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1na pp1  (MedChemExpress)


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    Structured Review

    MedChemExpress 1na pp1
    <t>PP1</t> analogs inhibit cell migration. Examples of HaCaT and MDA-MB-231 cell gaps observed upon wound making and 48 h later, in presence of DMSO or 5 µM of 1NM- and <t>1NA-PP1,</t> respectively.
    1na Pp1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 91/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/1na pp1/product/MedChemExpress
    Average 91 stars, based on 4 article reviews
    1na pp1 - by Bioz Stars, 2026-06
    91/100 stars

    Images

    1) Product Images from "Bulky PP1 analogs exert cellular effects independently from analog-sensitive kinase inhibition"

    Article Title: Bulky PP1 analogs exert cellular effects independently from analog-sensitive kinase inhibition

    Journal: Frontiers in Chemistry

    doi: 10.3389/fchem.2026.1812827

    PP1 analogs inhibit cell migration. Examples of HaCaT and MDA-MB-231 cell gaps observed upon wound making and 48 h later, in presence of DMSO or 5 µM of 1NM- and 1NA-PP1, respectively.
    Figure Legend Snippet: PP1 analogs inhibit cell migration. Examples of HaCaT and MDA-MB-231 cell gaps observed upon wound making and 48 h later, in presence of DMSO or 5 µM of 1NM- and 1NA-PP1, respectively.

    Techniques Used: Migration



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    Image Search Results


    PP1 analogs inhibit cell migration. Examples of HaCaT and MDA-MB-231 cell gaps observed upon wound making and 48 h later, in presence of DMSO or 5 µM of 1NM- and 1NA-PP1, respectively.

    Journal: Frontiers in Chemistry

    Article Title: Bulky PP1 analogs exert cellular effects independently from analog-sensitive kinase inhibition

    doi: 10.3389/fchem.2026.1812827

    Figure Lengend Snippet: PP1 analogs inhibit cell migration. Examples of HaCaT and MDA-MB-231 cell gaps observed upon wound making and 48 h later, in presence of DMSO or 5 µM of 1NM- and 1NA-PP1, respectively.

    Article Snippet: We prepared 10 mM stock solutions of 1NA-PP1 (MedChemExpress, HY-13941), 1NM-PP1 (MedChemExpress, HY-13942), 3MB-PP1 (Aobious, AOB3854), 3IB-PP1(Sigma, 529598) and 3MSB-PP1 in 100% DMSO and we stored aliquots at −20 °C.

    Techniques: Migration

    Fluoxetine modulates CaMKII-GSK3β-CREB signaling and ADAM10 expression in vitro. ( A ) Schematic diagram of the experimental design. SH-SY5Y cells were seeded and pretreated with fluoxetine (10 μM) for 12 h, followed by treatment with the CaMKII inhibitor 1-NA-PP1 (10 or 20 μM) or the GSK3β inhibitor IX (5 or 10 μM) for 1 h prior to cell harvest. ( B ) Representative Western blot analysis for phosphorylated and total forms of CaMKII (Thr286), GSK3β (Ser9), and CREB (Ser133). ( C ) Quantification of relative phosphorylation levels normalized to the corresponding total protein. ( D ) Representative Western blot analysis of signaling and APP-processing-related proteins following fluoxetine and/or GSK3β inhibitor treatment. ( E ) Quantification of protein expression levels normalized to β-actin (for protein) or to the corresponding total protein (for phosphorylated forms), as indicated. Data are presented as mean ± SEM ( n = 3 independent experiments). Individual data points represent independent biological replicates. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. fluoxetine alone; ns, not significant. Created in BioRender. Son, Y. (2026) https://BioRender.com/s91n646 (accessed on 31 January 2026).

    Journal: International Journal of Molecular Sciences

    Article Title: Fluoxetine Repurposing Mitigates Alzheimer’s Disease Pathology via the GSK3β–CREB–ADAM10 Axis

    doi: 10.3390/ijms27062676

    Figure Lengend Snippet: Fluoxetine modulates CaMKII-GSK3β-CREB signaling and ADAM10 expression in vitro. ( A ) Schematic diagram of the experimental design. SH-SY5Y cells were seeded and pretreated with fluoxetine (10 μM) for 12 h, followed by treatment with the CaMKII inhibitor 1-NA-PP1 (10 or 20 μM) or the GSK3β inhibitor IX (5 or 10 μM) for 1 h prior to cell harvest. ( B ) Representative Western blot analysis for phosphorylated and total forms of CaMKII (Thr286), GSK3β (Ser9), and CREB (Ser133). ( C ) Quantification of relative phosphorylation levels normalized to the corresponding total protein. ( D ) Representative Western blot analysis of signaling and APP-processing-related proteins following fluoxetine and/or GSK3β inhibitor treatment. ( E ) Quantification of protein expression levels normalized to β-actin (for protein) or to the corresponding total protein (for phosphorylated forms), as indicated. Data are presented as mean ± SEM ( n = 3 independent experiments). Individual data points represent independent biological replicates. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. fluoxetine alone; ns, not significant. Created in BioRender. Son, Y. (2026) https://BioRender.com/s91n646 (accessed on 31 January 2026).

    Article Snippet: After 24 h, 10 μM fluoxetine was added to the culture dishes for 12 h. 1-Naphthyl PP1 (1-NA-PP1, HY-13941), a CAMKII inhibitor, and GSK3 inhibitor IX (HY-10580), a GSK3β inhibitor, were purchased from MedChem Express (Princeton, NJ, USA).

    Techniques: Expressing, In Vitro, Western Blot, Phospho-proteomics, Control