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synaptophysin rabbit  (Novus Biologicals)


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    Structured Review

    Novus Biologicals synaptophysin rabbit
    Synaptophysin Rabbit, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 90 stars, based on 7 article reviews
    synaptophysin rabbit - by Bioz Stars, 2026-05
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    Alterations in PPP2R5C protein levels in NDEs from the plasma of AD patients (A) Representative TEM image of NDEs. Scale bars: 1 μm for low magnification and 100 nm for high magnification. (B) Nanoparticle tracking analysis of NDEs, confirming the expected size range. (C) Western blot analysis validation of NDEs and non-NDEs, using neuronal exosome markers, CD171 and <t>synaptophysin;</t> a microglia-derived exosome marker, Trem2; an astroglia-derived exosome marker, GLAST; and the exosome marker, Alix. (D) Label-free proteomic analysis of plasma NDEs showing differences in PPP2R5C protein levels among CN controls ( n = 4), pre-symptomatic familial AD mutation carriers (pre-FAD) ( n = 4), and familial AD (FAD) patients ( n = 5). (E) Targeted protein analysis comparing PPP2R5C protein levels in plasma NDEs across AD ( n = 20), aMCI ( n = 12), and CN groups ( n = 32). (F) Western blot analysis showed the difference in PPP2R5C levels in NDEs between AD, aMCI, and CN groups. All the western blot data are representative of three independent experiments. Quantification data are expressed as mean ± SEM (∗ p < 0.05 and ∗∗ p < 0.01 with Student’s t test).
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    Alterations in PPP2R5C protein levels in NDEs from the plasma of AD patients (A) Representative TEM image of NDEs. Scale bars: 1 μm for low magnification and 100 nm for high magnification. (B) Nanoparticle tracking analysis of NDEs, confirming the expected size range. (C) Western blot analysis validation of NDEs and non-NDEs, using neuronal exosome markers, CD171 and <t>synaptophysin;</t> a microglia-derived exosome marker, Trem2; an astroglia-derived exosome marker, GLAST; and the exosome marker, Alix. (D) Label-free proteomic analysis of plasma NDEs showing differences in PPP2R5C protein levels among CN controls ( n = 4), pre-symptomatic familial AD mutation carriers (pre-FAD) ( n = 4), and familial AD (FAD) patients ( n = 5). (E) Targeted protein analysis comparing PPP2R5C protein levels in plasma NDEs across AD ( n = 20), aMCI ( n = 12), and CN groups ( n = 32). (F) Western blot analysis showed the difference in PPP2R5C levels in NDEs between AD, aMCI, and CN groups. All the western blot data are representative of three independent experiments. Quantification data are expressed as mean ± SEM (∗ p < 0.05 and ∗∗ p < 0.01 with Student’s t test).
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    Proteintech rabbit polyclonal anti synaptophysin antibody
    Alterations in PPP2R5C protein levels in NDEs from the plasma of AD patients (A) Representative TEM image of NDEs. Scale bars: 1 μm for low magnification and 100 nm for high magnification. (B) Nanoparticle tracking analysis of NDEs, confirming the expected size range. (C) Western blot analysis validation of NDEs and non-NDEs, using neuronal exosome markers, CD171 and <t>synaptophysin;</t> a microglia-derived exosome marker, Trem2; an astroglia-derived exosome marker, GLAST; and the exosome marker, Alix. (D) Label-free proteomic analysis of plasma NDEs showing differences in PPP2R5C protein levels among CN controls ( n = 4), pre-symptomatic familial AD mutation carriers (pre-FAD) ( n = 4), and familial AD (FAD) patients ( n = 5). (E) Targeted protein analysis comparing PPP2R5C protein levels in plasma NDEs across AD ( n = 20), aMCI ( n = 12), and CN groups ( n = 32). (F) Western blot analysis showed the difference in PPP2R5C levels in NDEs between AD, aMCI, and CN groups. All the western blot data are representative of three independent experiments. Quantification data are expressed as mean ± SEM (∗ p < 0.05 and ∗∗ p < 0.01 with Student’s t test).
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    Cell Signaling Technology Inc synapsin 1
    CI-994 enhances spontaneous electrical activity and synaptic network formation in patient-specific iPSC-derived neurons carrying APOE ε4/ε4. A Spontaneous firing patterns in neurons derived from patient-specific iPSCs carrying APOE ε4/ε4 were measured by MED64 Presto for 8 weeks after differentiation from NPCs with the treatment of CI-994 at 4 µM. Each spike was indicated with a red arrow. P value was calculated by two-tailed, unpaired t-test at week 8. B The frequency of spontaneous firing was monitored in the iPSC-derived neurons for 8 weeks after differentiation and CI-994 treatment ( n = 8 technical replicates). C Extracellular recordings of spontaneous firing including burst firing (red brackets) in the iPSC-derived neurons were measured by MED64 Presto 8 weeks after differentiation and CI-994 treatment. D The incidence of burst firing was monitored in the iPSC neurons for 8 weeks after differentiation and CI-994 treatment ( n = 8 technical replicates). Data represents mean ± SEM. P value was calculated by two-tailed, unpaired t-test at week 8. E – G After the final MEA measurement, the neurons in each well were harvested, and the levels of <t>synapsin-1,</t> synaptophysin, β3-tubulin and β-actin in RIPA lysates were examined by Western blotting. Data represent mean ± SEM, n = 8 technical replicates. P values were calculated using two-tailed, unpaired t test
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    Image Search Results


    Alterations in PPP2R5C protein levels in NDEs from the plasma of AD patients (A) Representative TEM image of NDEs. Scale bars: 1 μm for low magnification and 100 nm for high magnification. (B) Nanoparticle tracking analysis of NDEs, confirming the expected size range. (C) Western blot analysis validation of NDEs and non-NDEs, using neuronal exosome markers, CD171 and synaptophysin; a microglia-derived exosome marker, Trem2; an astroglia-derived exosome marker, GLAST; and the exosome marker, Alix. (D) Label-free proteomic analysis of plasma NDEs showing differences in PPP2R5C protein levels among CN controls ( n = 4), pre-symptomatic familial AD mutation carriers (pre-FAD) ( n = 4), and familial AD (FAD) patients ( n = 5). (E) Targeted protein analysis comparing PPP2R5C protein levels in plasma NDEs across AD ( n = 20), aMCI ( n = 12), and CN groups ( n = 32). (F) Western blot analysis showed the difference in PPP2R5C levels in NDEs between AD, aMCI, and CN groups. All the western blot data are representative of three independent experiments. Quantification data are expressed as mean ± SEM (∗ p < 0.05 and ∗∗ p < 0.01 with Student’s t test).

    Journal: Cell Reports Medicine

    Article Title: Neuronal PPP2R5C in plasma is a potential biomarker for early diagnosis of Alzheimer’s disease

    doi: 10.1016/j.xcrm.2026.102631

    Figure Lengend Snippet: Alterations in PPP2R5C protein levels in NDEs from the plasma of AD patients (A) Representative TEM image of NDEs. Scale bars: 1 μm for low magnification and 100 nm for high magnification. (B) Nanoparticle tracking analysis of NDEs, confirming the expected size range. (C) Western blot analysis validation of NDEs and non-NDEs, using neuronal exosome markers, CD171 and synaptophysin; a microglia-derived exosome marker, Trem2; an astroglia-derived exosome marker, GLAST; and the exosome marker, Alix. (D) Label-free proteomic analysis of plasma NDEs showing differences in PPP2R5C protein levels among CN controls ( n = 4), pre-symptomatic familial AD mutation carriers (pre-FAD) ( n = 4), and familial AD (FAD) patients ( n = 5). (E) Targeted protein analysis comparing PPP2R5C protein levels in plasma NDEs across AD ( n = 20), aMCI ( n = 12), and CN groups ( n = 32). (F) Western blot analysis showed the difference in PPP2R5C levels in NDEs between AD, aMCI, and CN groups. All the western blot data are representative of three independent experiments. Quantification data are expressed as mean ± SEM (∗ p < 0.05 and ∗∗ p < 0.01 with Student’s t test).

    Article Snippet: Synaptophysin , Cell Signaling Technology, #36406 , RRID: AB_2799098.

    Techniques: Clinical Proteomics, Western Blot, Biomarker Discovery, Derivative Assay, Marker, Mutagenesis

    CI-994 enhances spontaneous electrical activity and synaptic network formation in patient-specific iPSC-derived neurons carrying APOE ε4/ε4. A Spontaneous firing patterns in neurons derived from patient-specific iPSCs carrying APOE ε4/ε4 were measured by MED64 Presto for 8 weeks after differentiation from NPCs with the treatment of CI-994 at 4 µM. Each spike was indicated with a red arrow. P value was calculated by two-tailed, unpaired t-test at week 8. B The frequency of spontaneous firing was monitored in the iPSC-derived neurons for 8 weeks after differentiation and CI-994 treatment ( n = 8 technical replicates). C Extracellular recordings of spontaneous firing including burst firing (red brackets) in the iPSC-derived neurons were measured by MED64 Presto 8 weeks after differentiation and CI-994 treatment. D The incidence of burst firing was monitored in the iPSC neurons for 8 weeks after differentiation and CI-994 treatment ( n = 8 technical replicates). Data represents mean ± SEM. P value was calculated by two-tailed, unpaired t-test at week 8. E – G After the final MEA measurement, the neurons in each well were harvested, and the levels of synapsin-1, synaptophysin, β3-tubulin and β-actin in RIPA lysates were examined by Western blotting. Data represent mean ± SEM, n = 8 technical replicates. P values were calculated using two-tailed, unpaired t test

    Journal: Alzheimer's Research & Therapy

    Article Title: CI-994 is a dual modulator of class I HDACs and Wnt/β-catenin signaling for the treatment of Alzheimer's disease

    doi: 10.1186/s13195-026-01982-0

    Figure Lengend Snippet: CI-994 enhances spontaneous electrical activity and synaptic network formation in patient-specific iPSC-derived neurons carrying APOE ε4/ε4. A Spontaneous firing patterns in neurons derived from patient-specific iPSCs carrying APOE ε4/ε4 were measured by MED64 Presto for 8 weeks after differentiation from NPCs with the treatment of CI-994 at 4 µM. Each spike was indicated with a red arrow. P value was calculated by two-tailed, unpaired t-test at week 8. B The frequency of spontaneous firing was monitored in the iPSC-derived neurons for 8 weeks after differentiation and CI-994 treatment ( n = 8 technical replicates). C Extracellular recordings of spontaneous firing including burst firing (red brackets) in the iPSC-derived neurons were measured by MED64 Presto 8 weeks after differentiation and CI-994 treatment. D The incidence of burst firing was monitored in the iPSC neurons for 8 weeks after differentiation and CI-994 treatment ( n = 8 technical replicates). Data represents mean ± SEM. P value was calculated by two-tailed, unpaired t-test at week 8. E – G After the final MEA measurement, the neurons in each well were harvested, and the levels of synapsin-1, synaptophysin, β3-tubulin and β-actin in RIPA lysates were examined by Western blotting. Data represent mean ± SEM, n = 8 technical replicates. P values were calculated using two-tailed, unpaired t test

    Article Snippet: The primary antibodies and their dilutions used in this study are as follows: LRP6 (Cell Signaling Technology, 3395S, 1:1000), anti-ADAM10 (Santa Cruz Biotechnology, 3395S, 1:1000), β-catenin (BD Biosciences, 610,154, 1:5000), acetyl-histone H3 (Cell Signaling Technology, 9649S, 1:1000), histone H3 (Cell Signaling Technology, 4499S, 1:1000), phospho-tau (AT8) (Fisher Healthcare, clone AT8, ENMN1020, 1:500), phospho-tau (AT180) (Fisher Healthcare, clone AT180, ENMN1040, 1:500), tau (Fisher Healthcare, clone HT7, clone HT7, ENMN1000, 1:1000), synaptophysin (Cell Signaling Technology, 36406S, 1:1000), synapsin-1 (Cell Signaling Technology, 5297S, 1:1000), β3-tubulin (Cell Signaling Technology, 5568S, 1:5000), β-actin (Cell Signaling Technology, 3700S and 4970S, 1:5000), and α-tubulin (Cell Signaling Technology, 2125S and 3873S, 1:5000).

    Techniques: Activity Assay, Derivative Assay, Two Tailed Test, Western Blot