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Hippocampal proteins from 7–9 months-old mice were probed with the following antibodies: 1. PP1, 2. <t>PP2A-A,</t> 3. PP2A-Bα, 4. PP2A-Bβ, 5. demPP2A-C, 6. PP2A-C, 7. PP2B, 8. PP5, 9. pPTEN, 10. PTEN. Two lanes from representative immunoblots are displayed for each condition. Dividing lines represent areas where lanes from the same blot were removed and the remaining lanes were spliced together. Quantification of demethylated or phosphorylated phosphatase was normalized to total phosphatase. Total protein expression was quantified vs. β-actin. There was no significant difference between STZ-injected mice and their controls (quantification data not shown). 11. PP2A activity: Results are expressed as percentage of control group (CTL). Data are mean ± SD. Asterisks indicate significant differences from controls, with **p < 0.01 and ***p < 0.001. Data from PP1, PP2A-Bβ, demPP2A-C, PP2A-C, pPTEN and PP2A activity following a normal distribution were analyzed with one-way ANOVA of variance followed by a Bonferroni’s post hoc test, while Kruskal-Wallis test followed by a Dunn’s post hoc test was used for PP2A-A, PP2A-Bα, PP2B, PP5 and PTEN analysis since data deviated from a normal distribution.
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R&D Systems human nectin 4 duoset elisa kit
Hippocampal proteins from 7–9 months-old mice were probed with the following antibodies: 1. PP1, 2. <t>PP2A-A,</t> 3. PP2A-Bα, 4. PP2A-Bβ, 5. demPP2A-C, 6. PP2A-C, 7. PP2B, 8. PP5, 9. pPTEN, 10. PTEN. Two lanes from representative immunoblots are displayed for each condition. Dividing lines represent areas where lanes from the same blot were removed and the remaining lanes were spliced together. Quantification of demethylated or phosphorylated phosphatase was normalized to total phosphatase. Total protein expression was quantified vs. β-actin. There was no significant difference between STZ-injected mice and their controls (quantification data not shown). 11. PP2A activity: Results are expressed as percentage of control group (CTL). Data are mean ± SD. Asterisks indicate significant differences from controls, with **p < 0.01 and ***p < 0.001. Data from PP1, PP2A-Bβ, demPP2A-C, PP2A-C, pPTEN and PP2A activity following a normal distribution were analyzed with one-way ANOVA of variance followed by a Bonferroni’s post hoc test, while Kruskal-Wallis test followed by a Dunn’s post hoc test was used for PP2A-A, PP2A-Bα, PP2B, PP5 and PTEN analysis since data deviated from a normal distribution.
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Hippocampal proteins from 7–9 months-old mice were probed with the following antibodies: 1. PP1, 2. <t>PP2A-A,</t> 3. PP2A-Bα, 4. PP2A-Bβ, 5. demPP2A-C, 6. PP2A-C, 7. PP2B, 8. PP5, 9. pPTEN, 10. PTEN. Two lanes from representative immunoblots are displayed for each condition. Dividing lines represent areas where lanes from the same blot were removed and the remaining lanes were spliced together. Quantification of demethylated or phosphorylated phosphatase was normalized to total phosphatase. Total protein expression was quantified vs. β-actin. There was no significant difference between STZ-injected mice and their controls (quantification data not shown). 11. PP2A activity: Results are expressed as percentage of control group (CTL). Data are mean ± SD. Asterisks indicate significant differences from controls, with **p < 0.01 and ***p < 0.001. Data from PP1, PP2A-Bβ, demPP2A-C, PP2A-C, pPTEN and PP2A activity following a normal distribution were analyzed with one-way ANOVA of variance followed by a Bonferroni’s post hoc test, while Kruskal-Wallis test followed by a Dunn’s post hoc test was used for PP2A-A, PP2A-Bα, PP2B, PP5 and PTEN analysis since data deviated from a normal distribution.
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Hippocampal proteins from 7–9 months-old mice were probed with the following antibodies: 1. PP1, 2. <t>PP2A-A,</t> 3. PP2A-Bα, 4. PP2A-Bβ, 5. demPP2A-C, 6. PP2A-C, 7. PP2B, 8. PP5, 9. pPTEN, 10. PTEN. Two lanes from representative immunoblots are displayed for each condition. Dividing lines represent areas where lanes from the same blot were removed and the remaining lanes were spliced together. Quantification of demethylated or phosphorylated phosphatase was normalized to total phosphatase. Total protein expression was quantified vs. β-actin. There was no significant difference between STZ-injected mice and their controls (quantification data not shown). 11. PP2A activity: Results are expressed as percentage of control group (CTL). Data are mean ± SD. Asterisks indicate significant differences from controls, with **p < 0.01 and ***p < 0.001. Data from PP1, PP2A-Bβ, demPP2A-C, PP2A-C, pPTEN and PP2A activity following a normal distribution were analyzed with one-way ANOVA of variance followed by a Bonferroni’s post hoc test, while Kruskal-Wallis test followed by a Dunn’s post hoc test was used for PP2A-A, PP2A-Bα, PP2B, PP5 and PTEN analysis since data deviated from a normal distribution.
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Hippocampal proteins from 7–9 months-old mice were probed with the following antibodies: 1. PP1, 2. <t>PP2A-A,</t> 3. PP2A-Bα, 4. PP2A-Bβ, 5. demPP2A-C, 6. PP2A-C, 7. PP2B, 8. PP5, 9. pPTEN, 10. PTEN. Two lanes from representative immunoblots are displayed for each condition. Dividing lines represent areas where lanes from the same blot were removed and the remaining lanes were spliced together. Quantification of demethylated or phosphorylated phosphatase was normalized to total phosphatase. Total protein expression was quantified vs. β-actin. There was no significant difference between STZ-injected mice and their controls (quantification data not shown). 11. PP2A activity: Results are expressed as percentage of control group (CTL). Data are mean ± SD. Asterisks indicate significant differences from controls, with **p < 0.01 and ***p < 0.001. Data from PP1, PP2A-Bβ, demPP2A-C, PP2A-C, pPTEN and PP2A activity following a normal distribution were analyzed with one-way ANOVA of variance followed by a Bonferroni’s post hoc test, while Kruskal-Wallis test followed by a Dunn’s post hoc test was used for PP2A-A, PP2A-Bα, PP2B, PP5 and PTEN analysis since data deviated from a normal distribution.
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Hippocampal proteins from 7–9 months-old mice were probed with the following antibodies: 1. PP1, 2. <t>PP2A-A,</t> 3. PP2A-Bα, 4. PP2A-Bβ, 5. demPP2A-C, 6. PP2A-C, 7. PP2B, 8. PP5, 9. pPTEN, 10. PTEN. Two lanes from representative immunoblots are displayed for each condition. Dividing lines represent areas where lanes from the same blot were removed and the remaining lanes were spliced together. Quantification of demethylated or phosphorylated phosphatase was normalized to total phosphatase. Total protein expression was quantified vs. β-actin. There was no significant difference between STZ-injected mice and their controls (quantification data not shown). 11. PP2A activity: Results are expressed as percentage of control group (CTL). Data are mean ± SD. Asterisks indicate significant differences from controls, with **p < 0.01 and ***p < 0.001. Data from PP1, PP2A-Bβ, demPP2A-C, PP2A-C, pPTEN and PP2A activity following a normal distribution were analyzed with one-way ANOVA of variance followed by a Bonferroni’s post hoc test, while Kruskal-Wallis test followed by a Dunn’s post hoc test was used for PP2A-A, PP2A-Bα, PP2B, PP5 and PTEN analysis since data deviated from a normal distribution.
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Hippocampal proteins from 7–9 months-old mice were probed with the following antibodies: 1. PP1, 2. <t>PP2A-A,</t> 3. PP2A-Bα, 4. PP2A-Bβ, 5. demPP2A-C, 6. PP2A-C, 7. PP2B, 8. PP5, 9. pPTEN, 10. PTEN. Two lanes from representative immunoblots are displayed for each condition. Dividing lines represent areas where lanes from the same blot were removed and the remaining lanes were spliced together. Quantification of demethylated or phosphorylated phosphatase was normalized to total phosphatase. Total protein expression was quantified vs. β-actin. There was no significant difference between STZ-injected mice and their controls (quantification data not shown). 11. PP2A activity: Results are expressed as percentage of control group (CTL). Data are mean ± SD. Asterisks indicate significant differences from controls, with **p < 0.01 and ***p < 0.001. Data from PP1, PP2A-Bβ, demPP2A-C, PP2A-C, pPTEN and PP2A activity following a normal distribution were analyzed with one-way ANOVA of variance followed by a Bonferroni’s post hoc test, while Kruskal-Wallis test followed by a Dunn’s post hoc test was used for PP2A-A, PP2A-Bα, PP2B, PP5 and PTEN analysis since data deviated from a normal distribution.
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Image Search Results


Hippocampal proteins from 7–9 months-old mice were probed with the following antibodies: 1. PP1, 2. PP2A-A, 3. PP2A-Bα, 4. PP2A-Bβ, 5. demPP2A-C, 6. PP2A-C, 7. PP2B, 8. PP5, 9. pPTEN, 10. PTEN. Two lanes from representative immunoblots are displayed for each condition. Dividing lines represent areas where lanes from the same blot were removed and the remaining lanes were spliced together. Quantification of demethylated or phosphorylated phosphatase was normalized to total phosphatase. Total protein expression was quantified vs. β-actin. There was no significant difference between STZ-injected mice and their controls (quantification data not shown). 11. PP2A activity: Results are expressed as percentage of control group (CTL). Data are mean ± SD. Asterisks indicate significant differences from controls, with **p < 0.01 and ***p < 0.001. Data from PP1, PP2A-Bβ, demPP2A-C, PP2A-C, pPTEN and PP2A activity following a normal distribution were analyzed with one-way ANOVA of variance followed by a Bonferroni’s post hoc test, while Kruskal-Wallis test followed by a Dunn’s post hoc test was used for PP2A-A, PP2A-Bα, PP2B, PP5 and PTEN analysis since data deviated from a normal distribution.

Journal: Scientific Reports

Article Title: Insulin deprivation induces PP2A inhibition and tau hyperphosphorylation in hTau mice, a model of Alzheimer’s disease-like tau pathology

doi: 10.1038/srep46359

Figure Lengend Snippet: Hippocampal proteins from 7–9 months-old mice were probed with the following antibodies: 1. PP1, 2. PP2A-A, 3. PP2A-Bα, 4. PP2A-Bβ, 5. demPP2A-C, 6. PP2A-C, 7. PP2B, 8. PP5, 9. pPTEN, 10. PTEN. Two lanes from representative immunoblots are displayed for each condition. Dividing lines represent areas where lanes from the same blot were removed and the remaining lanes were spliced together. Quantification of demethylated or phosphorylated phosphatase was normalized to total phosphatase. Total protein expression was quantified vs. β-actin. There was no significant difference between STZ-injected mice and their controls (quantification data not shown). 11. PP2A activity: Results are expressed as percentage of control group (CTL). Data are mean ± SD. Asterisks indicate significant differences from controls, with **p < 0.01 and ***p < 0.001. Data from PP1, PP2A-Bβ, demPP2A-C, PP2A-C, pPTEN and PP2A activity following a normal distribution were analyzed with one-way ANOVA of variance followed by a Bonferroni’s post hoc test, while Kruskal-Wallis test followed by a Dunn’s post hoc test was used for PP2A-A, PP2A-Bα, PP2B, PP5 and PTEN analysis since data deviated from a normal distribution.

Article Snippet: Brain PP2A activity was evaluated using a kit from R&D Systems according to the manufacturer’s instructions (Human/Mouse/Rat Active PP2A DuoSet IC, R&D Systems, Minneapolis, MN, USA).

Techniques: Western Blot, Expressing, Injection, Activity Assay

STZ injection induces insulin deprivation by destroying insulin-producing cells in pancreas. The resulting T1DM lead to PP2A inhibition in the brain, which induce tau hyperphosphorylation. Insulin injection 30 minutes before sacrifice partially restores physiological phosphorylation of tau comparable to non-T1DM mice without rescue of PP2A activity, suggesting involvement of different pathway.

Journal: Scientific Reports

Article Title: Insulin deprivation induces PP2A inhibition and tau hyperphosphorylation in hTau mice, a model of Alzheimer’s disease-like tau pathology

doi: 10.1038/srep46359

Figure Lengend Snippet: STZ injection induces insulin deprivation by destroying insulin-producing cells in pancreas. The resulting T1DM lead to PP2A inhibition in the brain, which induce tau hyperphosphorylation. Insulin injection 30 minutes before sacrifice partially restores physiological phosphorylation of tau comparable to non-T1DM mice without rescue of PP2A activity, suggesting involvement of different pathway.

Article Snippet: Brain PP2A activity was evaluated using a kit from R&D Systems according to the manufacturer’s instructions (Human/Mouse/Rat Active PP2A DuoSet IC, R&D Systems, Minneapolis, MN, USA).

Techniques: Injection, Inhibition, Activity Assay