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mouse anti map2 antibody  (Novus Biologicals)


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    Novus Biologicals mouse anti map2 antibody
    Effects of circulating amylin modulation on AD-like pathology in vivo and in human amylin-treated neonatal neurons (A–D) Heat maps comparing the brain tissue levels of pT231-tau, tau, Aβ 40 , and Aβ 42 in the same mice as in , , , , and (i.e., hA ON vs. hA i−OFF mice and hA OFF vs. hA i−ON mice). (E) Aβ immunofluorescence signal for Aβ (green) of cultured primary neurons incubated with human amylin (hAmylin; 1 μM for 4 h) or under control conditions (control). <t>MAP2</t> (blue) was used to identify the neurons. n = 86 neurons from 3 primary neonatal rat neuron cultures. (F) Total Aβ level secreted in the culture media by primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). Aβ was enriched by immunoprecipitation and measured by Western blot. (G) pTau and total Tau lysates from primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). pTau and Tau were enriched by immunoprecipitation and measured by western blot. Individual data points and mean ± s.e.m for three neuronal cultures. (H) Effect of amylin on pS214-tau in cultured murine astrocytes. Cells were incubated for 30 min under control conditions or in the presence of human amylin (15 μM) with and without the amylin receptor antagonist AC187 (10 μM) or PKA inhibitor H-89 (10 μM). pS214-tau was measured by ELISA. Individual data points and mean ± s.e.m for three cell cultures. (I) Representative images of IHC analyses of cortical slices from hA ON mice stained for amylin (top) and for total Aβ (bottom) ( n = 5 slices/mouse from n = 3 mice). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s multiple-comparisons test (H) and two-tail t test (E–G). See also .
    Mouse Anti Map2 Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 96/100, based on 159 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse anti map2 antibody/product/Novus Biologicals
    Average 96 stars, based on 159 article reviews
    mouse anti map2 antibody - by Bioz Stars, 2026-05
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    Images

    1) Product Images from "Peripheral amylin modulation rebalances brain glycolysis and Tau-Ser214 phosphorylation via cAMP-PKA signaling"

    Article Title: Peripheral amylin modulation rebalances brain glycolysis and Tau-Ser214 phosphorylation via cAMP-PKA signaling

    Journal: iScience

    doi: 10.1016/j.isci.2026.115157

    Effects of circulating amylin modulation on AD-like pathology in vivo and in human amylin-treated neonatal neurons (A–D) Heat maps comparing the brain tissue levels of pT231-tau, tau, Aβ 40 , and Aβ 42 in the same mice as in , , , , and (i.e., hA ON vs. hA i−OFF mice and hA OFF vs. hA i−ON mice). (E) Aβ immunofluorescence signal for Aβ (green) of cultured primary neurons incubated with human amylin (hAmylin; 1 μM for 4 h) or under control conditions (control). MAP2 (blue) was used to identify the neurons. n = 86 neurons from 3 primary neonatal rat neuron cultures. (F) Total Aβ level secreted in the culture media by primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). Aβ was enriched by immunoprecipitation and measured by Western blot. (G) pTau and total Tau lysates from primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). pTau and Tau were enriched by immunoprecipitation and measured by western blot. Individual data points and mean ± s.e.m for three neuronal cultures. (H) Effect of amylin on pS214-tau in cultured murine astrocytes. Cells were incubated for 30 min under control conditions or in the presence of human amylin (15 μM) with and without the amylin receptor antagonist AC187 (10 μM) or PKA inhibitor H-89 (10 μM). pS214-tau was measured by ELISA. Individual data points and mean ± s.e.m for three cell cultures. (I) Representative images of IHC analyses of cortical slices from hA ON mice stained for amylin (top) and for total Aβ (bottom) ( n = 5 slices/mouse from n = 3 mice). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s multiple-comparisons test (H) and two-tail t test (E–G). See also .
    Figure Legend Snippet: Effects of circulating amylin modulation on AD-like pathology in vivo and in human amylin-treated neonatal neurons (A–D) Heat maps comparing the brain tissue levels of pT231-tau, tau, Aβ 40 , and Aβ 42 in the same mice as in , , , , and (i.e., hA ON vs. hA i−OFF mice and hA OFF vs. hA i−ON mice). (E) Aβ immunofluorescence signal for Aβ (green) of cultured primary neurons incubated with human amylin (hAmylin; 1 μM for 4 h) or under control conditions (control). MAP2 (blue) was used to identify the neurons. n = 86 neurons from 3 primary neonatal rat neuron cultures. (F) Total Aβ level secreted in the culture media by primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). Aβ was enriched by immunoprecipitation and measured by Western blot. (G) pTau and total Tau lysates from primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). pTau and Tau were enriched by immunoprecipitation and measured by western blot. Individual data points and mean ± s.e.m for three neuronal cultures. (H) Effect of amylin on pS214-tau in cultured murine astrocytes. Cells were incubated for 30 min under control conditions or in the presence of human amylin (15 μM) with and without the amylin receptor antagonist AC187 (10 μM) or PKA inhibitor H-89 (10 μM). pS214-tau was measured by ELISA. Individual data points and mean ± s.e.m for three cell cultures. (I) Representative images of IHC analyses of cortical slices from hA ON mice stained for amylin (top) and for total Aβ (bottom) ( n = 5 slices/mouse from n = 3 mice). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s multiple-comparisons test (H) and two-tail t test (E–G). See also .

    Techniques Used: In Vivo, Immunofluorescence, Cell Culture, Incubation, Control, Immunoprecipitation, Western Blot, Enzyme-linked Immunosorbent Assay, Staining



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    Effects of circulating amylin modulation on AD-like pathology in vivo and in human amylin-treated neonatal neurons (A–D) Heat maps comparing the brain tissue levels of pT231-tau, tau, Aβ 40 , and Aβ 42 in the same mice as in , , , , and (i.e., hA ON vs. hA i−OFF mice and hA OFF vs. hA i−ON mice). (E) Aβ immunofluorescence signal for Aβ (green) of cultured primary neurons incubated with human amylin (hAmylin; 1 μM for 4 h) or under control conditions (control). <t>MAP2</t> (blue) was used to identify the neurons. n = 86 neurons from 3 primary neonatal rat neuron cultures. (F) Total Aβ level secreted in the culture media by primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). Aβ was enriched by immunoprecipitation and measured by Western blot. (G) pTau and total Tau lysates from primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). pTau and Tau were enriched by immunoprecipitation and measured by western blot. Individual data points and mean ± s.e.m for three neuronal cultures. (H) Effect of amylin on pS214-tau in cultured murine astrocytes. Cells were incubated for 30 min under control conditions or in the presence of human amylin (15 μM) with and without the amylin receptor antagonist AC187 (10 μM) or PKA inhibitor H-89 (10 μM). pS214-tau was measured by ELISA. Individual data points and mean ± s.e.m for three cell cultures. (I) Representative images of IHC analyses of cortical slices from hA ON mice stained for amylin (top) and for total Aβ (bottom) ( n = 5 slices/mouse from n = 3 mice). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s multiple-comparisons test (H) and two-tail t test (E–G). See also .
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    Effects of circulating amylin modulation on AD-like pathology in vivo and in human amylin-treated neonatal neurons (A–D) Heat maps comparing the brain tissue levels of pT231-tau, tau, Aβ 40 , and Aβ 42 in the same mice as in , , , , and (i.e., hA ON vs. hA i−OFF mice and hA OFF vs. hA i−ON mice). (E) Aβ immunofluorescence signal for Aβ (green) of cultured primary neurons incubated with human amylin (hAmylin; 1 μM for 4 h) or under control conditions (control). <t>MAP2</t> (blue) was used to identify the neurons. n = 86 neurons from 3 primary neonatal rat neuron cultures. (F) Total Aβ level secreted in the culture media by primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). Aβ was enriched by immunoprecipitation and measured by Western blot. (G) pTau and total Tau lysates from primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). pTau and Tau were enriched by immunoprecipitation and measured by western blot. Individual data points and mean ± s.e.m for three neuronal cultures. (H) Effect of amylin on pS214-tau in cultured murine astrocytes. Cells were incubated for 30 min under control conditions or in the presence of human amylin (15 μM) with and without the amylin receptor antagonist AC187 (10 μM) or PKA inhibitor H-89 (10 μM). pS214-tau was measured by ELISA. Individual data points and mean ± s.e.m for three cell cultures. (I) Representative images of IHC analyses of cortical slices from hA ON mice stained for amylin (top) and for total Aβ (bottom) ( n = 5 slices/mouse from n = 3 mice). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s multiple-comparisons test (H) and two-tail t test (E–G). See also .
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    Effects of circulating amylin modulation on AD-like pathology in vivo and in human amylin-treated neonatal neurons (A–D) Heat maps comparing the brain tissue levels of pT231-tau, tau, Aβ 40 , and Aβ 42 in the same mice as in , , , , and (i.e., hA ON vs. hA i−OFF mice and hA OFF vs. hA i−ON mice). (E) Aβ immunofluorescence signal for Aβ (green) of cultured primary neurons incubated with human amylin (hAmylin; 1 μM for 4 h) or under control conditions (control). <t>MAP2</t> (blue) was used to identify the neurons. n = 86 neurons from 3 primary neonatal rat neuron cultures. (F) Total Aβ level secreted in the culture media by primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). Aβ was enriched by immunoprecipitation and measured by Western blot. (G) pTau and total Tau lysates from primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). pTau and Tau were enriched by immunoprecipitation and measured by western blot. Individual data points and mean ± s.e.m for three neuronal cultures. (H) Effect of amylin on pS214-tau in cultured murine astrocytes. Cells were incubated for 30 min under control conditions or in the presence of human amylin (15 μM) with and without the amylin receptor antagonist AC187 (10 μM) or PKA inhibitor H-89 (10 μM). pS214-tau was measured by ELISA. Individual data points and mean ± s.e.m for three cell cultures. (I) Representative images of IHC analyses of cortical slices from hA ON mice stained for amylin (top) and for total Aβ (bottom) ( n = 5 slices/mouse from n = 3 mice). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s multiple-comparisons test (H) and two-tail t test (E–G). See also .
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    Effects of circulating amylin modulation on AD-like pathology in vivo and in human amylin-treated neonatal neurons (A–D) Heat maps comparing the brain tissue levels of pT231-tau, tau, Aβ 40 , and Aβ 42 in the same mice as in , , , , and (i.e., hA ON vs. hA i−OFF mice and hA OFF vs. hA i−ON mice). (E) Aβ immunofluorescence signal for Aβ (green) of cultured primary neurons incubated with human amylin (hAmylin; 1 μM for 4 h) or under control conditions (control). <t>MAP2</t> (blue) was used to identify the neurons. n = 86 neurons from 3 primary neonatal rat neuron cultures. (F) Total Aβ level secreted in the culture media by primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). Aβ was enriched by immunoprecipitation and measured by Western blot. (G) pTau and total Tau lysates from primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). pTau and Tau were enriched by immunoprecipitation and measured by western blot. Individual data points and mean ± s.e.m for three neuronal cultures. (H) Effect of amylin on pS214-tau in cultured murine astrocytes. Cells were incubated for 30 min under control conditions or in the presence of human amylin (15 μM) with and without the amylin receptor antagonist AC187 (10 μM) or PKA inhibitor H-89 (10 μM). pS214-tau was measured by ELISA. Individual data points and mean ± s.e.m for three cell cultures. (I) Representative images of IHC analyses of cortical slices from hA ON mice stained for amylin (top) and for total Aβ (bottom) ( n = 5 slices/mouse from n = 3 mice). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s multiple-comparisons test (H) and two-tail t test (E–G). See also .
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    CS2 treatment is protective in DA neurons derived from PD patient iPSCs. ( A ) Representative images of MitoTracker staining and ClpP-αSyn PLA in A53T αSyn or isogenic control (ISO) iPSCs-derived neurons (scale bar = 30 μm). ( B ) Representative images of ClpP-αSyn PLA in A53T αSyn or ISO iPSCs-derived neurons, which were treated with TAT or CS2 peptide (scale bar = 30 μm). Quantification of the average PLA puncta number in neurons ( n = 20 images per group, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM). ( C ) Representative blots of co-immunoprecipitation assay assessing ClpP-αSyn in A53T αSyn or ISO iPSCs-derived neurons, which were treated with TAT or CS2 peptide. Normalized ratio of ClpP to αSyn was shown in histogram ( n = 4, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM). ( D ) Representative images of ClpP staining in tyrosine dehydrogenase positive (TH + ) iPSCs-derived DA neurons treated with TAT or CS2 peptide (scale bar = 30 μm). Quantification of ClpP intensity in TH + neurons ( n = 6, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM). ( E ) Representative images of pS129-αSyn (pS129) staining in TH + iPSCs-derived DA neurons treated with TAT or CS2 peptide (scale bar = 30 μm). Quantification of pS129 intensity in TH + neurons ( n = 5–7, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM). ( F ) Representative images of PSD95, Synapsin1 (SYN1) and <t>MAP2</t> staining in iPSCs-derived neurons treated with TAT or CS2 peptide (scale bar = 30 μm). Quantification of the intensity of dendritic PSD95 and SYN1 ( n = 6–7, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM)
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    Image Search Results


    Effects of circulating amylin modulation on AD-like pathology in vivo and in human amylin-treated neonatal neurons (A–D) Heat maps comparing the brain tissue levels of pT231-tau, tau, Aβ 40 , and Aβ 42 in the same mice as in , , , , and (i.e., hA ON vs. hA i−OFF mice and hA OFF vs. hA i−ON mice). (E) Aβ immunofluorescence signal for Aβ (green) of cultured primary neurons incubated with human amylin (hAmylin; 1 μM for 4 h) or under control conditions (control). MAP2 (blue) was used to identify the neurons. n = 86 neurons from 3 primary neonatal rat neuron cultures. (F) Total Aβ level secreted in the culture media by primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). Aβ was enriched by immunoprecipitation and measured by Western blot. (G) pTau and total Tau lysates from primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). pTau and Tau were enriched by immunoprecipitation and measured by western blot. Individual data points and mean ± s.e.m for three neuronal cultures. (H) Effect of amylin on pS214-tau in cultured murine astrocytes. Cells were incubated for 30 min under control conditions or in the presence of human amylin (15 μM) with and without the amylin receptor antagonist AC187 (10 μM) or PKA inhibitor H-89 (10 μM). pS214-tau was measured by ELISA. Individual data points and mean ± s.e.m for three cell cultures. (I) Representative images of IHC analyses of cortical slices from hA ON mice stained for amylin (top) and for total Aβ (bottom) ( n = 5 slices/mouse from n = 3 mice). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s multiple-comparisons test (H) and two-tail t test (E–G). See also .

    Journal: iScience

    Article Title: Peripheral amylin modulation rebalances brain glycolysis and Tau-Ser214 phosphorylation via cAMP-PKA signaling

    doi: 10.1016/j.isci.2026.115157

    Figure Lengend Snippet: Effects of circulating amylin modulation on AD-like pathology in vivo and in human amylin-treated neonatal neurons (A–D) Heat maps comparing the brain tissue levels of pT231-tau, tau, Aβ 40 , and Aβ 42 in the same mice as in , , , , and (i.e., hA ON vs. hA i−OFF mice and hA OFF vs. hA i−ON mice). (E) Aβ immunofluorescence signal for Aβ (green) of cultured primary neurons incubated with human amylin (hAmylin; 1 μM for 4 h) or under control conditions (control). MAP2 (blue) was used to identify the neurons. n = 86 neurons from 3 primary neonatal rat neuron cultures. (F) Total Aβ level secreted in the culture media by primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). Aβ was enriched by immunoprecipitation and measured by Western blot. (G) pTau and total Tau lysates from primary neurons incubated with human amylin (hAmylin; 1 μM for 2 h) or under control conditions (control). pTau and Tau were enriched by immunoprecipitation and measured by western blot. Individual data points and mean ± s.e.m for three neuronal cultures. (H) Effect of amylin on pS214-tau in cultured murine astrocytes. Cells were incubated for 30 min under control conditions or in the presence of human amylin (15 μM) with and without the amylin receptor antagonist AC187 (10 μM) or PKA inhibitor H-89 (10 μM). pS214-tau was measured by ELISA. Individual data points and mean ± s.e.m for three cell cultures. (I) Representative images of IHC analyses of cortical slices from hA ON mice stained for amylin (top) and for total Aβ (bottom) ( n = 5 slices/mouse from n = 3 mice). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s multiple-comparisons test (H) and two-tail t test (E–G). See also .

    Article Snippet: Primary neuronal cells were detected with mouse anti-MAP2 antibody (NB300-213; Novus Biologicals; CO).

    Techniques: In Vivo, Immunofluorescence, Cell Culture, Incubation, Control, Immunoprecipitation, Western Blot, Enzyme-linked Immunosorbent Assay, Staining

    CS2 treatment is protective in DA neurons derived from PD patient iPSCs. ( A ) Representative images of MitoTracker staining and ClpP-αSyn PLA in A53T αSyn or isogenic control (ISO) iPSCs-derived neurons (scale bar = 30 μm). ( B ) Representative images of ClpP-αSyn PLA in A53T αSyn or ISO iPSCs-derived neurons, which were treated with TAT or CS2 peptide (scale bar = 30 μm). Quantification of the average PLA puncta number in neurons ( n = 20 images per group, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM). ( C ) Representative blots of co-immunoprecipitation assay assessing ClpP-αSyn in A53T αSyn or ISO iPSCs-derived neurons, which were treated with TAT or CS2 peptide. Normalized ratio of ClpP to αSyn was shown in histogram ( n = 4, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM). ( D ) Representative images of ClpP staining in tyrosine dehydrogenase positive (TH + ) iPSCs-derived DA neurons treated with TAT or CS2 peptide (scale bar = 30 μm). Quantification of ClpP intensity in TH + neurons ( n = 6, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM). ( E ) Representative images of pS129-αSyn (pS129) staining in TH + iPSCs-derived DA neurons treated with TAT or CS2 peptide (scale bar = 30 μm). Quantification of pS129 intensity in TH + neurons ( n = 5–7, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM). ( F ) Representative images of PSD95, Synapsin1 (SYN1) and MAP2 staining in iPSCs-derived neurons treated with TAT or CS2 peptide (scale bar = 30 μm). Quantification of the intensity of dendritic PSD95 and SYN1 ( n = 6–7, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM)

    Journal: Molecular Neurodegeneration

    Article Title: Disrupting α-Synuclein–ClpP interaction restores mitochondrial function and attenuates neuropathology in Parkinson’s disease models

    doi: 10.1186/s13024-025-00918-w

    Figure Lengend Snippet: CS2 treatment is protective in DA neurons derived from PD patient iPSCs. ( A ) Representative images of MitoTracker staining and ClpP-αSyn PLA in A53T αSyn or isogenic control (ISO) iPSCs-derived neurons (scale bar = 30 μm). ( B ) Representative images of ClpP-αSyn PLA in A53T αSyn or ISO iPSCs-derived neurons, which were treated with TAT or CS2 peptide (scale bar = 30 μm). Quantification of the average PLA puncta number in neurons ( n = 20 images per group, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM). ( C ) Representative blots of co-immunoprecipitation assay assessing ClpP-αSyn in A53T αSyn or ISO iPSCs-derived neurons, which were treated with TAT or CS2 peptide. Normalized ratio of ClpP to αSyn was shown in histogram ( n = 4, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM). ( D ) Representative images of ClpP staining in tyrosine dehydrogenase positive (TH + ) iPSCs-derived DA neurons treated with TAT or CS2 peptide (scale bar = 30 μm). Quantification of ClpP intensity in TH + neurons ( n = 6, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM). ( E ) Representative images of pS129-αSyn (pS129) staining in TH + iPSCs-derived DA neurons treated with TAT or CS2 peptide (scale bar = 30 μm). Quantification of pS129 intensity in TH + neurons ( n = 5–7, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM). ( F ) Representative images of PSD95, Synapsin1 (SYN1) and MAP2 staining in iPSCs-derived neurons treated with TAT or CS2 peptide (scale bar = 30 μm). Quantification of the intensity of dendritic PSD95 and SYN1 ( n = 6–7, one-way ANOVA with Tukey’s post-hoc test; data are mean ± SEM)

    Article Snippet: Antibodies against αSyn (Syn204) (2647, 1:500), and MAP2 (4542, 1:1000) were from Cell Signaling Technology.

    Techniques: Derivative Assay, Staining, Control, Co-Immunoprecipitation Assay