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cells  (Cytoskeleton Inc)


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    Structured Review

    Cytoskeleton Inc cells
    Cells, supplied by Cytoskeleton Inc, used in various techniques. Bioz Stars score: 96/100, based on 423 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rho+inhibitor/Rho+Inhibitor+I/pm42785467-395-16-26
    Average 96 stars, based on 423 article reviews
    cells - by Bioz Stars, 2026-10
    96/100 stars

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    Related Articles

    Sterility:

    Article Title: Piezo1 balances focal and reticular adhesions to enable EGFR clathrin-mediated endocytosis
    Article Snippet: .. 24h after serum starvation, cells were treated for indicated durations with DMSO (276855), 10μM Yoda1 (Tocris, 5586), 25μM Nocodazole (Sigma, M1404), 1μM A23187 (Biovision, 1501-10), all reconstituted in DMSO, 1μg/mL Rho Activator (Cytoskeleton Inc, CN03) or 2ng/mL EGF (Peprotech, 400-25), both reconstituted in sterile deionized H 2 O. Inhibitor experiments included a 30-min pre-treatment with 10μM Vilanterol (Sigma, SML3389, reconstituted in DMSO), 1μM GsMTx4 (Tocris, 4912), or 0.5μg/mL Rho Inhibitor (Cytoskeleton Inc, CT04-A) (both reconstituted in sterile deionized H 2 O). .. For 0Ca 2+ experiments, Ca 2+ -free DMEM (21068-028) was supplemented with 1% Pen/Strep and 1.2mM MgCl 2 (Sigma, M8266) to avoid integrin inhibition.

    Concentration Assay:

    Article Title: Spatiotemporal Insights into Glioma Oncostream Dynamics: Unraveling Formation, Stability, and Disassembly Pathways
    Article Snippet: .. The Rho inhibitor (Cytoskeleton, Inc, Cat# CT04) was administered at a concentration of 2 μg ml −1 , while the Rho activator I (Cytoskeleton, Inc, Cat# CN01) was similarly introduced at 2 μg ml −1 . ..

    Article Title: Spatiotemporal Insights into Glioma Oncostream Dynamics: Unraveling Formation, Stability, and Disassembly Pathways.
    Article Snippet: Glioblastoma (GBM) remains a challenge in Neuro-oncology, with a poor prognosis showing only a 5% survival rate beyond two years.. This is primarily due to its aggressiveness and intra-tumoral heterogeneity, which limits complete surgical resection and reduces the efficacy of existing treatments.. The existence of oncostreams—neuropathological structures comprising aligned spindle-like cells from both tumor and non-tumor originsis discovered earlier.

    Inhibition:

    Article Title: Sfrp1 inhibits lung fibroblast invasion during transition to injury-induced myofibroblasts
    Article Snippet: .. For RHO inhibition cells were seeded on top of the collagen and treated with 0.5 μg/ml RHO inhibitor (CT04; Cytoskeleton, Inc). ..

    Article Title: Targeting macrophage circadian rhythms with microcurrent stimulation to activate cancer immunity through phagocytic defense
    Article Snippet: .. The reagents added to the cultured cells were as follows: red fluorescent labeling of RAW264.7 (Figure D); CellTracker Deep Red Dye (5 μM for 2 h; Thermo Fisher Scientific), inhibition of actin polymerization in RAW264.7 and THP-1 (Figure H,I); Cytochalasin D (2 μM for 30 m; Sigma Aldrich), activation of NR1D1 (Figure B,F); SR9009 (100 nM for 24 h; Sigma Aldrich), inhibition of Rho activity in cultured mouse macrophages; Rho-inhibitor I, G-switch (1 μg/mL for 4 h; Cytoskeleton, Inc., Denver, CO, USA). .. To synchronize the cellular circadian clock, RAW264.7 cells and THP-1 cells were treated with 100 nmol/L dexamethasone (DEX, FUJIFILM Wako Pure Chemical Corporation, Osaka, Japan) for 2 h, as previously described .

    Recombinant:

    Article Title: RhoB supports rubella infection and impairs endothelial barrier integrity through downstream ROCK signaling
    Article Snippet: .. Recombinant human interferon (IFN)-β (Cat#300-02BC, PeproTech, Thermo Fisher Scientific) was used at 10 ng/ml, the ROCK1/2 inhibitor Y-27632-dihydrochlorid (Y-27632, Sigma-Aldrich, Merck) at 10 μM and the Rho Inhibitor I as a highly purified C3 transferase (C3, #CT04, Cytoskeleton Inc.) at 1 μg/ml. ..

    Purification:

    Article Title: RhoB supports rubella infection and impairs endothelial barrier integrity through downstream ROCK signaling
    Article Snippet: .. Recombinant human interferon (IFN)-β (Cat#300-02BC, PeproTech, Thermo Fisher Scientific) was used at 10 ng/ml, the ROCK1/2 inhibitor Y-27632-dihydrochlorid (Y-27632, Sigma-Aldrich, Merck) at 10 μM and the Rho Inhibitor I as a highly purified C3 transferase (C3, #CT04, Cytoskeleton Inc.) at 1 μg/ml. ..

    Cell Culture:

    Article Title: Fibrin Stiffness Regulates Phenotypic Plasticity of Metastatic Breast Cancer Cells.
    Article Snippet: .. Inhibitor Studies: 1–10 μm FGFR inhibitor (BGJ398, Selleckhem), 25– 50 μm calmodulin inhibitor (W7, Medchemexpress), 2 μg mL−1 Rho inhibitor (CT04, Cytoskeleton), or 30–100 μm RhoA inhibitor (Rhosin, Selleckhem) were added on day 0 or day 5 to cell culture medium of cells in 30 mg mL−1 fibrin. .. Cell death was assessed by incubating the cells with 1:2000 CellTox green (Promega) for 30 min before fixation, or by immunostaining cleaved caspase 3.

    Article Title: Targeting macrophage circadian rhythms with microcurrent stimulation to activate cancer immunity through phagocytic defense
    Article Snippet: .. The reagents added to the cultured cells were as follows: red fluorescent labeling of RAW264.7 (Figure D); CellTracker Deep Red Dye (5 μM for 2 h; Thermo Fisher Scientific), inhibition of actin polymerization in RAW264.7 and THP-1 (Figure H,I); Cytochalasin D (2 μM for 30 m; Sigma Aldrich), activation of NR1D1 (Figure B,F); SR9009 (100 nM for 24 h; Sigma Aldrich), inhibition of Rho activity in cultured mouse macrophages; Rho-inhibitor I, G-switch (1 μg/mL for 4 h; Cytoskeleton, Inc., Denver, CO, USA). .. To synchronize the cellular circadian clock, RAW264.7 cells and THP-1 cells were treated with 100 nmol/L dexamethasone (DEX, FUJIFILM Wako Pure Chemical Corporation, Osaka, Japan) for 2 h, as previously described .

    Labeling:

    Article Title: Targeting macrophage circadian rhythms with microcurrent stimulation to activate cancer immunity through phagocytic defense
    Article Snippet: .. The reagents added to the cultured cells were as follows: red fluorescent labeling of RAW264.7 (Figure D); CellTracker Deep Red Dye (5 μM for 2 h; Thermo Fisher Scientific), inhibition of actin polymerization in RAW264.7 and THP-1 (Figure H,I); Cytochalasin D (2 μM for 30 m; Sigma Aldrich), activation of NR1D1 (Figure B,F); SR9009 (100 nM for 24 h; Sigma Aldrich), inhibition of Rho activity in cultured mouse macrophages; Rho-inhibitor I, G-switch (1 μg/mL for 4 h; Cytoskeleton, Inc., Denver, CO, USA). .. To synchronize the cellular circadian clock, RAW264.7 cells and THP-1 cells were treated with 100 nmol/L dexamethasone (DEX, FUJIFILM Wako Pure Chemical Corporation, Osaka, Japan) for 2 h, as previously described .

    Activation Assay:

    Article Title: Targeting macrophage circadian rhythms with microcurrent stimulation to activate cancer immunity through phagocytic defense
    Article Snippet: .. The reagents added to the cultured cells were as follows: red fluorescent labeling of RAW264.7 (Figure D); CellTracker Deep Red Dye (5 μM for 2 h; Thermo Fisher Scientific), inhibition of actin polymerization in RAW264.7 and THP-1 (Figure H,I); Cytochalasin D (2 μM for 30 m; Sigma Aldrich), activation of NR1D1 (Figure B,F); SR9009 (100 nM for 24 h; Sigma Aldrich), inhibition of Rho activity in cultured mouse macrophages; Rho-inhibitor I, G-switch (1 μg/mL for 4 h; Cytoskeleton, Inc., Denver, CO, USA). .. To synchronize the cellular circadian clock, RAW264.7 cells and THP-1 cells were treated with 100 nmol/L dexamethasone (DEX, FUJIFILM Wako Pure Chemical Corporation, Osaka, Japan) for 2 h, as previously described .

    Activity Assay:

    Article Title: Targeting macrophage circadian rhythms with microcurrent stimulation to activate cancer immunity through phagocytic defense
    Article Snippet: .. The reagents added to the cultured cells were as follows: red fluorescent labeling of RAW264.7 (Figure D); CellTracker Deep Red Dye (5 μM for 2 h; Thermo Fisher Scientific), inhibition of actin polymerization in RAW264.7 and THP-1 (Figure H,I); Cytochalasin D (2 μM for 30 m; Sigma Aldrich), activation of NR1D1 (Figure B,F); SR9009 (100 nM for 24 h; Sigma Aldrich), inhibition of Rho activity in cultured mouse macrophages; Rho-inhibitor I, G-switch (1 μg/mL for 4 h; Cytoskeleton, Inc., Denver, CO, USA). .. To synchronize the cellular circadian clock, RAW264.7 cells and THP-1 cells were treated with 100 nmol/L dexamethasone (DEX, FUJIFILM Wako Pure Chemical Corporation, Osaka, Japan) for 2 h, as previously described .



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    Endothelial Epac1 coordinates VEGF/VEGFR2 signalling through actin cytoskeleton A . Ccn2 mRNA expression in CRISPR ctrl and Epac1 KO bEnd.3 cells after VEGF (50 ng/ml, 30 min). Data are normalized to untreated CRISPR ctrl and represent mean ± SEM of 3 independent experiments. B . Vegfr2 mRNA expression in CRISPR ctrl and Epac1 KO bEnd.3 cells after VEGF (50 ng/ml, 30 min). Data are normalized to untreated CRISPR ctrl and represent mean ± SEM of 3 independent experiments. C . Representative images of endothelial sprouting assay in bEnd.3 CRISPR ctrl and Epac1 KO cells. Spheroids were embedded in a collagen gel and incubated with VEGF (50 ng/ml, 24 h). D . Quantification of cumulative sprout length in CRISPR ctrl and Epac1 KO cells incubated with VEGF (50 ng/ml, 24 h). Data represent the mean cumulative sprout length ± SEM of 3 independent experiments, each totalling 10–15 spheroids/condition. Scale bars, 100 µm. E . Representative western blot image of GTP-bound RhoA, total RhoA and VEGFR2 in CRISPR ctrl and Epac1 KO bEnd.3 cells after VEGF (50 ng/ml, 30 min) or anlotinib (1 nM, 2 h) incubation. F . Representative western blot images and quantification of MLC2 expression and Ser19 phosphorylation of MLC2 in CRISPR ctrl and Epac1 KO bEnd.3 cells after VEGF treatment (100 ng/ml, 10 min). Data are normalized to untreated CRISPR ctrl cells and represent mean ± SEM of 3 independent experiments. G . TEAD luciferase reporter gene assay (HOPFlash) in CRISPR ctrl and Epac1 KO bEnd.3 cells. CRISPR ctrl was either untreated or treated with <t>CT04</t> (2 µg/ml, 120 min). Cells were co-transfected with renilla luciferase and normalized to renilla luciferase expression. Data are normalized to non-specific reporter gene activity using a TEAD-mutant binding domain (HIPFlash) and compared to CRISPR ctrl and represent mean ± SEM of 4 independent experiments. H . Ccn2 mRNA expression in bEnd.3 cells pre-incubation with CT04 (2 µg/ml, 2 h) and incubation with VEGF (50 ng/ml, 30 min). Data are normalized to untreated cells and represent mean ± SEM of 3 independent experiments. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001, n.s. p >0.05.
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    Image Search Results


    Endothelial Epac1 coordinates VEGF/VEGFR2 signalling through actin cytoskeleton A . Ccn2 mRNA expression in CRISPR ctrl and Epac1 KO bEnd.3 cells after VEGF (50 ng/ml, 30 min). Data are normalized to untreated CRISPR ctrl and represent mean ± SEM of 3 independent experiments. B . Vegfr2 mRNA expression in CRISPR ctrl and Epac1 KO bEnd.3 cells after VEGF (50 ng/ml, 30 min). Data are normalized to untreated CRISPR ctrl and represent mean ± SEM of 3 independent experiments. C . Representative images of endothelial sprouting assay in bEnd.3 CRISPR ctrl and Epac1 KO cells. Spheroids were embedded in a collagen gel and incubated with VEGF (50 ng/ml, 24 h). D . Quantification of cumulative sprout length in CRISPR ctrl and Epac1 KO cells incubated with VEGF (50 ng/ml, 24 h). Data represent the mean cumulative sprout length ± SEM of 3 independent experiments, each totalling 10–15 spheroids/condition. Scale bars, 100 µm. E . Representative western blot image of GTP-bound RhoA, total RhoA and VEGFR2 in CRISPR ctrl and Epac1 KO bEnd.3 cells after VEGF (50 ng/ml, 30 min) or anlotinib (1 nM, 2 h) incubation. F . Representative western blot images and quantification of MLC2 expression and Ser19 phosphorylation of MLC2 in CRISPR ctrl and Epac1 KO bEnd.3 cells after VEGF treatment (100 ng/ml, 10 min). Data are normalized to untreated CRISPR ctrl cells and represent mean ± SEM of 3 independent experiments. G . TEAD luciferase reporter gene assay (HOPFlash) in CRISPR ctrl and Epac1 KO bEnd.3 cells. CRISPR ctrl was either untreated or treated with CT04 (2 µg/ml, 120 min). Cells were co-transfected with renilla luciferase and normalized to renilla luciferase expression. Data are normalized to non-specific reporter gene activity using a TEAD-mutant binding domain (HIPFlash) and compared to CRISPR ctrl and represent mean ± SEM of 4 independent experiments. H . Ccn2 mRNA expression in bEnd.3 cells pre-incubation with CT04 (2 µg/ml, 2 h) and incubation with VEGF (50 ng/ml, 30 min). Data are normalized to untreated cells and represent mean ± SEM of 3 independent experiments. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001, n.s. p >0.05.

    Journal: Angiogenesis

    Article Title: Endothelial Epac1 facilitates YAP/TAZ controlled melanoma growth and angiogenesis

    doi: 10.1007/s10456-026-10080-6

    Figure Lengend Snippet: Endothelial Epac1 coordinates VEGF/VEGFR2 signalling through actin cytoskeleton A . Ccn2 mRNA expression in CRISPR ctrl and Epac1 KO bEnd.3 cells after VEGF (50 ng/ml, 30 min). Data are normalized to untreated CRISPR ctrl and represent mean ± SEM of 3 independent experiments. B . Vegfr2 mRNA expression in CRISPR ctrl and Epac1 KO bEnd.3 cells after VEGF (50 ng/ml, 30 min). Data are normalized to untreated CRISPR ctrl and represent mean ± SEM of 3 independent experiments. C . Representative images of endothelial sprouting assay in bEnd.3 CRISPR ctrl and Epac1 KO cells. Spheroids were embedded in a collagen gel and incubated with VEGF (50 ng/ml, 24 h). D . Quantification of cumulative sprout length in CRISPR ctrl and Epac1 KO cells incubated with VEGF (50 ng/ml, 24 h). Data represent the mean cumulative sprout length ± SEM of 3 independent experiments, each totalling 10–15 spheroids/condition. Scale bars, 100 µm. E . Representative western blot image of GTP-bound RhoA, total RhoA and VEGFR2 in CRISPR ctrl and Epac1 KO bEnd.3 cells after VEGF (50 ng/ml, 30 min) or anlotinib (1 nM, 2 h) incubation. F . Representative western blot images and quantification of MLC2 expression and Ser19 phosphorylation of MLC2 in CRISPR ctrl and Epac1 KO bEnd.3 cells after VEGF treatment (100 ng/ml, 10 min). Data are normalized to untreated CRISPR ctrl cells and represent mean ± SEM of 3 independent experiments. G . TEAD luciferase reporter gene assay (HOPFlash) in CRISPR ctrl and Epac1 KO bEnd.3 cells. CRISPR ctrl was either untreated or treated with CT04 (2 µg/ml, 120 min). Cells were co-transfected with renilla luciferase and normalized to renilla luciferase expression. Data are normalized to non-specific reporter gene activity using a TEAD-mutant binding domain (HIPFlash) and compared to CRISPR ctrl and represent mean ± SEM of 4 independent experiments. H . Ccn2 mRNA expression in bEnd.3 cells pre-incubation with CT04 (2 µg/ml, 2 h) and incubation with VEGF (50 ng/ml, 30 min). Data are normalized to untreated cells and represent mean ± SEM of 3 independent experiments. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001, n.s. p >0.05.

    Article Snippet: CT04 (#CT04-A) was obtained from Cytoskeleton, Inc. Anlotinib (#S8726) was from Selleckchem.

    Techniques: Expressing, CRISPR, Spheroids, Incubation, Western Blot, Phospho-proteomics, Luciferase, Reporter Gene Assay, Transfection, Activity Assay, Mutagenesis, Binding Assay

    VEGF leads to YAP/TAZ nuclear localization dependent on Rho/ROCK-mediated cytoskeletal dynamics A . Representative images of YAP (green) and TAZ (red) staining in HUVEC after pre-incubation with CT04 (2 µg/ml, 2 h) and incubation with VEGF (50 ng/ml, 1 h). Nuclei were counterstained with DAPI (not shown). Scale bars, 10 µm. B . Quantification of nuclear YAP and nuclear TAZ in HUVEC. Data are normalized to Basal and represent mean ± SEM of 4 independent experiments. C . Representative images of phalloidin staining of actin filaments (gray) in HUVEC after pre-incubation with CT04 (2 µg/ml, 2 h) and incubation with VEGF (50 ng/ml, 1 h). Nuclei were counterstained with DAPI (blue). D . Actin filaments were quantified. Data are normalized to untreated cells and represent mean ± SEM of 4 independent experiments. Scale bars, 10 µm. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001, n.s. p >0.05.

    Journal: Angiogenesis

    Article Title: Endothelial Epac1 facilitates YAP/TAZ controlled melanoma growth and angiogenesis

    doi: 10.1007/s10456-026-10080-6

    Figure Lengend Snippet: VEGF leads to YAP/TAZ nuclear localization dependent on Rho/ROCK-mediated cytoskeletal dynamics A . Representative images of YAP (green) and TAZ (red) staining in HUVEC after pre-incubation with CT04 (2 µg/ml, 2 h) and incubation with VEGF (50 ng/ml, 1 h). Nuclei were counterstained with DAPI (not shown). Scale bars, 10 µm. B . Quantification of nuclear YAP and nuclear TAZ in HUVEC. Data are normalized to Basal and represent mean ± SEM of 4 independent experiments. C . Representative images of phalloidin staining of actin filaments (gray) in HUVEC after pre-incubation with CT04 (2 µg/ml, 2 h) and incubation with VEGF (50 ng/ml, 1 h). Nuclei were counterstained with DAPI (blue). D . Actin filaments were quantified. Data are normalized to untreated cells and represent mean ± SEM of 4 independent experiments. Scale bars, 10 µm. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001, n.s. p >0.05.

    Article Snippet: CT04 (#CT04-A) was obtained from Cytoskeleton, Inc. Anlotinib (#S8726) was from Selleckchem.

    Techniques: Cytoskeletal, Staining, Incubation

    HeLa cells were serum-starved for 30 min, treated with DMSO or 5, 10, or 20 μM (A) Rac inhibitor EHop016, (B) cdc42 inhibitor ML141, (C) Rho inhibitor Y16, (D) ROCK inhibitor Y27632, (E) 20 μM Y16, Y27632, or EHop016 or (F) 20 μM ML141, EHop016, Y16, or all three, and challenged with 31–2,000 HU/ml SLO or PFO for 30 min at 37°C. Propidium iodide (PI) uptake was analyzed by flow cytometry. The LC 50 was calculated as described in the methods. Graphs show independent experiments and the mean ± SEM, n = 5 (A, B, D [SLO], B, C, [PFO]), n = 4 (A, D, E, [PFO], D, E, F [SLO]), n = 6 (C, SLO), or n = 3 (F, PFO). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 denote statistical significance using repeated-measures ANOVA between groups with Tukey post-test. SLO, streptolysin O; PFO, perfringolysin O.

    Journal: Life Science Alliance

    Article Title: Vav2 is a master regulator of repair against bacterial pore-forming toxins

    doi: 10.26508/lsa.202603633

    Figure Lengend Snippet: HeLa cells were serum-starved for 30 min, treated with DMSO or 5, 10, or 20 μM (A) Rac inhibitor EHop016, (B) cdc42 inhibitor ML141, (C) Rho inhibitor Y16, (D) ROCK inhibitor Y27632, (E) 20 μM Y16, Y27632, or EHop016 or (F) 20 μM ML141, EHop016, Y16, or all three, and challenged with 31–2,000 HU/ml SLO or PFO for 30 min at 37°C. Propidium iodide (PI) uptake was analyzed by flow cytometry. The LC 50 was calculated as described in the methods. Graphs show independent experiments and the mean ± SEM, n = 5 (A, B, D [SLO], B, C, [PFO]), n = 4 (A, D, E, [PFO], D, E, F [SLO]), n = 6 (C, SLO), or n = 3 (F, PFO). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 denote statistical significance using repeated-measures ANOVA between groups with Tukey post-test. SLO, streptolysin O; PFO, perfringolysin O.

    Article Snippet: Rho Inhibitor-Y16 (Cat# HY-12649) and ROCK1/2 inhibitor, Y-27632 dihydrochloride (Cat# HY-10583), were from MedChemExpress (NJ, USA).

    Techniques: Flow Cytometry