezing in contextual fear conditioning (two-way RM ANOVA; interaction effect, F (2,126) = 0.8953; p = 0.4111; genotype effect, F (1,63) = 0.4092; p = 0.5247; time effect, F (1.736,109.3) = 298; p < 0.0001; n = 31–34 per group).

    Journal: eNeuro

    Article Title: Parvalbumin Neuron–Targeted Loss of Alzheimer’s Disease Risk Gene BIN1 Is Insufficient to Drive Cognitive or Network Excitability Changes

    doi: 10.1523/ENEURO.0304-25.2026

    Figure Lengend Snippet: Older Bin1 -pvKO mice show mildly decreased exploratory behavior. Behavioral screening of 16–20-month-old Bin1- pvKO mice showed a significant decrease in A , the number of arm entrances in the Y maze (unpaired t test, t (64) = 2.247; p = 0.0281; n = 31–35 per group; split by sex in Extended Data Figure 3-1 A , B ) distance traveled in the Y maze (unpaired t test, t (64) = 2.220; p = 0.0300; n = 31–35 per group; split by sex in Extended Data Fig. 3-1 B ), but not in C , distance traveled in the elevated plus maze (unpaired t test, t (26) = 1.130; p = 0.2688; n = 12–16 per group), or D , total distance traveled in the open field (two-way RM ANOVA; interaction effect, F (9,576) = 0.3908; p = 0.9397; genotype effect, F (1,64) = 0.5156; p = 0.4753; time effect, F (1.808,115.7) = 61.76; p < 0.0001; n = 31–35 per group). Bin1- pvKO mice do not show differences in E , the percentage of time spent in the open arms of the elevated plus maze (Mann–Whitney test, U = 506; p = 0.6435; n = 31–35 per group); F , amount of time spent in the center of the open-field maze (Mann–Whitney test, U = 541; p = 0.9872; n = 31–35 per group); G , spontaneous alternations in the Y maze (Mann–Whitney test, U = 452.5; p = 0.3432; n = 30–35 per group); or H , the percentage of time freezing in contextual fear conditioning (two-way RM ANOVA; interaction effect, F (2,126) = 0.8953; p = 0.4111; genotype effect, F (1,63) = 0.4092; p = 0.5247; time effect, F (1.736,109.3) = 298; p < 0.0001; n = 31–34 per group).

    Article Snippet: Bin1 flox/flox mice were also crossed with Nestin-Cre mice (RRID:IMSR_JAX:00377) for knock-out validation ( ).

    Techniques: MANN-WHITNEY

    Machine learning–based pose estimation and behavioral clustering show no differences in Bin1- pvKO mice. A , Similarity dendrogram from KPMS behavioral clustering analysis following DLC pose estimation trained network. Syllables were sorted by dendrogram clustering, grouped by behavior class, and normalized to control syllable usage (two-way RM ANOVA of syllable usage across genotypes; interaction effect, F (36,1656) = 0.5730; p = 0.9806; effect of genotype, F (1,46) = 0.004145; p = 0.9489; effect of syllable, F (5.837,268.5) = 0.5730; p = 0.7471; n = 24 per group). B , Sum of percent time spent in each syllable group, color coded and clustered from panel A (two-way RM ANOVA of syllable group usage; interaction effect, F (6,276) = 0.4985; p = 0.8093; genotype effect, F (1,46) = 0.02772; p = 0.8685; syllable effect, F (1.960,90.16) = 349.1; p < 0.0001; n = 24 per group). C , Total distance traveled in the hour-long recording session, as tracked by the ezTrack software (unpaired t test, t (46) = 0.7510; p = 0.4565; n = 24 per group).

    Journal: eNeuro

    Article Title: Parvalbumin Neuron–Targeted Loss of Alzheimer’s Disease Risk Gene BIN1 Is Insufficient to Drive Cognitive or Network Excitability Changes

    doi: 10.1523/ENEURO.0304-25.2026

    Figure Lengend Snippet: Machine learning–based pose estimation and behavioral clustering show no differences in Bin1- pvKO mice. A , Similarity dendrogram from KPMS behavioral clustering analysis following DLC pose estimation trained network. Syllables were sorted by dendrogram clustering, grouped by behavior class, and normalized to control syllable usage (two-way RM ANOVA of syllable usage across genotypes; interaction effect, F (36,1656) = 0.5730; p = 0.9806; effect of genotype, F (1,46) = 0.004145; p = 0.9489; effect of syllable, F (5.837,268.5) = 0.5730; p = 0.7471; n = 24 per group). B , Sum of percent time spent in each syllable group, color coded and clustered from panel A (two-way RM ANOVA of syllable group usage; interaction effect, F (6,276) = 0.4985; p = 0.8093; genotype effect, F (1,46) = 0.02772; p = 0.8685; syllable effect, F (1.960,90.16) = 349.1; p < 0.0001; n = 24 per group). C , Total distance traveled in the hour-long recording session, as tracked by the ezTrack software (unpaired t test, t (46) = 0.7510; p = 0.4565; n = 24 per group).

    Article Snippet: Bin1 flox/flox mice were also crossed with Nestin-Cre mice (RRID:IMSR_JAX:00377) for knock-out validation ( ).

    Techniques: Control, Software

    Bin1- pvKO mice do not show increased PTZ-induced seizure susceptibility. A , Maximum seizure stage reached after PTZ (40 mg/kg) at 3–7 months (Mann–Whitney test, U = 371.5; p = 0.6426; n = 25–32 per group) and B , latency to each stage (two-way RM ANOVA; interaction effect, F (7,385) = 0.9376; p = 0.4771; genotype effect, F (1,55) = 0.1576; p = 0.6929; time effect, F (3.233,177.8) = 141.9; p < 0.0001; n = 25–32). C , Maximum seizure stage reached after PTZ (30 mg/kg; 40 mg/kg dose shown in ) at 16–20 months (Mann–Whitney test, U = 405.5; p = 0.3881; n = 30–31 per group) and D , latency to each stage (two-way RM ANOVA; interaction effect, F (7,413) = 2.161; p = 0.0367; genotype effect, F (1,59) = 0.3235; p = 0.5716; time effect, F (3.424,202.0) = 95.81; p < 0.0001; n = 30–31).

    Journal: eNeuro

    Article Title: Parvalbumin Neuron–Targeted Loss of Alzheimer’s Disease Risk Gene BIN1 Is Insufficient to Drive Cognitive or Network Excitability Changes

    doi: 10.1523/ENEURO.0304-25.2026

    Figure Lengend Snippet: Bin1- pvKO mice do not show increased PTZ-induced seizure susceptibility. A , Maximum seizure stage reached after PTZ (40 mg/kg) at 3–7 months (Mann–Whitney test, U = 371.5; p = 0.6426; n = 25–32 per group) and B , latency to each stage (two-way RM ANOVA; interaction effect, F (7,385) = 0.9376; p = 0.4771; genotype effect, F (1,55) = 0.1576; p = 0.6929; time effect, F (3.233,177.8) = 141.9; p < 0.0001; n = 25–32). C , Maximum seizure stage reached after PTZ (30 mg/kg; 40 mg/kg dose shown in ) at 16–20 months (Mann–Whitney test, U = 405.5; p = 0.3881; n = 30–31 per group) and D , latency to each stage (two-way RM ANOVA; interaction effect, F (7,413) = 2.161; p = 0.0367; genotype effect, F (1,59) = 0.3235; p = 0.5716; time effect, F (3.424,202.0) = 95.81; p < 0.0001; n = 30–31).

    Article Snippet: Bin1 flox/flox mice were also crossed with Nestin-Cre mice (RRID:IMSR_JAX:00377) for knock-out validation ( ).

    Techniques: MANN-WHITNEY

    Bin1- pvKO mice do not show spiking like that observed in AD models. A , Example waveforms used for spike classification in EEG recordings. B , Spike class per hour ( A , Welch’s t test, t (6.477) = 1.968; p = 0.0931; B , Mann–Whitney test, U = 18; p = 0.4557; C , U = 15.50; p = 0.2756; n = 7 per group). C , Total spikes per hour averaged over the entire recording (Mann–Whitney test, U = 19; p = 0.5350; n = 7 per group). D , Spikes per hour in hAPPJ20 mice (Mann–Whitney test, U = 0; p = 0.2000; n = 2–3 per group).

    Journal: eNeuro

    Article Title: Parvalbumin Neuron–Targeted Loss of Alzheimer’s Disease Risk Gene BIN1 Is Insufficient to Drive Cognitive or Network Excitability Changes

    doi: 10.1523/ENEURO.0304-25.2026

    Figure Lengend Snippet: Bin1- pvKO mice do not show spiking like that observed in AD models. A , Example waveforms used for spike classification in EEG recordings. B , Spike class per hour ( A , Welch’s t test, t (6.477) = 1.968; p = 0.0931; B , Mann–Whitney test, U = 18; p = 0.4557; C , U = 15.50; p = 0.2756; n = 7 per group). C , Total spikes per hour averaged over the entire recording (Mann–Whitney test, U = 19; p = 0.5350; n = 7 per group). D , Spikes per hour in hAPPJ20 mice (Mann–Whitney test, U = 0; p = 0.2000; n = 2–3 per group).

    Article Snippet: Bin1 flox/flox mice were also crossed with Nestin-Cre mice (RRID:IMSR_JAX:00377) for knock-out validation ( ).

    Techniques: MANN-WHITNEY

    Bin1- pvKO mice do not show major network alterations. A , Representative traces for control (left) and Bin1- pvKO (right) showing frequency band intensity, EEG traces, EMG traces, and locomotory activity during resting and active states. B , Delta power across activity states (two-way RM ANOVA, interaction, F (10,120) = 1.979; p = 0.0413; activity, F (1,12) = 84.80; p < 0.0001; genotype, F (1,12) = 2.392; p = 0.1479). C , Theta power across activity states (two-way RM ANOVA; interaction, F (10,120) = 0.5857; p = 0.8230; activity, F (1,12) = 66.99; p < 0.0001; genotype, F (1,12) = 0.1720; p = 0.6856). D , Alpha power across activity states (two-way RM ANOVA; interaction, F (10,120) = 1.137; p = 0.3404; activity, F (1,12) = 1.315; p = 0.2739; genotype, F (1,12) = 0.8494; p = 0.3749). E , Beta power across activity states (two-way RM ANOVA; interaction, F (10,120) = 0.5066; p = 0.8826; activity, F (1,12) = 6.997; p = 0.0214; genotype, F (1,12) = 0.3038; p = 0.5917). F , Gamma power across activity states (two-way RM ANOVA, interaction, F (10,120) = 0.2118; p = 0.9949; activity, F (1,12) = 266.2; p < 0.0001; genotype, F (1,12) = 0.009647; p = 0.9234). G , Average locomotor activity over the 24-h cycle (two-way RM ANOVA; interaction, F (23,276) = 0.353; p = 0.9977; time, F (4.054, 48.65) = 6.682; p = 0.0002; genotype, F (1,12) = 0.09613; p = 0.7618). H , Average normalized total power over the 24 h cycle (two-way RM ANOVA, interaction, F (23,276) = 1.356; p = 0.1316; time, F (5.287, 63.44) = 2.795; p = 0.0221; genotype, F (1,12) = 0.2240; p = 0.6445), individual power bands across the 24 h cycle shown in . I , Distribution of percent usage of each frequency band normalized to total power (two-way RM ANOVA, interaction, F (4,48) = 0.8896; p = 0.4774; frequency band, F (2.584, 31.01) = 107.4; p < 0.0001; genotype, F (1,12) = 0.2857; p = 0.6028). J , Percent time awake over a 24 h period (two-way RM ANOVA, time effect, F (7.114, 85.37) = 5.648; p < 0.0001; genotype effect, F (1,12) = 1.494; p = 0.2451; interaction effect, F (23,276) = 0.5560; p = 0.9526; n = 7 per group). K , Percent time in NREM over a 24 h period (two-way RM ANOVA, time effect, F (7.146, 85.75) = 5.435; p < 0.0001; genotype effect, F (1,12) = 1.198; p = 0.2953; interaction effect, F (23,276) = 0.5649; p = 0.9481; n = 7 per group). L , Percent time in REM over a 24 h period (two-way RM ANOVA; time effect, F (6.558, 78.70) = 4.918; p = 0.0002; genotype effect, F (1,12) = 0.2486; p = 0.6271; interaction effect, F (23,276) = 0.6717; p = 0.8720; n = 7 per group). Further sleep analysis shown in .

    Journal: eNeuro

    Article Title: Parvalbumin Neuron–Targeted Loss of Alzheimer’s Disease Risk Gene BIN1 Is Insufficient to Drive Cognitive or Network Excitability Changes

    doi: 10.1523/ENEURO.0304-25.2026

    Figure Lengend Snippet: Bin1- pvKO mice do not show major network alterations. A , Representative traces for control (left) and Bin1- pvKO (right) showing frequency band intensity, EEG traces, EMG traces, and locomotory activity during resting and active states. B , Delta power across activity states (two-way RM ANOVA, interaction, F (10,120) = 1.979; p = 0.0413; activity, F (1,12) = 84.80; p < 0.0001; genotype, F (1,12) = 2.392; p = 0.1479). C , Theta power across activity states (two-way RM ANOVA; interaction, F (10,120) = 0.5857; p = 0.8230; activity, F (1,12) = 66.99; p < 0.0001; genotype, F (1,12) = 0.1720; p = 0.6856). D , Alpha power across activity states (two-way RM ANOVA; interaction, F (10,120) = 1.137; p = 0.3404; activity, F (1,12) = 1.315; p = 0.2739; genotype, F (1,12) = 0.8494; p = 0.3749). E , Beta power across activity states (two-way RM ANOVA; interaction, F (10,120) = 0.5066; p = 0.8826; activity, F (1,12) = 6.997; p = 0.0214; genotype, F (1,12) = 0.3038; p = 0.5917). F , Gamma power across activity states (two-way RM ANOVA, interaction, F (10,120) = 0.2118; p = 0.9949; activity, F (1,12) = 266.2; p < 0.0001; genotype, F (1,12) = 0.009647; p = 0.9234). G , Average locomotor activity over the 24-h cycle (two-way RM ANOVA; interaction, F (23,276) = 0.353; p = 0.9977; time, F (4.054, 48.65) = 6.682; p = 0.0002; genotype, F (1,12) = 0.09613; p = 0.7618). H , Average normalized total power over the 24 h cycle (two-way RM ANOVA, interaction, F (23,276) = 1.356; p = 0.1316; time, F (5.287, 63.44) = 2.795; p = 0.0221; genotype, F (1,12) = 0.2240; p = 0.6445), individual power bands across the 24 h cycle shown in . I , Distribution of percent usage of each frequency band normalized to total power (two-way RM ANOVA, interaction, F (4,48) = 0.8896; p = 0.4774; frequency band, F (2.584, 31.01) = 107.4; p < 0.0001; genotype, F (1,12) = 0.2857; p = 0.6028). J , Percent time awake over a 24 h period (two-way RM ANOVA, time effect, F (7.114, 85.37) = 5.648; p < 0.0001; genotype effect, F (1,12) = 1.494; p = 0.2451; interaction effect, F (23,276) = 0.5560; p = 0.9526; n = 7 per group). K , Percent time in NREM over a 24 h period (two-way RM ANOVA, time effect, F (7.146, 85.75) = 5.435; p < 0.0001; genotype effect, F (1,12) = 1.198; p = 0.2953; interaction effect, F (23,276) = 0.5649; p = 0.9481; n = 7 per group). L , Percent time in REM over a 24 h period (two-way RM ANOVA; time effect, F (6.558, 78.70) = 4.918; p = 0.0002; genotype effect, F (1,12) = 0.2486; p = 0.6271; interaction effect, F (23,276) = 0.6717; p = 0.8720; n = 7 per group). Further sleep analysis shown in .

    Article Snippet: Bin1 flox/flox mice were also crossed with Nestin-Cre mice (RRID:IMSR_JAX:00377) for knock-out validation ( ).

    Techniques: Control, Activity Assay