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cdc42 inhibitor ml141  (MedChemExpress)


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    Structured Review

    MedChemExpress cdc42 inhibitor ml141
    Cdc42 Inhibitor Ml141, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cdc42/ML141/pmc13311001-251-14-17
    Average 95 stars, based on 42 article reviews
    cdc42 inhibitor ml141 - by Bioz Stars, 2026-09
    95/100 stars

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    Related Articles

    Activity Assay:

    Article Title: Celsr2-mediated morphological polarization and functional phenotype of reactive astrocytes in neural repair.
    Article Snippet: .. To inhibit Cdc42 or Rac1 activity, cultured astrocytes were incubated with 5 μM ML141 (HY-12755, MCE, New Jersey, USA) or 50 μM NSC23766 (HY-15723A, MCE, NJ, USA) for 24 h before starving and scratching as described (Chaker et al., 2018; Jiang et al., 2020). ..

    Article Title: Proton pump inhibitors enhance macropinocytosis‐mediated extracellular vesicle endocytosis by inducing membrane v‐ATPase assembly
    Article Snippet: Cells were treated with 10 μM KM91104 or 10 nM Baf‐A1, or 10 μM azathioprine (Selleck) to inhibit the activity of v‐ATPase or RAC1, respectively. .. Cells were treated with 10 μM Dynasore (MedChemExpress), CDC42‐IN‐1 (Selleck) or NAV‐2729 (MedChemExpress) to inhibit the activity of dynamin, CDC42 and ARF6, respectively. ..

    Cell Culture:

    Article Title: Celsr2-mediated morphological polarization and functional phenotype of reactive astrocytes in neural repair.
    Article Snippet: .. To inhibit Cdc42 or Rac1 activity, cultured astrocytes were incubated with 5 μM ML141 (HY-12755, MCE, New Jersey, USA) or 50 μM NSC23766 (HY-15723A, MCE, NJ, USA) for 24 h before starving and scratching as described (Chaker et al., 2018; Jiang et al., 2020). ..

    Incubation:

    Article Title: Celsr2-mediated morphological polarization and functional phenotype of reactive astrocytes in neural repair.
    Article Snippet: .. To inhibit Cdc42 or Rac1 activity, cultured astrocytes were incubated with 5 μM ML141 (HY-12755, MCE, New Jersey, USA) or 50 μM NSC23766 (HY-15723A, MCE, NJ, USA) for 24 h before starving and scratching as described (Chaker et al., 2018; Jiang et al., 2020). ..



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    a , Immunoblots showing cleaved Notch1 (c-Notch1) and total Notch1 in MVECs treated with S1P for 1-hour ± γ-secretase inhibitor DAPT; quantification below (mean ± SEM). b , Fluorescent micrographs of YFP-Notch1 reporter intensity after S1P treatment; quantification below. Scale bar, 50 μm. c-d , Fold change in HES1 and HEY1 gene expression levels in (c) MVECs after S1P ± DAPT treatment, and in (d) mouse tissues after intravenous injection of S1P ± DAPT. e , Evans blue dye leakage in mouse dermis 1-hour post-injection with DMSO, S1P, or S1P + DAPT. Scale bar, 5 mm. f-i , Quantified dye leakage in (f) dermis, (g) lung, (h) liver, and (i) kidney, measured via absorbance. j , Heat maps of dextran dye diffusion in engineered microvessels ± S1P. Scale bar, 50 μm. k-l , Diffusive permeability in microvessels lined with (k) DAPT-vs. DMSO-treated or (l) NOTCH1 KO vs. SCR KO MVECs (mean ± SD). m , Micrographs of VE-cadherin (magenta), actin (green), and nuclei (blue) staining in microvessels. Scale bar, 50 μm. n-o , Mean corrected intensities of junctional (n) VE-cadherin and (o) actin from (m). p , Rac1 activity (PBD pull-down). Active/total Rac1 quantification below. q , Schematic of canonical Notch signaling. r , HES1 / HEY1 gene expression levels in dominant negative-MAML-GFP (DN-MAML-GFP) normalized to GFP expressing cells. s , Permeability in DN-MAML-GFP vs GFP-lined microvessels ± S1P. t , Schematic of Notch cortical pathway mediated by its transmembrane domain (TMD). u , Permeability in TMD-RFP vs RFP-lined microvessels ± S1P. v , Permeability in TMD-RFP vs RFP-lined microvessels ± clinical S1P receptor degrader fingolimod.

    Journal: bioRxiv

    Article Title: Sphingosine-1-phosphate cross-talks to Notch via a S1PR1-Dll4-MPDZ complex to regulate endothelial barrier function

    doi: 10.64898/2026.05.20.726610

    Figure Lengend Snippet: a , Immunoblots showing cleaved Notch1 (c-Notch1) and total Notch1 in MVECs treated with S1P for 1-hour ± γ-secretase inhibitor DAPT; quantification below (mean ± SEM). b , Fluorescent micrographs of YFP-Notch1 reporter intensity after S1P treatment; quantification below. Scale bar, 50 μm. c-d , Fold change in HES1 and HEY1 gene expression levels in (c) MVECs after S1P ± DAPT treatment, and in (d) mouse tissues after intravenous injection of S1P ± DAPT. e , Evans blue dye leakage in mouse dermis 1-hour post-injection with DMSO, S1P, or S1P + DAPT. Scale bar, 5 mm. f-i , Quantified dye leakage in (f) dermis, (g) lung, (h) liver, and (i) kidney, measured via absorbance. j , Heat maps of dextran dye diffusion in engineered microvessels ± S1P. Scale bar, 50 μm. k-l , Diffusive permeability in microvessels lined with (k) DAPT-vs. DMSO-treated or (l) NOTCH1 KO vs. SCR KO MVECs (mean ± SD). m , Micrographs of VE-cadherin (magenta), actin (green), and nuclei (blue) staining in microvessels. Scale bar, 50 μm. n-o , Mean corrected intensities of junctional (n) VE-cadherin and (o) actin from (m). p , Rac1 activity (PBD pull-down). Active/total Rac1 quantification below. q , Schematic of canonical Notch signaling. r , HES1 / HEY1 gene expression levels in dominant negative-MAML-GFP (DN-MAML-GFP) normalized to GFP expressing cells. s , Permeability in DN-MAML-GFP vs GFP-lined microvessels ± S1P. t , Schematic of Notch cortical pathway mediated by its transmembrane domain (TMD). u , Permeability in TMD-RFP vs RFP-lined microvessels ± S1P. v , Permeability in TMD-RFP vs RFP-lined microvessels ± clinical S1P receptor degrader fingolimod.

    Article Snippet: PAK-PBD beads to bind active Rac1 (PAK-02) were purchased from Cytoskeleton and reconstituted according to the manufacturer’s instructions.

    Techniques: Western Blot, Gene Expression, Injection, Diffusion-based Assay, Permeability, Staining, Activity Assay, Dominant Negative Mutation, Expressing