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Santa Cruz Biotechnology mouse anti catd
Mouse Anti Catd, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 663 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+anti+catd/cathepsin+D+Antibody/pmc10996108-54-15-18
Average 96 stars, based on 663 article reviews

mouse anti catd - by Bioz Stars, 2026-10

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Article Title: Prominent tauopathy and intracellular β-amyloid accumulation triggered by genetic deletion of cathepsin D: implications for Alzheimer disease pathogenesis
Article Snippet: Protein extracts were run on 8% SDS–PAGE gels (ThermoFisher, Waltham, MA), transferred to nitrocellulose and probed with the following antibodies (and dilutions, sources): mouse anti-CatD (1:1000; Santa Cruz Biotechnologies, Santa Cruz, CA; Cat. No. sc-377,299); TAU-5 (1:1000; Abcam, Boston, MA; Cat. No. Ab80579); PHF-1 (1:1000; [ ]); C3 (1:500; MilliporeSigma, Burlington, MA; Cat. No. MAB5430-C); P44 (1:1000; [ ]); and GAPDH (1:10000; Bio design Meridian Life Science, Memphis, TN; Cat. No. H86504M).

Article Title: Prominent tauopathy and intracellular β-amyloid accumulation triggered by genetic deletion of cathepsin D: implications for Alzheimer disease pathogenesis
Article Snippet: Another subset of brain sections was immunostained with the following primary antibodies (and dilutions, sources): mouse anti-CatD (1:1000; Santa Cruz Biotechnologies, Santa Cruz, CA; Cat. No. sc-377,299); 33.1.1.1, targeting all Aβ species (1:1000; [ , ]); rabbit anti-ubiquitin (1:1000; Dako North America, Inc., Carpinteria, CA); mouse anti-GFAP (1:2000; Santa Cruz Biotechnologies, Santa Cruz, CA; Cat. No. sc-33,673); CP13, targeting tau phosphorylated at Ser202 (1:1000 or 1:2000; [ ]); PHF-1, targeting tau phosphorylated at Ser396 and Ser404 (1:1000 or 1:2000; [ ]); or AT180, targeting tau phosphorylated at Thr213 (1:1000; [ ]); then visualized by treatment with 3,3’-diaminobenzidine (DAB) with appropriate horse-radish peroxidase-conjugated secondary antibodies, as described [ ].

Article Title: Prominent tauopathy and intracellular β-amyloid accumulation triggered by genetic deletion of cathepsin D: Implications for Alzheimer disease pathogenesis
Article Snippet: Another subset of brain sections was immunostained with the following primary antibodies (and dilutions, sources): mouse anti-CatD (1:1000; Santa Cruz Biotechnologies, Santa Cruz, CA; Cat. No. sc-377299); 33.1.1.1, targeting all Aβ species (1:1000; [28, 30]); rabbit anti-ubiquitin (1:1000; Dako North America, Inc., Carpinteria, CA); mouse antiGFAP (1:2000; Santa Cruz Biotechnologies, Santa Cruz, CA; Cat. No. sc-33673); CP13, targeting tau phosphorylated at Ser202 (1:1000 or 1:2000; [31]); or PHF-1, targeting tau phosphorylated at Ser396 and Ser404 (1:1000 or 1:2000; [32]), then visualized by treatment with 3,3'-diaminobenzidine (DAB) with appropriate horse-radish peroxidase-conjugated secondary antibodies, as described [26].

Article Title: Prominent tauopathy and intracellular β-amyloid accumulation triggered by genetic deletion of cathepsin D: Implications for Alzheimer disease pathogenesis
Article Snippet: Protein extracts were run on 8% SDS–PAGE gels (ThermoFisher, Waltham, MA), transferred to nitrocellulose and probed with the following antibodies (and dilutions, sources): mouse anti-CatD (1:1000; Santa Cruz Biotechnologies, Santa Cruz, CA; Cat. No. sc-377299); TAU-5 (1:1000; Abcam, Boston, MA; Cat. No. Ab80579); PHF-1 (1:1000; [32]); C3 (1:500; MilliporeSigma, Burlington, MA; Cat. No. MAB5430-C); P44 (1:1000; [35]); and GAPDH (1:10000; Bio design Meridian Life Science, Memphis, TN; Cat. No. H86504M).

Image Search Results

Loss of NHE6 increases MVB fusion with the PM and exosome secretion. A , Representative TIRF image depicting MVB-PM fusion and exosome release as developed from . Widefield image of neuron cotransfected with mCherry and CD63-pHluorin expression constructs. White inset, Location of MVB-PM fusion and the zoomed in panels on the right. Each panel represents the progression of a CD63-pHluorin fusion event with the PM with the number of seconds indicated below the panel. Scale bars: large, 10 µm; small, 1 µm. B , Quantification of full MVB-PM fusion/exosome release events per cell over 5 min in WT and Nhe6 -/Y male littermate mouse primary hippocampal neurons at 14 DIV (WT n = 28 cells from 7 mice, Nhe6 -/Y n = 18 cells from 7 mice, 5 litters, p = 0.009, Glass's Δ = 2.27). C , Quantification of full MVB-PM fusion/exosome release events per cell over 5 min in WT and Nhe6 -/Y male mouse primary hippocampal neurons at 14 DIV under the following conditions: untreated (same as in B ), U18666A (positive control) (WT n = 14 cells from 5 mice, Nhe6 -/Y n = 14 cells from 5 mice, 3 litters), bafilomycin A1 (positive control) (WT n = 14 cells from 7 mice, Nhe6 -/Y n = 16 cells from 6 mice, 4 litters, Kruskal–Wallis test with Dunn's test: WT untreated compared with WT bafilomycin A1 p = 0.002, Glass's Δ = 3.04). D , E , CD63 western blot ( D ) and quantification ( E ) in WT and Nhe6 -/Y male littermate mouse primary hippocampal neurons at 14 DIV (WT n = 5 cultures, Nhe6 -/Y n = 5 cultures, 5 litters, p = 0.02, Glass's Δ = 1.68). F , Released β-Hex enzyme activity following short-term incubation in Tyrode's solution followed by treatment with either ionomycin or DMSO (WT n = 9, Nhe6 -/Y n = 9, 8 litters). G , Released CatD enzyme activity following short-term incubation in Tyrode's solution followed by treatment with either ionomycin or DMSO (WT n = 6, Nhe6 -/Y n = 6, 5 litters). H , Released LDH activity across all β-Hex (WT n = 5, Nhe6 -/Y n = 5, 5 litters) and CatD (WT n = 4, Nhe6 -/Y n = 4, 3 litters) experiments. Data are mean ± SEM. Unpaired two-tailed Student's t test ( C , WT- Nhe6 -/Y : bafilomycin A1) with Welch's correction ( E ), Mann–Whitney test ( B , C , WT- Nhe6 -/Y : U18666A), Kruskal–Wallis test with Dunn's test ( C , differences between treatments by genotype), two-way ANOVA with Tukey's multiple comparisons test ( F , G , H ).

Journal: The Journal of Neuroscience

Article Title: Loss of Christianson Syndrome Na + /H + Exchanger 6 (NHE6) Causes Abnormal Endosome Maturation and Trafficking Underlying Lysosome Dysfunction in Neurons

doi: 10.1523/JNEUROSCI.1244-20.2021

Figure Lengend Snippet: Loss of NHE6 increases MVB fusion with the PM and exosome secretion. A , Representative TIRF image depicting MVB-PM fusion and exosome release as developed from . Widefield image of neuron cotransfected with mCherry and CD63-pHluorin expression constructs. White inset, Location of MVB-PM fusion and the zoomed in panels on the right. Each panel represents the progression of a CD63-pHluorin fusion event with the PM with the number of seconds indicated below the panel. Scale bars: large, 10 µm; small, 1 µm. B , Quantification of full MVB-PM fusion/exosome release events per cell over 5 min in WT and Nhe6 -/Y male littermate mouse primary hippocampal neurons at 14 DIV (WT n = 28 cells from 7 mice, Nhe6 -/Y n = 18 cells from 7 mice, 5 litters, p = 0.009, Glass's Δ = 2.27). C , Quantification of full MVB-PM fusion/exosome release events per cell over 5 min in WT and Nhe6 -/Y male mouse primary hippocampal neurons at 14 DIV under the following conditions: untreated (same as in B ), U18666A (positive control) (WT n = 14 cells from 5 mice, Nhe6 -/Y n = 14 cells from 5 mice, 3 litters), bafilomycin A1 (positive control) (WT n = 14 cells from 7 mice, Nhe6 -/Y n = 16 cells from 6 mice, 4 litters, Kruskal–Wallis test with Dunn's test: WT untreated compared with WT bafilomycin A1 p = 0.002, Glass's Δ = 3.04). D , E , CD63 western blot ( D ) and quantification ( E ) in WT and Nhe6 -/Y male littermate mouse primary hippocampal neurons at 14 DIV (WT n = 5 cultures, Nhe6 -/Y n = 5 cultures, 5 litters, p = 0.02, Glass's Δ = 1.68). F , Released β-Hex enzyme activity following short-term incubation in Tyrode's solution followed by treatment with either ionomycin or DMSO (WT n = 9, Nhe6 -/Y n = 9, 8 litters). G , Released CatD enzyme activity following short-term incubation in Tyrode's solution followed by treatment with either ionomycin or DMSO (WT n = 6, Nhe6 -/Y n = 6, 5 litters). H , Released LDH activity across all β-Hex (WT n = 5, Nhe6 -/Y n = 5, 5 litters) and CatD (WT n = 4, Nhe6 -/Y n = 4, 3 litters) experiments. Data are mean ± SEM. Unpaired two-tailed Student's t test ( C , WT- Nhe6 -/Y : bafilomycin A1) with Welch's correction ( E ), Mann–Whitney test ( B , C , WT- Nhe6 -/Y : U18666A), Kruskal–Wallis test with Dunn's test ( C , differences between treatments by genotype), two-way ANOVA with Tukey's multiple comparisons test ( F , G , H ).

Article Snippet: The following antibodies were used for western blot: actin (Sigma, A3853, Ms, 1:1000), CatD (R&D Systems, AF1029, Gt, 1:1000), CD63 (Abcam, EPR21151-ab217345, Rb, 1:1000), ci-mannose 6-phosphate receptor (M6PR) (Cell Signaling Technology, 14364S, Rb, 1:500), GAPDH (Sigma, G8795, Ms, 1:40 000), LAMP1 (DSHB, 1D4B, Rt, 1:1000), RAB5 (Cell Signaling Technology, 3547, Rb, 1:1000), and RAB7 (Sigma, R8779, Ms, 1:1000).

Techniques: Expressing, Construct, Positive Control, Western Blot, Activity Assay, Incubation, Two Tailed Test, MANN-WHITNEY

Figure 12. Loss of NHE6 increases MVB fusion with the PM and exosome secretion. A, Representative TIRF image depicting MVB-PM fusion and exosome release as developed from Verweij et al. (2018). Widefield image of neuron cotransfected with mCherry and CD63-pHluorin expression constructs. White inset, Location of MVB-PM fusion and the zoomed in panels on the right. Each panel represents the progression of a CD63-pHluorin fusion event with the PM with the number of seconds indicated below the panel. Scale bars: large, 10mm; small, 1 mm. B, Quantification of full MVB-PM fusion/exosome release events per cell over 5 min in WT and Nhe6-/Y male littermate mouse primary hippocampal neurons at 14 DIV (WT n = 28 cells from 7 mice, Nhe6-/Y n = 18 cells from 7 mice, 5 litters, p = 0.009, Glass’s D = 2.27). C, Quantification of full MVB-PM fusion/exosome release events per cell over 5 min in WT and Nhe6-/Y male mouse primary hippocampal neurons at 14 DIV under the following conditions: untreated (same as in B), U18666A (positive control) (WT n = 14 cells from 5 mice, Nhe6-/Y n = 14 cells from 5 mice, 3 litters), bafilomycin A1 (positive control) (WT n = 14 cells from 7 mice, Nhe6-/Y n = 16 cells from 6 mice, 4 litters, Kruskal–Wallis test with Dunn’s test: WT untreated compared with WT bafilomycin A1 p = 0.002, Glass’s D = 3.04). D, E, CD63 western blot (D) and quantification (E) in WT and Nhe6-/Y male littermate mouse primary hippocampal neurons at 14 DIV (WT n = 5 cultures, Nhe6-/Y n = 5 cultures, 5 litters, p = 0.02, Glass’s D = 1.68). F, Released b -Hex enzyme activity following short-term incubation in Tyrode’s solution followed by treatment with either ionomycin or DMSO (WT n = 9, Nhe6-/Y n = 9, 8 litters). G, Released CatD enzyme activity following short-term incubation in Tyrode’s solution followed by treatment with either ionomycin or DMSO (WT n = 6, Nhe6-/Y n = 6, 5 litters). H, Released LDH activity across all b -Hex (WT n = 5, Nhe6-/Y n = 5, 5 litters) and CatD (WT n = 4, Nhe6-/Y n = 4, 3 litters) experiments. Data are mean 6 SEM. Unpaired two-tailed Student’s t test (C, WT-Nhe6-/Y: bafilomycin A1) with Welch’s correction (E), Mann–Whitney test (B,C, WT-Nhe6-/Y: U18666A), Kruskal–Wallis test with Dunn’s test (C, differences between treatments by genotype), two-way ANOVA with Tukey’s multiple comparisons test (F,G,H).

Journal: The Journal of Neuroscience

Article Title: Loss of Christianson Syndrome Na⁺/H⁺ Exchanger 6 (NHE6) Causes Abnormal Endosome Maturation and Trafficking Underlying Lysosome Dysfunction in Neurons

doi: 10.1523/jneurosci.1244-20.2021

Figure Lengend Snippet: Figure 12. Loss of NHE6 increases MVB fusion with the PM and exosome secretion. A, Representative TIRF image depicting MVB-PM fusion and exosome release as developed from Verweij et al. (2018). Widefield image of neuron cotransfected with mCherry and CD63-pHluorin expression constructs. White inset, Location of MVB-PM fusion and the zoomed in panels on the right. Each panel represents the progression of a CD63-pHluorin fusion event with the PM with the number of seconds indicated below the panel. Scale bars: large, 10mm; small, 1 mm. B, Quantification of full MVB-PM fusion/exosome release events per cell over 5 min in WT and Nhe6-/Y male littermate mouse primary hippocampal neurons at 14 DIV (WT n = 28 cells from 7 mice, Nhe6-/Y n = 18 cells from 7 mice, 5 litters, p = 0.009, Glass’s D = 2.27). C, Quantification of full MVB-PM fusion/exosome release events per cell over 5 min in WT and Nhe6-/Y male mouse primary hippocampal neurons at 14 DIV under the following conditions: untreated (same as in B), U18666A (positive control) (WT n = 14 cells from 5 mice, Nhe6-/Y n = 14 cells from 5 mice, 3 litters), bafilomycin A1 (positive control) (WT n = 14 cells from 7 mice, Nhe6-/Y n = 16 cells from 6 mice, 4 litters, Kruskal–Wallis test with Dunn’s test: WT untreated compared with WT bafilomycin A1 p = 0.002, Glass’s D = 3.04). D, E, CD63 western blot (D) and quantification (E) in WT and Nhe6-/Y male littermate mouse primary hippocampal neurons at 14 DIV (WT n = 5 cultures, Nhe6-/Y n = 5 cultures, 5 litters, p = 0.02, Glass’s D = 1.68). F, Released b -Hex enzyme activity following short-term incubation in Tyrode’s solution followed by treatment with either ionomycin or DMSO (WT n = 9, Nhe6-/Y n = 9, 8 litters). G, Released CatD enzyme activity following short-term incubation in Tyrode’s solution followed by treatment with either ionomycin or DMSO (WT n = 6, Nhe6-/Y n = 6, 5 litters). H, Released LDH activity across all b -Hex (WT n = 5, Nhe6-/Y n = 5, 5 litters) and CatD (WT n = 4, Nhe6-/Y n = 4, 3 litters) experiments. Data are mean 6 SEM. Unpaired two-tailed Student’s t test (C, WT-Nhe6-/Y: bafilomycin A1) with Welch’s correction (E), Mann–Whitney test (B,C, WT-Nhe6-/Y: U18666A), Kruskal–Wallis test with Dunn’s test (C, differences between treatments by genotype), two-way ANOVA with Tukey’s multiple comparisons test (F,G,H).