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rabbit antibody against psap  (Proteintech)


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    Structured Review

    Proteintech rabbit antibody against psap
    Increased protein levels of <t>PSAP</t> and PGRN within the SFO of SAP-D −/− mice a – b) , Coronal brain section at 0.7–0.8 mm posterior to bregma containing the SFO. a: DAPI staining. a-2: Enlarged view of the white square in a-1. SFO: subfornical organ, 3V: third ventricle. b; Double immunofluorescent staining of PSAP (red) and PGRN (green) in 10-month-old female WT and SAP-D −/− mice. DAPI (blue) staining showed the nuclei ( a and b ). Scale bar, 500 μm ( a and b ). White arrowheads indicate the SFO regions ( b ). c) Cerebral region from 3-, 6-, and 10-month-old male and female mice containing the SFO (0.7–0.8 mm posterior to ∗bregma) used for protein extraction and Western blot ( d – h ) using anti- PSAP, PGRN, and <t>GAPDH</t> <t>antibodies.</t> Quantification normalized to GAPDH expression and represented as the mean ± SD of three mice for each group. and indicate the individual values in each group ( e , f , h ). d – f) PSAP and PGRN protein levels in the SFO were remarkably increased. Their quantification by densitometric analysis is represented in e for male and f for female, respectively. e ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effects of genotype (F(1,24) = 547.7, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.51, −62.43]), with no effect of age ( p = 0.46) or genotype × age interaction ( p = 0.47). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 354.2, p < 0.0001, ηp 2 = 0.48, 95 % CI [−46.39, −37.22]), with no effect of age ( p = 0.73) or genotype × age interaction ( p = 0.76). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.87, 95 % CI [−52.71, −28.91]), 6 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−52.82, −29.02]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−52.32, −28.52]). f ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 611.1, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.42, −62.95]), with no effect of age ( p = 0.07) or genotype × age interaction (p = 0.07). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 273.5, p < 0.0001, ηp 2 = 0.47, 95 % CI [−63.96, −49.76]), with no effect of age ( p = 0.71) or genotype × age interaction (p = 0.70). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.31, 95 % CI [−73.43, −36.60]), 6 M ( p < 0.0001, Cohen's d = 5.71, 95 % CI [−73.04, −36.22]), and 10 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−73.08, −36.26]). g – h ) Comparison of PSAP and PGRN protein expression in the SFO, whole cerebrum, and cerebellum. The quantitative analysis is shown in h . h ) For PSAP/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 30.06, p = 0.0007, η 2 = 0.90), but not in WT mice ( p = 0.3461). Tukey's post hoc tests showed significant differences for SFO versus cerebellum ( p = 0.0010, Cohen's d = 5.26, 95 % CI [46.80, 119.1]) as well as and cerebrum versus cerebellum ( p = 0.0018, Cohen's d = 9.34, 95 % CI [38.39, 110.6]). There was no significant difference for SFO versus cerebrum ( p = 0.76, Cohen's d = 0.47, 95 % CI [−27.71, 44.54]). For PGRN/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 54.42, p = 0.0001, η 2 = 0.94), but not in WT mice ( p = 0.6327). Tukey's post hoc tests showed significant differences for SFO versus cerebrum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]) as well as and SFO versus cerebellum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]), but not for cerebrum versus cerebellum ( p = 0.3274, Cohen's d = 6.06, 95 % CI [−7.72, 23.92]). ns: no significant difference. ∗∗∗∗ p < 0.0001. ∗∗∗ p < 0.001. ∗∗ p < 0.01.
    Rabbit Antibody Against Psap, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 35 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+antibody+against+psap/pmc12720004-219-6-13?v=Proteintech
    Average 94 stars, based on 35 article reviews
    rabbit antibody against psap - by Bioz Stars, 2026-08
    94/100 stars

    Images

    1) Product Images from "Accumulation of prosaposin and progranulin around the subfornical organ induces polydipsia in SAP-D-deficient mice"

    Article Title: Accumulation of prosaposin and progranulin around the subfornical organ induces polydipsia in SAP-D-deficient mice

    Journal: Biochemistry and Biophysics Reports

    doi: 10.1016/j.bbrep.2025.102388

    Increased protein levels of PSAP and PGRN within the SFO of SAP-D −/− mice a – b) , Coronal brain section at 0.7–0.8 mm posterior to bregma containing the SFO. a: DAPI staining. a-2: Enlarged view of the white square in a-1. SFO: subfornical organ, 3V: third ventricle. b; Double immunofluorescent staining of PSAP (red) and PGRN (green) in 10-month-old female WT and SAP-D −/− mice. DAPI (blue) staining showed the nuclei ( a and b ). Scale bar, 500 μm ( a and b ). White arrowheads indicate the SFO regions ( b ). c) Cerebral region from 3-, 6-, and 10-month-old male and female mice containing the SFO (0.7–0.8 mm posterior to ∗bregma) used for protein extraction and Western blot ( d – h ) using anti- PSAP, PGRN, and GAPDH antibodies. Quantification normalized to GAPDH expression and represented as the mean ± SD of three mice for each group. and indicate the individual values in each group ( e , f , h ). d – f) PSAP and PGRN protein levels in the SFO were remarkably increased. Their quantification by densitometric analysis is represented in e for male and f for female, respectively. e ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effects of genotype (F(1,24) = 547.7, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.51, −62.43]), with no effect of age ( p = 0.46) or genotype × age interaction ( p = 0.47). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 354.2, p < 0.0001, ηp 2 = 0.48, 95 % CI [−46.39, −37.22]), with no effect of age ( p = 0.73) or genotype × age interaction ( p = 0.76). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.87, 95 % CI [−52.71, −28.91]), 6 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−52.82, −29.02]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−52.32, −28.52]). f ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 611.1, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.42, −62.95]), with no effect of age ( p = 0.07) or genotype × age interaction (p = 0.07). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 273.5, p < 0.0001, ηp 2 = 0.47, 95 % CI [−63.96, −49.76]), with no effect of age ( p = 0.71) or genotype × age interaction (p = 0.70). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.31, 95 % CI [−73.43, −36.60]), 6 M ( p < 0.0001, Cohen's d = 5.71, 95 % CI [−73.04, −36.22]), and 10 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−73.08, −36.26]). g – h ) Comparison of PSAP and PGRN protein expression in the SFO, whole cerebrum, and cerebellum. The quantitative analysis is shown in h . h ) For PSAP/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 30.06, p = 0.0007, η 2 = 0.90), but not in WT mice ( p = 0.3461). Tukey's post hoc tests showed significant differences for SFO versus cerebellum ( p = 0.0010, Cohen's d = 5.26, 95 % CI [46.80, 119.1]) as well as and cerebrum versus cerebellum ( p = 0.0018, Cohen's d = 9.34, 95 % CI [38.39, 110.6]). There was no significant difference for SFO versus cerebrum ( p = 0.76, Cohen's d = 0.47, 95 % CI [−27.71, 44.54]). For PGRN/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 54.42, p = 0.0001, η 2 = 0.94), but not in WT mice ( p = 0.6327). Tukey's post hoc tests showed significant differences for SFO versus cerebrum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]) as well as and SFO versus cerebellum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]), but not for cerebrum versus cerebellum ( p = 0.3274, Cohen's d = 6.06, 95 % CI [−7.72, 23.92]). ns: no significant difference. ∗∗∗∗ p < 0.0001. ∗∗∗ p < 0.001. ∗∗ p < 0.01.
    Figure Legend Snippet: Increased protein levels of PSAP and PGRN within the SFO of SAP-D −/− mice a – b) , Coronal brain section at 0.7–0.8 mm posterior to bregma containing the SFO. a: DAPI staining. a-2: Enlarged view of the white square in a-1. SFO: subfornical organ, 3V: third ventricle. b; Double immunofluorescent staining of PSAP (red) and PGRN (green) in 10-month-old female WT and SAP-D −/− mice. DAPI (blue) staining showed the nuclei ( a and b ). Scale bar, 500 μm ( a and b ). White arrowheads indicate the SFO regions ( b ). c) Cerebral region from 3-, 6-, and 10-month-old male and female mice containing the SFO (0.7–0.8 mm posterior to ∗bregma) used for protein extraction and Western blot ( d – h ) using anti- PSAP, PGRN, and GAPDH antibodies. Quantification normalized to GAPDH expression and represented as the mean ± SD of three mice for each group. and indicate the individual values in each group ( e , f , h ). d – f) PSAP and PGRN protein levels in the SFO were remarkably increased. Their quantification by densitometric analysis is represented in e for male and f for female, respectively. e ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effects of genotype (F(1,24) = 547.7, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.51, −62.43]), with no effect of age ( p = 0.46) or genotype × age interaction ( p = 0.47). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 354.2, p < 0.0001, ηp 2 = 0.48, 95 % CI [−46.39, −37.22]), with no effect of age ( p = 0.73) or genotype × age interaction ( p = 0.76). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.87, 95 % CI [−52.71, −28.91]), 6 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−52.82, −29.02]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−52.32, −28.52]). f ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 611.1, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.42, −62.95]), with no effect of age ( p = 0.07) or genotype × age interaction (p = 0.07). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 273.5, p < 0.0001, ηp 2 = 0.47, 95 % CI [−63.96, −49.76]), with no effect of age ( p = 0.71) or genotype × age interaction (p = 0.70). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.31, 95 % CI [−73.43, −36.60]), 6 M ( p < 0.0001, Cohen's d = 5.71, 95 % CI [−73.04, −36.22]), and 10 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−73.08, −36.26]). g – h ) Comparison of PSAP and PGRN protein expression in the SFO, whole cerebrum, and cerebellum. The quantitative analysis is shown in h . h ) For PSAP/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 30.06, p = 0.0007, η 2 = 0.90), but not in WT mice ( p = 0.3461). Tukey's post hoc tests showed significant differences for SFO versus cerebellum ( p = 0.0010, Cohen's d = 5.26, 95 % CI [46.80, 119.1]) as well as and cerebrum versus cerebellum ( p = 0.0018, Cohen's d = 9.34, 95 % CI [38.39, 110.6]). There was no significant difference for SFO versus cerebrum ( p = 0.76, Cohen's d = 0.47, 95 % CI [−27.71, 44.54]). For PGRN/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 54.42, p = 0.0001, η 2 = 0.94), but not in WT mice ( p = 0.6327). Tukey's post hoc tests showed significant differences for SFO versus cerebrum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]) as well as and SFO versus cerebellum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]), but not for cerebrum versus cerebellum ( p = 0.3274, Cohen's d = 6.06, 95 % CI [−7.72, 23.92]). ns: no significant difference. ∗∗∗∗ p < 0.0001. ∗∗∗ p < 0.001. ∗∗ p < 0.01.

    Techniques Used: Staining, Protein Extraction, Western Blot, Expressing, Comparison

    Increased PSAP and PGRN immunostaining in the SFO and its surrounding tissues in SAP-D −/− mice a) Double immunofluorescent staining of PSAP (red) and PGRN (green) around the SFO in 10-month-old female WT and SAP-D −/− mice. The white dotted lines enclose the SFO. b ) enlarged white ⅰ-iv squares in a, as indicated. White arrowheads indicate co-staining with anti-PGRN and PSAP antibodies. Open arrowheads indicate staining with PGRN alone. Nuclei are labeled by DAPI (blue) staining. All scale bars, 20 μm.
    Figure Legend Snippet: Increased PSAP and PGRN immunostaining in the SFO and its surrounding tissues in SAP-D −/− mice a) Double immunofluorescent staining of PSAP (red) and PGRN (green) around the SFO in 10-month-old female WT and SAP-D −/− mice. The white dotted lines enclose the SFO. b ) enlarged white ⅰ-iv squares in a, as indicated. White arrowheads indicate co-staining with anti-PGRN and PSAP antibodies. Open arrowheads indicate staining with PGRN alone. Nuclei are labeled by DAPI (blue) staining. All scale bars, 20 μm.

    Techniques Used: Immunostaining, Staining, Labeling

    Lysosomal localization of PSAP and PGRN expression around the SFO a) Immunofluorescence staining of LAMP1 (green) around the SFO in 10-month-old female WT and SAP-D −/− mice. Nuclei are labeled by DAPI (blue) staining. b) Quantification of LAMP1-stained areas in ( a ) relative to WT (%). The results of Student's t-tests for each panel are as follows: left panel, p = 0.0059, Cohen's d = 2.35 (95 % CI: 15.89, 67.66); and right panel: p = 0.0061, Cohen's d = 2.33 (95 % CI: 51.06, 220.89). Data are shown as the mean ± SD (n = 5). c) Triple immunofluorescent staining of PSAP (red), PGRN (green), and LAMP1 (cyan) around the SFO of 10-month-old female SAP-D −/− mice. Enlarged images indicated by the white squares (ⅰ-iv) were shown in c. d) Localization rate of PGRN or PSAP to LAMP1 in the SFO. The results of Student's t-tests for each panel are as follows: left panel, p = 0.0008, Cohen's d = 2.24 (95 % CI: -40.90, -13.73); and right panel, p = 0.2341, Cohen's d = 0.64 (95 % CI: 26.80, 7.17). Data are shown as the mean ± SD (n = 6 for WT-SFO and n = 8 for SAP-D −/− -SFO). e) Same experiment as in (c) on microglia/macrophage co-expressing PSAP and PGRN, or PGRN only, in the boundary and fornix regions of SAP-D −/− mice. Single image for each antibody was shown in white, while double or triple merged images were presented with red (PSAP or PGRN), green (LAMP1 or PGRN), or cyan (LAMP1) as indicated. and indicate the individual values in each group (b and d). ns: no significant difference. ∗∗∗ p < 0.001. ∗∗ p < 0.01. All scale bars, 10 μm.
    Figure Legend Snippet: Lysosomal localization of PSAP and PGRN expression around the SFO a) Immunofluorescence staining of LAMP1 (green) around the SFO in 10-month-old female WT and SAP-D −/− mice. Nuclei are labeled by DAPI (blue) staining. b) Quantification of LAMP1-stained areas in ( a ) relative to WT (%). The results of Student's t-tests for each panel are as follows: left panel, p = 0.0059, Cohen's d = 2.35 (95 % CI: 15.89, 67.66); and right panel: p = 0.0061, Cohen's d = 2.33 (95 % CI: 51.06, 220.89). Data are shown as the mean ± SD (n = 5). c) Triple immunofluorescent staining of PSAP (red), PGRN (green), and LAMP1 (cyan) around the SFO of 10-month-old female SAP-D −/− mice. Enlarged images indicated by the white squares (ⅰ-iv) were shown in c. d) Localization rate of PGRN or PSAP to LAMP1 in the SFO. The results of Student's t-tests for each panel are as follows: left panel, p = 0.0008, Cohen's d = 2.24 (95 % CI: -40.90, -13.73); and right panel, p = 0.2341, Cohen's d = 0.64 (95 % CI: 26.80, 7.17). Data are shown as the mean ± SD (n = 6 for WT-SFO and n = 8 for SAP-D −/− -SFO). e) Same experiment as in (c) on microglia/macrophage co-expressing PSAP and PGRN, or PGRN only, in the boundary and fornix regions of SAP-D −/− mice. Single image for each antibody was shown in white, while double or triple merged images were presented with red (PSAP or PGRN), green (LAMP1 or PGRN), or cyan (LAMP1) as indicated. and indicate the individual values in each group (b and d). ns: no significant difference. ∗∗∗ p < 0.001. ∗∗ p < 0.01. All scale bars, 10 μm.

    Techniques Used: Expressing, Immunofluorescence, Staining, Labeling



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    Proteintech rabbit antibody against psap
    Increased protein levels of <t>PSAP</t> and PGRN within the SFO of SAP-D −/− mice a – b) , Coronal brain section at 0.7–0.8 mm posterior to bregma containing the SFO. a: DAPI staining. a-2: Enlarged view of the white square in a-1. SFO: subfornical organ, 3V: third ventricle. b; Double immunofluorescent staining of PSAP (red) and PGRN (green) in 10-month-old female WT and SAP-D −/− mice. DAPI (blue) staining showed the nuclei ( a and b ). Scale bar, 500 μm ( a and b ). White arrowheads indicate the SFO regions ( b ). c) Cerebral region from 3-, 6-, and 10-month-old male and female mice containing the SFO (0.7–0.8 mm posterior to ∗bregma) used for protein extraction and Western blot ( d – h ) using anti- PSAP, PGRN, and <t>GAPDH</t> <t>antibodies.</t> Quantification normalized to GAPDH expression and represented as the mean ± SD of three mice for each group. and indicate the individual values in each group ( e , f , h ). d – f) PSAP and PGRN protein levels in the SFO were remarkably increased. Their quantification by densitometric analysis is represented in e for male and f for female, respectively. e ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effects of genotype (F(1,24) = 547.7, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.51, −62.43]), with no effect of age ( p = 0.46) or genotype × age interaction ( p = 0.47). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 354.2, p < 0.0001, ηp 2 = 0.48, 95 % CI [−46.39, −37.22]), with no effect of age ( p = 0.73) or genotype × age interaction ( p = 0.76). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.87, 95 % CI [−52.71, −28.91]), 6 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−52.82, −29.02]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−52.32, −28.52]). f ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 611.1, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.42, −62.95]), with no effect of age ( p = 0.07) or genotype × age interaction (p = 0.07). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 273.5, p < 0.0001, ηp 2 = 0.47, 95 % CI [−63.96, −49.76]), with no effect of age ( p = 0.71) or genotype × age interaction (p = 0.70). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.31, 95 % CI [−73.43, −36.60]), 6 M ( p < 0.0001, Cohen's d = 5.71, 95 % CI [−73.04, −36.22]), and 10 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−73.08, −36.26]). g – h ) Comparison of PSAP and PGRN protein expression in the SFO, whole cerebrum, and cerebellum. The quantitative analysis is shown in h . h ) For PSAP/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 30.06, p = 0.0007, η 2 = 0.90), but not in WT mice ( p = 0.3461). Tukey's post hoc tests showed significant differences for SFO versus cerebellum ( p = 0.0010, Cohen's d = 5.26, 95 % CI [46.80, 119.1]) as well as and cerebrum versus cerebellum ( p = 0.0018, Cohen's d = 9.34, 95 % CI [38.39, 110.6]). There was no significant difference for SFO versus cerebrum ( p = 0.76, Cohen's d = 0.47, 95 % CI [−27.71, 44.54]). For PGRN/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 54.42, p = 0.0001, η 2 = 0.94), but not in WT mice ( p = 0.6327). Tukey's post hoc tests showed significant differences for SFO versus cerebrum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]) as well as and SFO versus cerebellum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]), but not for cerebrum versus cerebellum ( p = 0.3274, Cohen's d = 6.06, 95 % CI [−7.72, 23.92]). ns: no significant difference. ∗∗∗∗ p < 0.0001. ∗∗∗ p < 0.001. ∗∗ p < 0.01.
    Rabbit Antibody Against Psap, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+antibody+against+psap/pmc12720004-219-6-13?v=Proteintech
    Average 94 stars, based on 1 article reviews
    rabbit antibody against psap - by Bioz Stars, 2026-08
    94/100 stars
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    GL Biochem polyclonal rabbit antibody against the mature peptide of sp -acp (pqitfsrswvpqamide)
    Increased protein levels of <t>PSAP</t> and PGRN within the SFO of SAP-D −/− mice a – b) , Coronal brain section at 0.7–0.8 mm posterior to bregma containing the SFO. a: DAPI staining. a-2: Enlarged view of the white square in a-1. SFO: subfornical organ, 3V: third ventricle. b; Double immunofluorescent staining of PSAP (red) and PGRN (green) in 10-month-old female WT and SAP-D −/− mice. DAPI (blue) staining showed the nuclei ( a and b ). Scale bar, 500 μm ( a and b ). White arrowheads indicate the SFO regions ( b ). c) Cerebral region from 3-, 6-, and 10-month-old male and female mice containing the SFO (0.7–0.8 mm posterior to ∗bregma) used for protein extraction and Western blot ( d – h ) using anti- PSAP, PGRN, and <t>GAPDH</t> <t>antibodies.</t> Quantification normalized to GAPDH expression and represented as the mean ± SD of three mice for each group. and indicate the individual values in each group ( e , f , h ). d – f) PSAP and PGRN protein levels in the SFO were remarkably increased. Their quantification by densitometric analysis is represented in e for male and f for female, respectively. e ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effects of genotype (F(1,24) = 547.7, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.51, −62.43]), with no effect of age ( p = 0.46) or genotype × age interaction ( p = 0.47). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 354.2, p < 0.0001, ηp 2 = 0.48, 95 % CI [−46.39, −37.22]), with no effect of age ( p = 0.73) or genotype × age interaction ( p = 0.76). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.87, 95 % CI [−52.71, −28.91]), 6 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−52.82, −29.02]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−52.32, −28.52]). f ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 611.1, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.42, −62.95]), with no effect of age ( p = 0.07) or genotype × age interaction (p = 0.07). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 273.5, p < 0.0001, ηp 2 = 0.47, 95 % CI [−63.96, −49.76]), with no effect of age ( p = 0.71) or genotype × age interaction (p = 0.70). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.31, 95 % CI [−73.43, −36.60]), 6 M ( p < 0.0001, Cohen's d = 5.71, 95 % CI [−73.04, −36.22]), and 10 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−73.08, −36.26]). g – h ) Comparison of PSAP and PGRN protein expression in the SFO, whole cerebrum, and cerebellum. The quantitative analysis is shown in h . h ) For PSAP/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 30.06, p = 0.0007, η 2 = 0.90), but not in WT mice ( p = 0.3461). Tukey's post hoc tests showed significant differences for SFO versus cerebellum ( p = 0.0010, Cohen's d = 5.26, 95 % CI [46.80, 119.1]) as well as and cerebrum versus cerebellum ( p = 0.0018, Cohen's d = 9.34, 95 % CI [38.39, 110.6]). There was no significant difference for SFO versus cerebrum ( p = 0.76, Cohen's d = 0.47, 95 % CI [−27.71, 44.54]). For PGRN/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 54.42, p = 0.0001, η 2 = 0.94), but not in WT mice ( p = 0.6327). Tukey's post hoc tests showed significant differences for SFO versus cerebrum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]) as well as and SFO versus cerebellum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]), but not for cerebrum versus cerebellum ( p = 0.3274, Cohen's d = 6.06, 95 % CI [−7.72, 23.92]). ns: no significant difference. ∗∗∗∗ p < 0.0001. ∗∗∗ p < 0.001. ∗∗ p < 0.01.
    Polyclonal Rabbit Antibody Against The Mature Peptide Of Sp Acp (Pqitfsrswvpqamide), supplied by GL Biochem, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Jackson Immuno biotinylated donkey antibody against rabbit immunoglobulin g
    Increased protein levels of <t>PSAP</t> and PGRN within the SFO of SAP-D −/− mice a – b) , Coronal brain section at 0.7–0.8 mm posterior to bregma containing the SFO. a: DAPI staining. a-2: Enlarged view of the white square in a-1. SFO: subfornical organ, 3V: third ventricle. b; Double immunofluorescent staining of PSAP (red) and PGRN (green) in 10-month-old female WT and SAP-D −/− mice. DAPI (blue) staining showed the nuclei ( a and b ). Scale bar, 500 μm ( a and b ). White arrowheads indicate the SFO regions ( b ). c) Cerebral region from 3-, 6-, and 10-month-old male and female mice containing the SFO (0.7–0.8 mm posterior to ∗bregma) used for protein extraction and Western blot ( d – h ) using anti- PSAP, PGRN, and <t>GAPDH</t> <t>antibodies.</t> Quantification normalized to GAPDH expression and represented as the mean ± SD of three mice for each group. and indicate the individual values in each group ( e , f , h ). d – f) PSAP and PGRN protein levels in the SFO were remarkably increased. Their quantification by densitometric analysis is represented in e for male and f for female, respectively. e ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effects of genotype (F(1,24) = 547.7, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.51, −62.43]), with no effect of age ( p = 0.46) or genotype × age interaction ( p = 0.47). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 354.2, p < 0.0001, ηp 2 = 0.48, 95 % CI [−46.39, −37.22]), with no effect of age ( p = 0.73) or genotype × age interaction ( p = 0.76). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.87, 95 % CI [−52.71, −28.91]), 6 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−52.82, −29.02]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−52.32, −28.52]). f ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 611.1, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.42, −62.95]), with no effect of age ( p = 0.07) or genotype × age interaction (p = 0.07). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 273.5, p < 0.0001, ηp 2 = 0.47, 95 % CI [−63.96, −49.76]), with no effect of age ( p = 0.71) or genotype × age interaction (p = 0.70). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.31, 95 % CI [−73.43, −36.60]), 6 M ( p < 0.0001, Cohen's d = 5.71, 95 % CI [−73.04, −36.22]), and 10 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−73.08, −36.26]). g – h ) Comparison of PSAP and PGRN protein expression in the SFO, whole cerebrum, and cerebellum. The quantitative analysis is shown in h . h ) For PSAP/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 30.06, p = 0.0007, η 2 = 0.90), but not in WT mice ( p = 0.3461). Tukey's post hoc tests showed significant differences for SFO versus cerebellum ( p = 0.0010, Cohen's d = 5.26, 95 % CI [46.80, 119.1]) as well as and cerebrum versus cerebellum ( p = 0.0018, Cohen's d = 9.34, 95 % CI [38.39, 110.6]). There was no significant difference for SFO versus cerebrum ( p = 0.76, Cohen's d = 0.47, 95 % CI [−27.71, 44.54]). For PGRN/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 54.42, p = 0.0001, η 2 = 0.94), but not in WT mice ( p = 0.6327). Tukey's post hoc tests showed significant differences for SFO versus cerebrum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]) as well as and SFO versus cerebellum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]), but not for cerebrum versus cerebellum ( p = 0.3274, Cohen's d = 6.06, 95 % CI [−7.72, 23.92]). ns: no significant difference. ∗∗∗∗ p < 0.0001. ∗∗∗ p < 0.001. ∗∗ p < 0.01.
    Biotinylated Donkey Antibody Against Rabbit Immunoglobulin G, supplied by Jackson Immuno, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Sino Biological rabbit polyclonal antibody against sars cov 2 sp rbd
    Increased protein levels of <t>PSAP</t> and PGRN within the SFO of SAP-D −/− mice a – b) , Coronal brain section at 0.7–0.8 mm posterior to bregma containing the SFO. a: DAPI staining. a-2: Enlarged view of the white square in a-1. SFO: subfornical organ, 3V: third ventricle. b; Double immunofluorescent staining of PSAP (red) and PGRN (green) in 10-month-old female WT and SAP-D −/− mice. DAPI (blue) staining showed the nuclei ( a and b ). Scale bar, 500 μm ( a and b ). White arrowheads indicate the SFO regions ( b ). c) Cerebral region from 3-, 6-, and 10-month-old male and female mice containing the SFO (0.7–0.8 mm posterior to ∗bregma) used for protein extraction and Western blot ( d – h ) using anti- PSAP, PGRN, and <t>GAPDH</t> <t>antibodies.</t> Quantification normalized to GAPDH expression and represented as the mean ± SD of three mice for each group. and indicate the individual values in each group ( e , f , h ). d – f) PSAP and PGRN protein levels in the SFO were remarkably increased. Their quantification by densitometric analysis is represented in e for male and f for female, respectively. e ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effects of genotype (F(1,24) = 547.7, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.51, −62.43]), with no effect of age ( p = 0.46) or genotype × age interaction ( p = 0.47). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 354.2, p < 0.0001, ηp 2 = 0.48, 95 % CI [−46.39, −37.22]), with no effect of age ( p = 0.73) or genotype × age interaction ( p = 0.76). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.87, 95 % CI [−52.71, −28.91]), 6 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−52.82, −29.02]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−52.32, −28.52]). f ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 611.1, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.42, −62.95]), with no effect of age ( p = 0.07) or genotype × age interaction (p = 0.07). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 273.5, p < 0.0001, ηp 2 = 0.47, 95 % CI [−63.96, −49.76]), with no effect of age ( p = 0.71) or genotype × age interaction (p = 0.70). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.31, 95 % CI [−73.43, −36.60]), 6 M ( p < 0.0001, Cohen's d = 5.71, 95 % CI [−73.04, −36.22]), and 10 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−73.08, −36.26]). g – h ) Comparison of PSAP and PGRN protein expression in the SFO, whole cerebrum, and cerebellum. The quantitative analysis is shown in h . h ) For PSAP/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 30.06, p = 0.0007, η 2 = 0.90), but not in WT mice ( p = 0.3461). Tukey's post hoc tests showed significant differences for SFO versus cerebellum ( p = 0.0010, Cohen's d = 5.26, 95 % CI [46.80, 119.1]) as well as and cerebrum versus cerebellum ( p = 0.0018, Cohen's d = 9.34, 95 % CI [38.39, 110.6]). There was no significant difference for SFO versus cerebrum ( p = 0.76, Cohen's d = 0.47, 95 % CI [−27.71, 44.54]). For PGRN/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 54.42, p = 0.0001, η 2 = 0.94), but not in WT mice ( p = 0.6327). Tukey's post hoc tests showed significant differences for SFO versus cerebrum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]) as well as and SFO versus cerebellum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]), but not for cerebrum versus cerebellum ( p = 0.3274, Cohen's d = 6.06, 95 % CI [−7.72, 23.92]). ns: no significant difference. ∗∗∗∗ p < 0.0001. ∗∗∗ p < 0.001. ∗∗ p < 0.01.
    Rabbit Polyclonal Antibody Against Sars Cov 2 Sp Rbd, supplied by Sino Biological, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Sino Biological sars-cov / sars-cov-2 spike antibody, rabbit mab
    Increased protein levels of <t>PSAP</t> and PGRN within the SFO of SAP-D −/− mice a – b) , Coronal brain section at 0.7–0.8 mm posterior to bregma containing the SFO. a: DAPI staining. a-2: Enlarged view of the white square in a-1. SFO: subfornical organ, 3V: third ventricle. b; Double immunofluorescent staining of PSAP (red) and PGRN (green) in 10-month-old female WT and SAP-D −/− mice. DAPI (blue) staining showed the nuclei ( a and b ). Scale bar, 500 μm ( a and b ). White arrowheads indicate the SFO regions ( b ). c) Cerebral region from 3-, 6-, and 10-month-old male and female mice containing the SFO (0.7–0.8 mm posterior to ∗bregma) used for protein extraction and Western blot ( d – h ) using anti- PSAP, PGRN, and <t>GAPDH</t> <t>antibodies.</t> Quantification normalized to GAPDH expression and represented as the mean ± SD of three mice for each group. and indicate the individual values in each group ( e , f , h ). d – f) PSAP and PGRN protein levels in the SFO were remarkably increased. Their quantification by densitometric analysis is represented in e for male and f for female, respectively. e ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effects of genotype (F(1,24) = 547.7, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.51, −62.43]), with no effect of age ( p = 0.46) or genotype × age interaction ( p = 0.47). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 354.2, p < 0.0001, ηp 2 = 0.48, 95 % CI [−46.39, −37.22]), with no effect of age ( p = 0.73) or genotype × age interaction ( p = 0.76). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.87, 95 % CI [−52.71, −28.91]), 6 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−52.82, −29.02]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−52.32, −28.52]). f ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 611.1, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.42, −62.95]), with no effect of age ( p = 0.07) or genotype × age interaction (p = 0.07). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 273.5, p < 0.0001, ηp 2 = 0.47, 95 % CI [−63.96, −49.76]), with no effect of age ( p = 0.71) or genotype × age interaction (p = 0.70). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.31, 95 % CI [−73.43, −36.60]), 6 M ( p < 0.0001, Cohen's d = 5.71, 95 % CI [−73.04, −36.22]), and 10 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−73.08, −36.26]). g – h ) Comparison of PSAP and PGRN protein expression in the SFO, whole cerebrum, and cerebellum. The quantitative analysis is shown in h . h ) For PSAP/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 30.06, p = 0.0007, η 2 = 0.90), but not in WT mice ( p = 0.3461). Tukey's post hoc tests showed significant differences for SFO versus cerebellum ( p = 0.0010, Cohen's d = 5.26, 95 % CI [46.80, 119.1]) as well as and cerebrum versus cerebellum ( p = 0.0018, Cohen's d = 9.34, 95 % CI [38.39, 110.6]). There was no significant difference for SFO versus cerebrum ( p = 0.76, Cohen's d = 0.47, 95 % CI [−27.71, 44.54]). For PGRN/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 54.42, p = 0.0001, η 2 = 0.94), but not in WT mice ( p = 0.6327). Tukey's post hoc tests showed significant differences for SFO versus cerebrum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]) as well as and SFO versus cerebellum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]), but not for cerebrum versus cerebellum ( p = 0.3274, Cohen's d = 6.06, 95 % CI [−7.72, 23.92]). ns: no significant difference. ∗∗∗∗ p < 0.0001. ∗∗∗ p < 0.001. ∗∗ p < 0.01.
    Sars Cov / Sars Cov 2 Spike Antibody, Rabbit Mab, supplied by Sino Biological, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs rabbit polyclonal antibodies against mouse
    Increased protein levels of <t>PSAP</t> and PGRN within the SFO of SAP-D −/− mice a – b) , Coronal brain section at 0.7–0.8 mm posterior to bregma containing the SFO. a: DAPI staining. a-2: Enlarged view of the white square in a-1. SFO: subfornical organ, 3V: third ventricle. b; Double immunofluorescent staining of PSAP (red) and PGRN (green) in 10-month-old female WT and SAP-D −/− mice. DAPI (blue) staining showed the nuclei ( a and b ). Scale bar, 500 μm ( a and b ). White arrowheads indicate the SFO regions ( b ). c) Cerebral region from 3-, 6-, and 10-month-old male and female mice containing the SFO (0.7–0.8 mm posterior to ∗bregma) used for protein extraction and Western blot ( d – h ) using anti- PSAP, PGRN, and <t>GAPDH</t> <t>antibodies.</t> Quantification normalized to GAPDH expression and represented as the mean ± SD of three mice for each group. and indicate the individual values in each group ( e , f , h ). d – f) PSAP and PGRN protein levels in the SFO were remarkably increased. Their quantification by densitometric analysis is represented in e for male and f for female, respectively. e ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effects of genotype (F(1,24) = 547.7, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.51, −62.43]), with no effect of age ( p = 0.46) or genotype × age interaction ( p = 0.47). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 354.2, p < 0.0001, ηp 2 = 0.48, 95 % CI [−46.39, −37.22]), with no effect of age ( p = 0.73) or genotype × age interaction ( p = 0.76). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.87, 95 % CI [−52.71, −28.91]), 6 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−52.82, −29.02]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−52.32, −28.52]). f ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 611.1, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.42, −62.95]), with no effect of age ( p = 0.07) or genotype × age interaction (p = 0.07). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 273.5, p < 0.0001, ηp 2 = 0.47, 95 % CI [−63.96, −49.76]), with no effect of age ( p = 0.71) or genotype × age interaction (p = 0.70). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.31, 95 % CI [−73.43, −36.60]), 6 M ( p < 0.0001, Cohen's d = 5.71, 95 % CI [−73.04, −36.22]), and 10 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−73.08, −36.26]). g – h ) Comparison of PSAP and PGRN protein expression in the SFO, whole cerebrum, and cerebellum. The quantitative analysis is shown in h . h ) For PSAP/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 30.06, p = 0.0007, η 2 = 0.90), but not in WT mice ( p = 0.3461). Tukey's post hoc tests showed significant differences for SFO versus cerebellum ( p = 0.0010, Cohen's d = 5.26, 95 % CI [46.80, 119.1]) as well as and cerebrum versus cerebellum ( p = 0.0018, Cohen's d = 9.34, 95 % CI [38.39, 110.6]). There was no significant difference for SFO versus cerebrum ( p = 0.76, Cohen's d = 0.47, 95 % CI [−27.71, 44.54]). For PGRN/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 54.42, p = 0.0001, η 2 = 0.94), but not in WT mice ( p = 0.6327). Tukey's post hoc tests showed significant differences for SFO versus cerebrum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]) as well as and SFO versus cerebellum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]), but not for cerebrum versus cerebellum ( p = 0.3274, Cohen's d = 6.06, 95 % CI [−7.72, 23.92]). ns: no significant difference. ∗∗∗∗ p < 0.0001. ∗∗∗ p < 0.001. ∗∗ p < 0.01.
    Rabbit Polyclonal Antibodies Against Mouse, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam rabbit polyclonal primary antibody against sp d
    Increased protein levels of <t>PSAP</t> and PGRN within the SFO of SAP-D −/− mice a – b) , Coronal brain section at 0.7–0.8 mm posterior to bregma containing the SFO. a: DAPI staining. a-2: Enlarged view of the white square in a-1. SFO: subfornical organ, 3V: third ventricle. b; Double immunofluorescent staining of PSAP (red) and PGRN (green) in 10-month-old female WT and SAP-D −/− mice. DAPI (blue) staining showed the nuclei ( a and b ). Scale bar, 500 μm ( a and b ). White arrowheads indicate the SFO regions ( b ). c) Cerebral region from 3-, 6-, and 10-month-old male and female mice containing the SFO (0.7–0.8 mm posterior to ∗bregma) used for protein extraction and Western blot ( d – h ) using anti- PSAP, PGRN, and <t>GAPDH</t> <t>antibodies.</t> Quantification normalized to GAPDH expression and represented as the mean ± SD of three mice for each group. and indicate the individual values in each group ( e , f , h ). d – f) PSAP and PGRN protein levels in the SFO were remarkably increased. Their quantification by densitometric analysis is represented in e for male and f for female, respectively. e ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effects of genotype (F(1,24) = 547.7, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.51, −62.43]), with no effect of age ( p = 0.46) or genotype × age interaction ( p = 0.47). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 354.2, p < 0.0001, ηp 2 = 0.48, 95 % CI [−46.39, −37.22]), with no effect of age ( p = 0.73) or genotype × age interaction ( p = 0.76). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.87, 95 % CI [−52.71, −28.91]), 6 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−52.82, −29.02]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−52.32, −28.52]). f ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 611.1, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.42, −62.95]), with no effect of age ( p = 0.07) or genotype × age interaction (p = 0.07). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 273.5, p < 0.0001, ηp 2 = 0.47, 95 % CI [−63.96, −49.76]), with no effect of age ( p = 0.71) or genotype × age interaction (p = 0.70). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.31, 95 % CI [−73.43, −36.60]), 6 M ( p < 0.0001, Cohen's d = 5.71, 95 % CI [−73.04, −36.22]), and 10 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−73.08, −36.26]). g – h ) Comparison of PSAP and PGRN protein expression in the SFO, whole cerebrum, and cerebellum. The quantitative analysis is shown in h . h ) For PSAP/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 30.06, p = 0.0007, η 2 = 0.90), but not in WT mice ( p = 0.3461). Tukey's post hoc tests showed significant differences for SFO versus cerebellum ( p = 0.0010, Cohen's d = 5.26, 95 % CI [46.80, 119.1]) as well as and cerebrum versus cerebellum ( p = 0.0018, Cohen's d = 9.34, 95 % CI [38.39, 110.6]). There was no significant difference for SFO versus cerebrum ( p = 0.76, Cohen's d = 0.47, 95 % CI [−27.71, 44.54]). For PGRN/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 54.42, p = 0.0001, η 2 = 0.94), but not in WT mice ( p = 0.6327). Tukey's post hoc tests showed significant differences for SFO versus cerebrum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]) as well as and SFO versus cerebellum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]), but not for cerebrum versus cerebellum ( p = 0.3274, Cohen's d = 6.06, 95 % CI [−7.72, 23.92]). ns: no significant difference. ∗∗∗∗ p < 0.0001. ∗∗∗ p < 0.001. ∗∗ p < 0.01.
    Rabbit Polyclonal Primary Antibody Against Sp D, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs rabbit anti human monoclonal antibodies against eta
    Immunostaining of sections of stenotic valve from a patient with rheumatic fever. Top left. ET-1 staining associated with fibrotic regions and neovascularization. Top middle. <t>ETA</t> receptor staining of fibrotic region and neovascularization. Top right. H + E-stained section. Lower left. No ET-3 immunostaining. Lower <t>middle.</t> <t>ETB</t> receptor immunostaining of fibrotic region and neovascularization. Lower right. Negative control. ET=endothelin; ETA=endothelin receptor A; ETB=endothelin receptor B
    Rabbit Anti Human Monoclonal Antibodies Against Eta, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Increased protein levels of PSAP and PGRN within the SFO of SAP-D −/− mice a – b) , Coronal brain section at 0.7–0.8 mm posterior to bregma containing the SFO. a: DAPI staining. a-2: Enlarged view of the white square in a-1. SFO: subfornical organ, 3V: third ventricle. b; Double immunofluorescent staining of PSAP (red) and PGRN (green) in 10-month-old female WT and SAP-D −/− mice. DAPI (blue) staining showed the nuclei ( a and b ). Scale bar, 500 μm ( a and b ). White arrowheads indicate the SFO regions ( b ). c) Cerebral region from 3-, 6-, and 10-month-old male and female mice containing the SFO (0.7–0.8 mm posterior to ∗bregma) used for protein extraction and Western blot ( d – h ) using anti- PSAP, PGRN, and GAPDH antibodies. Quantification normalized to GAPDH expression and represented as the mean ± SD of three mice for each group. and indicate the individual values in each group ( e , f , h ). d – f) PSAP and PGRN protein levels in the SFO were remarkably increased. Their quantification by densitometric analysis is represented in e for male and f for female, respectively. e ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effects of genotype (F(1,24) = 547.7, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.51, −62.43]), with no effect of age ( p = 0.46) or genotype × age interaction ( p = 0.47). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 354.2, p < 0.0001, ηp 2 = 0.48, 95 % CI [−46.39, −37.22]), with no effect of age ( p = 0.73) or genotype × age interaction ( p = 0.76). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.87, 95 % CI [−52.71, −28.91]), 6 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−52.82, −29.02]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−52.32, −28.52]). f ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 611.1, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.42, −62.95]), with no effect of age ( p = 0.07) or genotype × age interaction (p = 0.07). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 273.5, p < 0.0001, ηp 2 = 0.47, 95 % CI [−63.96, −49.76]), with no effect of age ( p = 0.71) or genotype × age interaction (p = 0.70). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.31, 95 % CI [−73.43, −36.60]), 6 M ( p < 0.0001, Cohen's d = 5.71, 95 % CI [−73.04, −36.22]), and 10 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−73.08, −36.26]). g – h ) Comparison of PSAP and PGRN protein expression in the SFO, whole cerebrum, and cerebellum. The quantitative analysis is shown in h . h ) For PSAP/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 30.06, p = 0.0007, η 2 = 0.90), but not in WT mice ( p = 0.3461). Tukey's post hoc tests showed significant differences for SFO versus cerebellum ( p = 0.0010, Cohen's d = 5.26, 95 % CI [46.80, 119.1]) as well as and cerebrum versus cerebellum ( p = 0.0018, Cohen's d = 9.34, 95 % CI [38.39, 110.6]). There was no significant difference for SFO versus cerebrum ( p = 0.76, Cohen's d = 0.47, 95 % CI [−27.71, 44.54]). For PGRN/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 54.42, p = 0.0001, η 2 = 0.94), but not in WT mice ( p = 0.6327). Tukey's post hoc tests showed significant differences for SFO versus cerebrum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]) as well as and SFO versus cerebellum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]), but not for cerebrum versus cerebellum ( p = 0.3274, Cohen's d = 6.06, 95 % CI [−7.72, 23.92]). ns: no significant difference. ∗∗∗∗ p < 0.0001. ∗∗∗ p < 0.001. ∗∗ p < 0.01.

    Journal: Biochemistry and Biophysics Reports

    Article Title: Accumulation of prosaposin and progranulin around the subfornical organ induces polydipsia in SAP-D-deficient mice

    doi: 10.1016/j.bbrep.2025.102388

    Figure Lengend Snippet: Increased protein levels of PSAP and PGRN within the SFO of SAP-D −/− mice a – b) , Coronal brain section at 0.7–0.8 mm posterior to bregma containing the SFO. a: DAPI staining. a-2: Enlarged view of the white square in a-1. SFO: subfornical organ, 3V: third ventricle. b; Double immunofluorescent staining of PSAP (red) and PGRN (green) in 10-month-old female WT and SAP-D −/− mice. DAPI (blue) staining showed the nuclei ( a and b ). Scale bar, 500 μm ( a and b ). White arrowheads indicate the SFO regions ( b ). c) Cerebral region from 3-, 6-, and 10-month-old male and female mice containing the SFO (0.7–0.8 mm posterior to ∗bregma) used for protein extraction and Western blot ( d – h ) using anti- PSAP, PGRN, and GAPDH antibodies. Quantification normalized to GAPDH expression and represented as the mean ± SD of three mice for each group. and indicate the individual values in each group ( e , f , h ). d – f) PSAP and PGRN protein levels in the SFO were remarkably increased. Their quantification by densitometric analysis is represented in e for male and f for female, respectively. e ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effects of genotype (F(1,24) = 547.7, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.51, −62.43]), with no effect of age ( p = 0.46) or genotype × age interaction ( p = 0.47). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 354.2, p < 0.0001, ηp 2 = 0.48, 95 % CI [−46.39, −37.22]), with no effect of age ( p = 0.73) or genotype × age interaction ( p = 0.76). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.87, 95 % CI [−52.71, −28.91]), 6 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−52.82, −29.02]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−52.32, −28.52]). f ) For PSAP/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 611.1, p < 0.0001, ηp 2 = 0.48, 95 % CI [−74.42, −62.95]), with no effect of age ( p = 0.07) or genotype × age interaction (p = 0.07). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 9.99, 95 % CI [−86.30, −54.96]), 6 M ( p < 0.0001, Cohen's d = 7.24, 95 % CI [−79.04, −47.70]), and 10 M ( p < 0.0001, Cohen's d = 8.77, 95 % CI [−87.09, −55.75]). For PGRN/GAPDH, two-way ANOVA revealed a significant main effect of genotype (F(1,24) = 273.5, p < 0.0001, ηp 2 = 0.47, 95 % CI [−63.96, −49.76]), with no effect of age ( p = 0.71) or genotype × age interaction (p = 0.70). Post-hoc Tukey's tests showed that SAP-D −/− differed from WT at 3 M ( p < 0.0001, Cohen's d = 7.31, 95 % CI [−73.43, −36.60]), 6 M ( p < 0.0001, Cohen's d = 5.71, 95 % CI [−73.04, −36.22]), and 10 M ( p < 0.0001, Cohen's d = 5.35, 95 % CI [−73.08, −36.26]). g – h ) Comparison of PSAP and PGRN protein expression in the SFO, whole cerebrum, and cerebellum. The quantitative analysis is shown in h . h ) For PSAP/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 30.06, p = 0.0007, η 2 = 0.90), but not in WT mice ( p = 0.3461). Tukey's post hoc tests showed significant differences for SFO versus cerebellum ( p = 0.0010, Cohen's d = 5.26, 95 % CI [46.80, 119.1]) as well as and cerebrum versus cerebellum ( p = 0.0018, Cohen's d = 9.34, 95 % CI [38.39, 110.6]). There was no significant difference for SFO versus cerebrum ( p = 0.76, Cohen's d = 0.47, 95 % CI [−27.71, 44.54]). For PGRN/GAPDH, one-way ANOVA revealed a significant effect in SAP-D −/− mice (F(2,6) = 54.42, p = 0.0001, η 2 = 0.94), but not in WT mice ( p = 0.6327). Tukey's post hoc tests showed significant differences for SFO versus cerebrum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]) as well as and SFO versus cerebellum ( p = 0.0005, Cohen's d = 5.43, 95 % CI [26.19, 57.84]), but not for cerebrum versus cerebellum ( p = 0.3274, Cohen's d = 6.06, 95 % CI [−7.72, 23.92]). ns: no significant difference. ∗∗∗∗ p < 0.0001. ∗∗∗ p < 0.001. ∗∗ p < 0.01.

    Article Snippet: The primary antibodies used were a rabbit antibody against PSAP (dilution 1:100, 10801-1-AP, Proteintech Group Inc., IL, USA), a sheep antibody against PGRN (dilution 1:100, AF 2557, R&D Systems Inc., MN, USA), a guinea pig antibody against c-Fos (dilution 1:500, 226308, Synaptic Systems GmbH, Göttingen, Germany), a rat antibody against CD68-FITC conjugated (dilution 1:500, MCA1957FA, BIO-RAD Laboratories Inc., CA, USA), and a rat antibody against LAMP1 (dilution 1:100, ab25245, Abcam, Cambridge, UK).

    Techniques: Staining, Protein Extraction, Western Blot, Expressing, Comparison

    Increased PSAP and PGRN immunostaining in the SFO and its surrounding tissues in SAP-D −/− mice a) Double immunofluorescent staining of PSAP (red) and PGRN (green) around the SFO in 10-month-old female WT and SAP-D −/− mice. The white dotted lines enclose the SFO. b ) enlarged white ⅰ-iv squares in a, as indicated. White arrowheads indicate co-staining with anti-PGRN and PSAP antibodies. Open arrowheads indicate staining with PGRN alone. Nuclei are labeled by DAPI (blue) staining. All scale bars, 20 μm.

    Journal: Biochemistry and Biophysics Reports

    Article Title: Accumulation of prosaposin and progranulin around the subfornical organ induces polydipsia in SAP-D-deficient mice

    doi: 10.1016/j.bbrep.2025.102388

    Figure Lengend Snippet: Increased PSAP and PGRN immunostaining in the SFO and its surrounding tissues in SAP-D −/− mice a) Double immunofluorescent staining of PSAP (red) and PGRN (green) around the SFO in 10-month-old female WT and SAP-D −/− mice. The white dotted lines enclose the SFO. b ) enlarged white ⅰ-iv squares in a, as indicated. White arrowheads indicate co-staining with anti-PGRN and PSAP antibodies. Open arrowheads indicate staining with PGRN alone. Nuclei are labeled by DAPI (blue) staining. All scale bars, 20 μm.

    Article Snippet: The primary antibodies used were a rabbit antibody against PSAP (dilution 1:100, 10801-1-AP, Proteintech Group Inc., IL, USA), a sheep antibody against PGRN (dilution 1:100, AF 2557, R&D Systems Inc., MN, USA), a guinea pig antibody against c-Fos (dilution 1:500, 226308, Synaptic Systems GmbH, Göttingen, Germany), a rat antibody against CD68-FITC conjugated (dilution 1:500, MCA1957FA, BIO-RAD Laboratories Inc., CA, USA), and a rat antibody against LAMP1 (dilution 1:100, ab25245, Abcam, Cambridge, UK).

    Techniques: Immunostaining, Staining, Labeling

    Lysosomal localization of PSAP and PGRN expression around the SFO a) Immunofluorescence staining of LAMP1 (green) around the SFO in 10-month-old female WT and SAP-D −/− mice. Nuclei are labeled by DAPI (blue) staining. b) Quantification of LAMP1-stained areas in ( a ) relative to WT (%). The results of Student's t-tests for each panel are as follows: left panel, p = 0.0059, Cohen's d = 2.35 (95 % CI: 15.89, 67.66); and right panel: p = 0.0061, Cohen's d = 2.33 (95 % CI: 51.06, 220.89). Data are shown as the mean ± SD (n = 5). c) Triple immunofluorescent staining of PSAP (red), PGRN (green), and LAMP1 (cyan) around the SFO of 10-month-old female SAP-D −/− mice. Enlarged images indicated by the white squares (ⅰ-iv) were shown in c. d) Localization rate of PGRN or PSAP to LAMP1 in the SFO. The results of Student's t-tests for each panel are as follows: left panel, p = 0.0008, Cohen's d = 2.24 (95 % CI: -40.90, -13.73); and right panel, p = 0.2341, Cohen's d = 0.64 (95 % CI: 26.80, 7.17). Data are shown as the mean ± SD (n = 6 for WT-SFO and n = 8 for SAP-D −/− -SFO). e) Same experiment as in (c) on microglia/macrophage co-expressing PSAP and PGRN, or PGRN only, in the boundary and fornix regions of SAP-D −/− mice. Single image for each antibody was shown in white, while double or triple merged images were presented with red (PSAP or PGRN), green (LAMP1 or PGRN), or cyan (LAMP1) as indicated. and indicate the individual values in each group (b and d). ns: no significant difference. ∗∗∗ p < 0.001. ∗∗ p < 0.01. All scale bars, 10 μm.

    Journal: Biochemistry and Biophysics Reports

    Article Title: Accumulation of prosaposin and progranulin around the subfornical organ induces polydipsia in SAP-D-deficient mice

    doi: 10.1016/j.bbrep.2025.102388

    Figure Lengend Snippet: Lysosomal localization of PSAP and PGRN expression around the SFO a) Immunofluorescence staining of LAMP1 (green) around the SFO in 10-month-old female WT and SAP-D −/− mice. Nuclei are labeled by DAPI (blue) staining. b) Quantification of LAMP1-stained areas in ( a ) relative to WT (%). The results of Student's t-tests for each panel are as follows: left panel, p = 0.0059, Cohen's d = 2.35 (95 % CI: 15.89, 67.66); and right panel: p = 0.0061, Cohen's d = 2.33 (95 % CI: 51.06, 220.89). Data are shown as the mean ± SD (n = 5). c) Triple immunofluorescent staining of PSAP (red), PGRN (green), and LAMP1 (cyan) around the SFO of 10-month-old female SAP-D −/− mice. Enlarged images indicated by the white squares (ⅰ-iv) were shown in c. d) Localization rate of PGRN or PSAP to LAMP1 in the SFO. The results of Student's t-tests for each panel are as follows: left panel, p = 0.0008, Cohen's d = 2.24 (95 % CI: -40.90, -13.73); and right panel, p = 0.2341, Cohen's d = 0.64 (95 % CI: 26.80, 7.17). Data are shown as the mean ± SD (n = 6 for WT-SFO and n = 8 for SAP-D −/− -SFO). e) Same experiment as in (c) on microglia/macrophage co-expressing PSAP and PGRN, or PGRN only, in the boundary and fornix regions of SAP-D −/− mice. Single image for each antibody was shown in white, while double or triple merged images were presented with red (PSAP or PGRN), green (LAMP1 or PGRN), or cyan (LAMP1) as indicated. and indicate the individual values in each group (b and d). ns: no significant difference. ∗∗∗ p < 0.001. ∗∗ p < 0.01. All scale bars, 10 μm.

    Article Snippet: The primary antibodies used were a rabbit antibody against PSAP (dilution 1:100, 10801-1-AP, Proteintech Group Inc., IL, USA), a sheep antibody against PGRN (dilution 1:100, AF 2557, R&D Systems Inc., MN, USA), a guinea pig antibody against c-Fos (dilution 1:500, 226308, Synaptic Systems GmbH, Göttingen, Germany), a rat antibody against CD68-FITC conjugated (dilution 1:500, MCA1957FA, BIO-RAD Laboratories Inc., CA, USA), and a rat antibody against LAMP1 (dilution 1:100, ab25245, Abcam, Cambridge, UK).

    Techniques: Expressing, Immunofluorescence, Staining, Labeling

    Immunostaining of sections of stenotic valve from a patient with rheumatic fever. Top left. ET-1 staining associated with fibrotic regions and neovascularization. Top middle. ETA receptor staining of fibrotic region and neovascularization. Top right. H + E-stained section. Lower left. No ET-3 immunostaining. Lower middle. ETB receptor immunostaining of fibrotic region and neovascularization. Lower right. Negative control. ET=endothelin; ETA=endothelin receptor A; ETB=endothelin receptor B

    Journal: Revista Brasileira de Cirurgia Cardiovascular : órgão oficial da Sociedade Brasileira de Cirurgia Cardiovascular

    Article Title: Analysis of immunostaining and western blotting of endothelin 1 and its receptors in mitral stenosis

    doi: 10.5935/1678-9741.20150004

    Figure Lengend Snippet: Immunostaining of sections of stenotic valve from a patient with rheumatic fever. Top left. ET-1 staining associated with fibrotic regions and neovascularization. Top middle. ETA receptor staining of fibrotic region and neovascularization. Top right. H + E-stained section. Lower left. No ET-3 immunostaining. Lower middle. ETB receptor immunostaining of fibrotic region and neovascularization. Lower right. Negative control. ET=endothelin; ETA=endothelin receptor A; ETB=endothelin receptor B

    Article Snippet: Antibodies and their dilution: Mouse anti-human monoclonal antibody against endothelial cells (CD31, clone JC70A, 1:100, DakoCytomation, Denmark); rabbit anti-human monoclonal antibody against ET-1 and ET-3 (1:250, R & D Labs), rabbit anti-human monoclonal antibodies against ETA and ETB receptors (both 1:200, Alomone Labs, Israel) and AS02/Thy-1 for fibroblasts (1:200, DakoCytomation, Denmark).

    Techniques: Immunostaining, Staining, Negative Control