jasplakinolide  (Cayman Chemical)

 
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    Name:
    Jasplakinolide
    Description:
    Jasplakinolide is a natural macrocyclic peptide first isolated from a marine sponge It potently inhibits the proliferation of PC3 prostate carcinoma cells IC 35 nM by binding F actin KD 15 nM This binding of jasplakinolide to actin which is competitive with phalloidin stabilizes actin filaments in vitro but disrupts actin filaments and induces irregular polymerization of monomeric actin in vivo This compound is used to investigate the role of actin in diverse cellular roles such as motility transport and development
    Catalog Number:
    11705
    Price:
    $165
    Purity:
    ≥98%
    Size:
    50 µg
    Product Aliases:
    NSC 613009
    Formula:
    A solid
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    Structured Review

    Cayman Chemical jasplakinolide
    Ultrastructural analysis of non-small cell lung cancer (NSCLC) A549 cell spheroids. Representative images of NSCLC A549 cells showing cell surface architecture in a 2D adhesive culture dish ( left panel ) and a 3D poly-HEMA-coated dish ( right panel ). The images were taken after 3 days of culturing. The cells in the 2D monolayer culture were treated with 1 µM <t>jasplakinolide</t> for 1 h. Then, the cells were cultured on 2D tissue culture dishes or poly-HEMA-coated dishes. Upper panel: The representative transmission electron microscopy images of NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. Middle panel: The representative scanning electron microscopy images of NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. Lower panel: The phase-contrast micrographs showing the morphologies of human NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. White arrowhead indicates tight junction; Black arrowhead indicates protrusion. Note the adherens junctions and protrusions. Original magnification: ×1000. Scale bar: 200 μm.
    Jasplakinolide is a natural macrocyclic peptide first isolated from a marine sponge It potently inhibits the proliferation of PC3 prostate carcinoma cells IC 35 nM by binding F actin KD 15 nM This binding of jasplakinolide to actin which is competitive with phalloidin stabilizes actin filaments in vitro but disrupts actin filaments and induces irregular polymerization of monomeric actin in vivo This compound is used to investigate the role of actin in diverse cellular roles such as motility transport and development
    https://www.bioz.com/result/jasplakinolide/product/Cayman Chemical
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    jasplakinolide - by Bioz Stars, 2021-07
    95/100 stars

    Images

    1) Product Images from "AQP3 Increases Intercellular Cohesion in NSCLC A549 Cell Spheroids through Exploratory Cell Protrusions"

    Article Title: AQP3 Increases Intercellular Cohesion in NSCLC A549 Cell Spheroids through Exploratory Cell Protrusions

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms22084287

    Ultrastructural analysis of non-small cell lung cancer (NSCLC) A549 cell spheroids. Representative images of NSCLC A549 cells showing cell surface architecture in a 2D adhesive culture dish ( left panel ) and a 3D poly-HEMA-coated dish ( right panel ). The images were taken after 3 days of culturing. The cells in the 2D monolayer culture were treated with 1 µM jasplakinolide for 1 h. Then, the cells were cultured on 2D tissue culture dishes or poly-HEMA-coated dishes. Upper panel: The representative transmission electron microscopy images of NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. Middle panel: The representative scanning electron microscopy images of NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. Lower panel: The phase-contrast micrographs showing the morphologies of human NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. White arrowhead indicates tight junction; Black arrowhead indicates protrusion. Note the adherens junctions and protrusions. Original magnification: ×1000. Scale bar: 200 μm.
    Figure Legend Snippet: Ultrastructural analysis of non-small cell lung cancer (NSCLC) A549 cell spheroids. Representative images of NSCLC A549 cells showing cell surface architecture in a 2D adhesive culture dish ( left panel ) and a 3D poly-HEMA-coated dish ( right panel ). The images were taken after 3 days of culturing. The cells in the 2D monolayer culture were treated with 1 µM jasplakinolide for 1 h. Then, the cells were cultured on 2D tissue culture dishes or poly-HEMA-coated dishes. Upper panel: The representative transmission electron microscopy images of NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. Middle panel: The representative scanning electron microscopy images of NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. Lower panel: The phase-contrast micrographs showing the morphologies of human NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. White arrowhead indicates tight junction; Black arrowhead indicates protrusion. Note the adherens junctions and protrusions. Original magnification: ×1000. Scale bar: 200 μm.

    Techniques Used: Cell Culture, Transmission Assay, Electron Microscopy

    Protrusion controls migration and invasion of A549 cancer cells. ( A ) The phase-contrast micrograph of the migration of NSCLC A549 cells (left) and quantification (right) in the Transwell assay. The quantification of migrated cells treated with jasplakinolide represents three independent experiments, and the values represent the mean ± SEM of triplicate samples. The differences in expression levels were evaluated for significance using unpaired two-tailed t-test. * p
    Figure Legend Snippet: Protrusion controls migration and invasion of A549 cancer cells. ( A ) The phase-contrast micrograph of the migration of NSCLC A549 cells (left) and quantification (right) in the Transwell assay. The quantification of migrated cells treated with jasplakinolide represents three independent experiments, and the values represent the mean ± SEM of triplicate samples. The differences in expression levels were evaluated for significance using unpaired two-tailed t-test. * p

    Techniques Used: Migration, Transwell Assay, Expressing, Two Tailed Test

    2) Product Images from "The cerebral cavernous malformation disease causing gene KRIT1 participates in intestinal epithelial barrier maintenance and regulation"

    Article Title: The cerebral cavernous malformation disease causing gene KRIT1 participates in intestinal epithelial barrier maintenance and regulation

    Journal: The FASEB Journal

    doi: 10.1096/fj.201800343R

    KRIT1 is required for myosin II contraction–induced epithelial barrier regulation. A ) TER of the monomeric actin–binding drug latrunculin A (LatA; 0.5 μM) treated control (blue diamonds) and KRIT1 knockdown monolayers (red diamonds). Results of 3 independent experiments are shown. Data points from the same individual experiments are connected by gray lines. B ) TER of actin polymerization inducer jasplakinolide (jas; 2 μM) treated control (blue diamonds) and KRIT1 knockdown monolayers. Results of 3 independent experiments are shown. Data points from the same individual experiments are connected by gray lines. C ) TER of myosin II motor inhibitor blebbistatin (blebb; 50 μM) treated control (blue diamonds) and KRIT1 knockdown (red diamonds) monolayers. Results of 4 independent experiments are shown. Data points from the same individual experiments are connected by gray lines. D ) Relative TER of blebbistatin (blebb; 50 μM) treated KRIT1 knockdown monolayers stably transfected with Tet-inducible EGFP-KRIT1 plasmid with (green diamonds) or without (red diamonds) doxycycline-induced EGFP-KRIT1 expression. Results of 4 independent experiments are shown. Data points from the same individual experiments are connect by gray lines. E , F ) Immunofluorescent microscopy of apical F-actin (green) and ZO-1 (red) in control and KRIT1 knockdown monolayers. X-y presentation. Scale bar, 10 μm ( E ). X-z presentation. Scale bar, 5 μm ( F ). G ) Quantification of distance between the tip of the apical actin cytoskeleton and the plane of the tight junction, as marked by ZO-1. Sixty cells from multiple fields were measured for each condition. β-gal, β-galactosidase; NS, not significant ( P > 0.05). # P ≤ 0.01.
    Figure Legend Snippet: KRIT1 is required for myosin II contraction–induced epithelial barrier regulation. A ) TER of the monomeric actin–binding drug latrunculin A (LatA; 0.5 μM) treated control (blue diamonds) and KRIT1 knockdown monolayers (red diamonds). Results of 3 independent experiments are shown. Data points from the same individual experiments are connected by gray lines. B ) TER of actin polymerization inducer jasplakinolide (jas; 2 μM) treated control (blue diamonds) and KRIT1 knockdown monolayers. Results of 3 independent experiments are shown. Data points from the same individual experiments are connected by gray lines. C ) TER of myosin II motor inhibitor blebbistatin (blebb; 50 μM) treated control (blue diamonds) and KRIT1 knockdown (red diamonds) monolayers. Results of 4 independent experiments are shown. Data points from the same individual experiments are connected by gray lines. D ) Relative TER of blebbistatin (blebb; 50 μM) treated KRIT1 knockdown monolayers stably transfected with Tet-inducible EGFP-KRIT1 plasmid with (green diamonds) or without (red diamonds) doxycycline-induced EGFP-KRIT1 expression. Results of 4 independent experiments are shown. Data points from the same individual experiments are connect by gray lines. E , F ) Immunofluorescent microscopy of apical F-actin (green) and ZO-1 (red) in control and KRIT1 knockdown monolayers. X-y presentation. Scale bar, 10 μm ( E ). X-z presentation. Scale bar, 5 μm ( F ). G ) Quantification of distance between the tip of the apical actin cytoskeleton and the plane of the tight junction, as marked by ZO-1. Sixty cells from multiple fields were measured for each condition. β-gal, β-galactosidase; NS, not significant ( P > 0.05). # P ≤ 0.01.

    Techniques Used: Binding Assay, Stable Transfection, Transfection, Plasmid Preparation, Expressing, Microscopy

    3) Product Images from "CB1 receptor-mediated inhibitory LTD triggers presynaptic remodeling via protein synthesis and ubiquitination"

    Article Title: CB1 receptor-mediated inhibitory LTD triggers presynaptic remodeling via protein synthesis and ubiquitination

    Journal: bioRxiv

    doi: 10.1101/2020.01.09.900464

    CB 1 -iLTD involves actin remodeling via Rac1 and Arp2/3 A. Left , representative single boutons reconstructed in 3D. Right , quantification of bouton volume normalized to control. Activation of CB 1 receptors with WIN for 25 min led to decreased bouton volume that was blocked by treatment with jasplakinolide (JSK, 250 nM). Summary data expressed as normalized change from Vehicle ± S.E.M.. WIN + Veh: 0.89 ± 0.01 vs. JSK + WIN: 0.98 ± 0.01, U = 2.92E6, Z = 6.356, **** indicates p
    Figure Legend Snippet: CB 1 -iLTD involves actin remodeling via Rac1 and Arp2/3 A. Left , representative single boutons reconstructed in 3D. Right , quantification of bouton volume normalized to control. Activation of CB 1 receptors with WIN for 25 min led to decreased bouton volume that was blocked by treatment with jasplakinolide (JSK, 250 nM). Summary data expressed as normalized change from Vehicle ± S.E.M.. WIN + Veh: 0.89 ± 0.01 vs. JSK + WIN: 0.98 ± 0.01, U = 2.92E6, Z = 6.356, **** indicates p

    Techniques Used: Activation Assay

    4) Product Images from "HIV-1 Vpu promotes phagocytosis of infected CD4+ T cells by macrophages through downregulation of CD47"

    Article Title: HIV-1 Vpu promotes phagocytosis of infected CD4+ T cells by macrophages through downregulation of CD47

    Journal: bioRxiv

    doi: 10.1101/2021.03.16.435750

    Inhibition of phagocytosis hinders productive infection of MDMs by T/F virus. (A) Experimental strategy for coculture of infected CD4 + T cells, with autologous MDMs pretreated with Jasplakinolide (Jasp), analysis of phagocytosis and MDM productive infection. Pretreated MDMs (1 h with Jasp or vehicle (DMSO)) were cocultured for 6 h with WITO-infected CD4 + T cells in the presence of Jasp or DMSO. MDMs were also cocultured for 2 h with the same number of pHrodo-treated CD4 + T cells and analyzed for phagocytosis by flow cytometry. MDMs were maintained in culture after washing-off T cells and collected at the indicated time points for intracellular Gag staining and flow cytometry analysis. Evaluation of infectious virus production was determined as described above using the TZM-bl assay. (B) Inhibition of phagocytosis by Jasp. Representative flow cytometry dot-plots of MDMs (CD11b + ) with percentage of pHrodo + populations corresponding to phagocytosis of CD4 + T cells by MDMs (top) and summary graph (bottom), analyzed by Mann-Whitney U-test, (*, P
    Figure Legend Snippet: Inhibition of phagocytosis hinders productive infection of MDMs by T/F virus. (A) Experimental strategy for coculture of infected CD4 + T cells, with autologous MDMs pretreated with Jasplakinolide (Jasp), analysis of phagocytosis and MDM productive infection. Pretreated MDMs (1 h with Jasp or vehicle (DMSO)) were cocultured for 6 h with WITO-infected CD4 + T cells in the presence of Jasp or DMSO. MDMs were also cocultured for 2 h with the same number of pHrodo-treated CD4 + T cells and analyzed for phagocytosis by flow cytometry. MDMs were maintained in culture after washing-off T cells and collected at the indicated time points for intracellular Gag staining and flow cytometry analysis. Evaluation of infectious virus production was determined as described above using the TZM-bl assay. (B) Inhibition of phagocytosis by Jasp. Representative flow cytometry dot-plots of MDMs (CD11b + ) with percentage of pHrodo + populations corresponding to phagocytosis of CD4 + T cells by MDMs (top) and summary graph (bottom), analyzed by Mann-Whitney U-test, (*, P

    Techniques Used: Inhibition, Infection, Flow Cytometry, Staining, MANN-WHITNEY

    5) Product Images from "Mechanosensitive subcellular rheostasis drives emergent single-cell mechanical homeostasis"

    Article Title: Mechanosensitive subcellular rheostasis drives emergent single-cell mechanical homeostasis

    Journal: Nature materials

    doi: 10.1038/nmat4654

    Subcellular cytoskeleton (CSK) tension and focal adhesion (FA) followed distinct mechanosensitive rheostasis to drive single-cell mechanical homeostasis. ( a b ) Heterogeneous rheostatic paths for subcellular CSK tension ( a ) and FA ( b ). Results from REF-52 fibroblasts under 8% static equibiaxial stretch were grouped into subsets based on ground-state CSK tension values at t = 0 min ( F 0 ). Average result from each subset was plotted using the rainbow spectrum (from purple to red ). Whole-cell average response ( black ) was included for referencing single-cell homeostasis. Data represents the mean ± s.e.m with n = 10. ( c-f ) Dependence of subcellular rheostasis on ground-state values of CSK tension and FA size. Changes in CSK tension ( c d ) and FA size ( e f ) during Phase I ( t = 0 - 1 min; c e ) and phase II ( t = 1 - 30 min; d f ) were color-coded in two-dimensional ground-state CSK tension - FA size diagrams obtained at t = 0 min. Red dashed lines in d and f marked average ground-state values of CSK tension and FA size as well as a transition boundary between reinforcement and relaxation for subcellular rheostasis during Phase II . ( g-j ) Responses of subcellular CSK tension ( top ) and FA ( bottom ) rheostasis to pharmacological inhibitors in REF-52 fibroblasts under 8% static equibiaxial stretch ( g : nocodazole; h : blebbistatin; i : jasplakinolide; j : cytochalasin D). Results were grouped into subsets based on ground-state CSK tension values at t = 0 min ( F 0 ). Whole-cell average responses ( black ) were included to indicate changes in single-cell homeostasis. Data represents the mean ± s.e.m with n = 10. ( k ) Force - lifetime diagram of the catch-slip bond between α 5 β 1 integrin and FNIII 7-10 , with or without treatments of antibody TS2/16 as indicated (from Ref. [ 23 ]). ( l ) Response of subcellular CSK tension ( left ) and FA ( right ) rheostasis to TS2/16 treatment in human mesenchymal stem cells (HUMSCs) under 8% static equibiaxial stretch. Results were grouped into subsets based on ground-state CSK tension values at t = 0 min ( F 0 ). Whole-cell average response ( black ) was included to indicate changes in single-cell homeostasis. Data represents the mean ± s.e.m with n = 11. In g-i and l , hollow red arrowheads indicated suppressed FA reinforcement in Phase I , and solid red arrowheads marked suppressed FA relaxation in Phase II . P -values were calculated using student’s paired sample t -test comparing data before ( t = 0 min) and after ( t = 1 or 30 min) stretch. N.S. , statistically not significant and P > 0.05. *, P
    Figure Legend Snippet: Subcellular cytoskeleton (CSK) tension and focal adhesion (FA) followed distinct mechanosensitive rheostasis to drive single-cell mechanical homeostasis. ( a b ) Heterogeneous rheostatic paths for subcellular CSK tension ( a ) and FA ( b ). Results from REF-52 fibroblasts under 8% static equibiaxial stretch were grouped into subsets based on ground-state CSK tension values at t = 0 min ( F 0 ). Average result from each subset was plotted using the rainbow spectrum (from purple to red ). Whole-cell average response ( black ) was included for referencing single-cell homeostasis. Data represents the mean ± s.e.m with n = 10. ( c-f ) Dependence of subcellular rheostasis on ground-state values of CSK tension and FA size. Changes in CSK tension ( c d ) and FA size ( e f ) during Phase I ( t = 0 - 1 min; c e ) and phase II ( t = 1 - 30 min; d f ) were color-coded in two-dimensional ground-state CSK tension - FA size diagrams obtained at t = 0 min. Red dashed lines in d and f marked average ground-state values of CSK tension and FA size as well as a transition boundary between reinforcement and relaxation for subcellular rheostasis during Phase II . ( g-j ) Responses of subcellular CSK tension ( top ) and FA ( bottom ) rheostasis to pharmacological inhibitors in REF-52 fibroblasts under 8% static equibiaxial stretch ( g : nocodazole; h : blebbistatin; i : jasplakinolide; j : cytochalasin D). Results were grouped into subsets based on ground-state CSK tension values at t = 0 min ( F 0 ). Whole-cell average responses ( black ) were included to indicate changes in single-cell homeostasis. Data represents the mean ± s.e.m with n = 10. ( k ) Force - lifetime diagram of the catch-slip bond between α 5 β 1 integrin and FNIII 7-10 , with or without treatments of antibody TS2/16 as indicated (from Ref. [ 23 ]). ( l ) Response of subcellular CSK tension ( left ) and FA ( right ) rheostasis to TS2/16 treatment in human mesenchymal stem cells (HUMSCs) under 8% static equibiaxial stretch. Results were grouped into subsets based on ground-state CSK tension values at t = 0 min ( F 0 ). Whole-cell average response ( black ) was included to indicate changes in single-cell homeostasis. Data represents the mean ± s.e.m with n = 11. In g-i and l , hollow red arrowheads indicated suppressed FA reinforcement in Phase I , and solid red arrowheads marked suppressed FA relaxation in Phase II . P -values were calculated using student’s paired sample t -test comparing data before ( t = 0 min) and after ( t = 1 or 30 min) stretch. N.S. , statistically not significant and P > 0.05. *, P

    Techniques Used:

    6) Product Images from "Short-Lived Cages Restrict Protein Diffusion in the Plasma Membrane"

    Article Title: Short-Lived Cages Restrict Protein Diffusion in the Plasma Membrane

    Journal: Scientific Reports

    doi: 10.1038/srep34987

    Cages are Structures Distinct from Actin-Based Corrals. The impact of actin stabilization (Jasplakinolide (Jasp) + Belbbistatin (Bleb)) and destabilization (Latrunculin B, LatB) were assessed on CD93 corralling and cage strength. ( a ) Effect of actin destabilization and stabilization on CD93 corralling. ( b ) Effect of actin stabilization and destabilization on the frequency and size of actin-based corrals, measured as fraction of total CD93 tracks. ( c ) Actin stabilization and destabilization do not affect cage strength at early lag times (τ = 0.1 s). ( d ) Rate of CD93 cage decay following stabilization or destabilization of the actin cytoskeleton. Data are expressed as mean ± SEM ( a,c,d ) or as mean ( b ) of 4 independent experiments. * , † p
    Figure Legend Snippet: Cages are Structures Distinct from Actin-Based Corrals. The impact of actin stabilization (Jasplakinolide (Jasp) + Belbbistatin (Bleb)) and destabilization (Latrunculin B, LatB) were assessed on CD93 corralling and cage strength. ( a ) Effect of actin destabilization and stabilization on CD93 corralling. ( b ) Effect of actin stabilization and destabilization on the frequency and size of actin-based corrals, measured as fraction of total CD93 tracks. ( c ) Actin stabilization and destabilization do not affect cage strength at early lag times (τ = 0.1 s). ( d ) Rate of CD93 cage decay following stabilization or destabilization of the actin cytoskeleton. Data are expressed as mean ± SEM ( a,c,d ) or as mean ( b ) of 4 independent experiments. * , † p

    Techniques Used:

    7) Product Images from "CB1-receptor-mediated inhibitory LTD triggers presynaptic remodeling via protein synthesis and ubiquitination"

    Article Title: CB1-receptor-mediated inhibitory LTD triggers presynaptic remodeling via protein synthesis and ubiquitination

    Journal: eLife

    doi: 10.7554/eLife.54812

    Individual bouton sizes are altered by CB 1 -iLTD and dependent on actin dynamics but actin inhibitors have no effect on basal transmission. ( A ) Quantification of bouton volume normalized to control by slice. Activation of CB 1 receptors with WIN for 25 min led to decreased bouton volume that was blocked by treatment with jasplakinolide (JSK, 250 nM). Superplot shows individual bouton volume values color-coded by slice in swarmplot with solid larger dots overlaid representing mean bouton volume per slice. Overall mean of each slice is given by solid black circle with 95% CI represented by the vertical black line. Control: 1.0 ± 0.02 vs. WIN 1 hr: 0.88 ± 0.02 vs. WIN + JSK: 0.97 ± 0.02 vs. JSK: 0.95 ± 0.02 (Mean ± S.E.M.); F[3,20]=7.33, p=0.0017, one-way ANOVA with post-hoc Tukey test for multiple comparisons. WIN 1 hr vs. Control: CI [−0.20,–0.04], p=0.0016, WIN 1 hr vs. WIN + JSK: CI [−0.17,–0.017], p=0.012. n = number of slices (three images/slice, one slice/rat, six rats). 95% Confidence intervals (CI) are given as CI[lower CI, upper CI]. p-Values are exact. ( B ) JSK (250 nM) had no effect on baseline. JSK: 97.76 ± 2.8, one-sample t-test, p > 0.05. For all electrophysiology figures, averaged summary data expressed as normalized change from baseline ± S.E.M. and n = number of slices ( s ), number of animals ( a ). ( C ) NSC application on baseline caused decreased PPR (measured at 35–45 min) suggesting a presynaptic target. Pre: 0.65 ± 0.06 vs. NSC: 0.57 ± 0.08, paired-sample t-test, p
    Figure Legend Snippet: Individual bouton sizes are altered by CB 1 -iLTD and dependent on actin dynamics but actin inhibitors have no effect on basal transmission. ( A ) Quantification of bouton volume normalized to control by slice. Activation of CB 1 receptors with WIN for 25 min led to decreased bouton volume that was blocked by treatment with jasplakinolide (JSK, 250 nM). Superplot shows individual bouton volume values color-coded by slice in swarmplot with solid larger dots overlaid representing mean bouton volume per slice. Overall mean of each slice is given by solid black circle with 95% CI represented by the vertical black line. Control: 1.0 ± 0.02 vs. WIN 1 hr: 0.88 ± 0.02 vs. WIN + JSK: 0.97 ± 0.02 vs. JSK: 0.95 ± 0.02 (Mean ± S.E.M.); F[3,20]=7.33, p=0.0017, one-way ANOVA with post-hoc Tukey test for multiple comparisons. WIN 1 hr vs. Control: CI [−0.20,–0.04], p=0.0016, WIN 1 hr vs. WIN + JSK: CI [−0.17,–0.017], p=0.012. n = number of slices (three images/slice, one slice/rat, six rats). 95% Confidence intervals (CI) are given as CI[lower CI, upper CI]. p-Values are exact. ( B ) JSK (250 nM) had no effect on baseline. JSK: 97.76 ± 2.8, one-sample t-test, p > 0.05. For all electrophysiology figures, averaged summary data expressed as normalized change from baseline ± S.E.M. and n = number of slices ( s ), number of animals ( a ). ( C ) NSC application on baseline caused decreased PPR (measured at 35–45 min) suggesting a presynaptic target. Pre: 0.65 ± 0.06 vs. NSC: 0.57 ± 0.08, paired-sample t-test, p

    Techniques Used: Transmission Assay, Activation Assay

    8) Product Images from "T-Plastin reinforces membrane protrusions to bridge matrix gaps during cell migration"

    Article Title: T-Plastin reinforces membrane protrusions to bridge matrix gaps during cell migration

    Journal: Nature Communications

    doi: 10.1038/s41467-020-18586-3

    Selective association of T-Plastin with extending but not retracting protrusions. a HUVEC expressing T-Plastin-mRuby3 and F-tractin-mCitrine were plated sparsely and imaged over time. The ratio of T-Plastin over F-tractin is shown as a parula colormap with yellow and blue indicating high (99th percentile) or low (3rd percentile) enrichment of T-Plastin, respectively and is the same scale in all panels using the parula colormap. The cell edge from each previous timepoint image is shown as a red outline; protrusions are present outside the red line while retractions lie within. Subregions blown up for clarity are denoted with a white asterisk. b Regions from of the cell edge from ( a ) were divided into windows for kymographic analysis of cell edge velocity and T-Plastin enrichment. Arrows depict edge velocities for each window between frames. c Kymographs of window edge velocities with protrusions shown in red (positive, +0.65 µm/s) and retractions in blue (negative, −0.65 µm/s). Parula kymograph shows the corresponding ratio of T-Plastin over F-tractin at same scale as ( a ) in the same windows analyzed for edge velocity. Dotted box shows region blown up in ( d ). d Region from ( c ) with protrusion areas highlighted in black and corresponding regions of T-Plastin enrichment also highlighted. e Temporal cross-correlation analysis of protrusion events shown in ( a – d ). Cross-correlation coefficients of T-Plastin (purple) and F-tractin (green) are shown relative the incidence of protrusion at 0 min. f Similar to ( a ), except cells also expressed MYL9-mTurq to mark myosin activity. Cells were treated with CK666 where indicated. g Similar to ( f ), except cells were first treated with 300 nM Jasplakinolide then CK666. Bars, 5 µm.
    Figure Legend Snippet: Selective association of T-Plastin with extending but not retracting protrusions. a HUVEC expressing T-Plastin-mRuby3 and F-tractin-mCitrine were plated sparsely and imaged over time. The ratio of T-Plastin over F-tractin is shown as a parula colormap with yellow and blue indicating high (99th percentile) or low (3rd percentile) enrichment of T-Plastin, respectively and is the same scale in all panels using the parula colormap. The cell edge from each previous timepoint image is shown as a red outline; protrusions are present outside the red line while retractions lie within. Subregions blown up for clarity are denoted with a white asterisk. b Regions from of the cell edge from ( a ) were divided into windows for kymographic analysis of cell edge velocity and T-Plastin enrichment. Arrows depict edge velocities for each window between frames. c Kymographs of window edge velocities with protrusions shown in red (positive, +0.65 µm/s) and retractions in blue (negative, −0.65 µm/s). Parula kymograph shows the corresponding ratio of T-Plastin over F-tractin at same scale as ( a ) in the same windows analyzed for edge velocity. Dotted box shows region blown up in ( d ). d Region from ( c ) with protrusion areas highlighted in black and corresponding regions of T-Plastin enrichment also highlighted. e Temporal cross-correlation analysis of protrusion events shown in ( a – d ). Cross-correlation coefficients of T-Plastin (purple) and F-tractin (green) are shown relative the incidence of protrusion at 0 min. f Similar to ( a ), except cells also expressed MYL9-mTurq to mark myosin activity. Cells were treated with CK666 where indicated. g Similar to ( f ), except cells were first treated with 300 nM Jasplakinolide then CK666. Bars, 5 µm.

    Techniques Used: Expressing, Activity Assay

    9) Product Images from "RhoA effectors LOK/SLK activate ERM proteins to locally inhibit RhoA and define apical morphology"

    Article Title: RhoA effectors LOK/SLK activate ERM proteins to locally inhibit RhoA and define apical morphology

    Journal: bioRxiv

    doi: 10.1101/2020.07.02.185298

    Increased actin polymerization in ERM or LOK/SLK knockout cells leads to junctional defects and mechanical stiffening of the cell. (A) Jeg3 cells treated with DMSO, 500nM Jaspakinolide or 100ng/mL Latrunculin B for 30 min before immunostaining with ZO-1 and actin. Magenta arrows point to actin gaps at junctions while blue arrows represent actin present at cell junctions. Scale bars, 10 μm. (B) Quantification of tortuosity between tight junction markers as described in Figure 3 . Jasplakinolide treatment increases tortuosity values, while Latrunculin B rescues tortuosity to wildtype levels. N ≥ 10 cells per condition. Lines represent mean±SEM. P-values were calculated with Welch’s t-test (* p≤0.05, ** p≤0.01, *** p≤0.001). (C) Comparison of actin levels between apical and basolateral regions after treatment with drugs as visualized in panel A. N ≥ 21 cells per condition. Bars show mean±SEM. (D) Averaged force indentation curves for WT Jeg3 (blue), ezrin -/- radixin -/- (green) and LOK -/- SLK -/- (magenta); semi-transparent area around each line represents the SEM of the data. A steeper curve indicates a stiffer cell. (E) Young’s modulus stiffness parameters; black line indicates each condition’s mean value (WT N=356, ezrin -/- radixin -/- N=304, LOK -/- SLK -/- N=431). Both KO conditions were significantly stiffer than WT cells (*** p=
    Figure Legend Snippet: Increased actin polymerization in ERM or LOK/SLK knockout cells leads to junctional defects and mechanical stiffening of the cell. (A) Jeg3 cells treated with DMSO, 500nM Jaspakinolide or 100ng/mL Latrunculin B for 30 min before immunostaining with ZO-1 and actin. Magenta arrows point to actin gaps at junctions while blue arrows represent actin present at cell junctions. Scale bars, 10 μm. (B) Quantification of tortuosity between tight junction markers as described in Figure 3 . Jasplakinolide treatment increases tortuosity values, while Latrunculin B rescues tortuosity to wildtype levels. N ≥ 10 cells per condition. Lines represent mean±SEM. P-values were calculated with Welch’s t-test (* p≤0.05, ** p≤0.01, *** p≤0.001). (C) Comparison of actin levels between apical and basolateral regions after treatment with drugs as visualized in panel A. N ≥ 21 cells per condition. Bars show mean±SEM. (D) Averaged force indentation curves for WT Jeg3 (blue), ezrin -/- radixin -/- (green) and LOK -/- SLK -/- (magenta); semi-transparent area around each line represents the SEM of the data. A steeper curve indicates a stiffer cell. (E) Young’s modulus stiffness parameters; black line indicates each condition’s mean value (WT N=356, ezrin -/- radixin -/- N=304, LOK -/- SLK -/- N=431). Both KO conditions were significantly stiffer than WT cells (*** p=

    Techniques Used: Knock-Out, Immunostaining

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    other:

    Article Title: CB1-receptor-mediated inhibitory LTD triggers presynaptic remodeling via protein synthesis and ubiquitination
    Article Snippet: CNQX, D-APV, SR 141716, and WIN 55,212–2 were acquired from the NIMH Chemical Synthesis and Drug Supply Program; salts for making cutting, ACSF, ziram, and intracellular recording solutions from Sigma Aldrich (St. Louis, MO); AM251, NSC-23766, MG-132, DAMGO, cycloheximide from Tocris Bioscience (Bristol UK); jasplakinolide, anisomycin, PYR41 from Cayman Chemical (Ann Arbor, MI); CK-666 from EMD Millipore.

    Article Title: CB1 receptor-mediated inhibitory LTD triggers presynaptic remodeling via protein synthesis and ubiquitination
    Article Snippet: CNQX, D-APV, SR 141716, and WIN were acquired from the NIMH Chemical Synthesis and Drug Supply Program; salts for making cutting, ACSF, ziram, and intracellular recording solutions from Sigma Aldrich (St. Louis, MO, USA); AM251, NSC-23766, MG-132, DAMGO, cycloheximide from Tocris Bioscience (Bristol UK); jasplakinolide, anisomycin, PYR41 from Cayman Chemical (Ann Arbor, MI, USA); CK-666 from EMD Millipore.

    Concentration Assay:

    Article Title: AQP3 Increases Intercellular Cohesion in NSCLC A549 Cell Spheroids through Exploratory Cell Protrusions
    Article Snippet: .. Jasplakinolide and Y-27632 (Cayman Chemical, Ann Arbor, MI, USA) dissolved in dimethyl sulfoxide (Sigma-Aldrich, St. Louis, MO, USA) to reach a concentration of 1 mM. ..

    Activity Assay:

    Article Title: Mechanosensitive subcellular rheostasis drives emergent single-cell mechanical homeostasis
    Article Snippet: To reduce background fluorescence, phenol red-free growth medium (Invitrogen) was used during live-cell fluorescence imaging. .. To perturb the actin cytoskeleton (CSK) in REF-52 fibroblasts, small-molecule inhibitors targeting the CSK integrity and tension, including 50 nM nocodazole (Sigma-Aldrich), which depolymerizes microtubules and impedes FA disassembly ; 10 μM blebbistatin (Cayman Chemical, Ann Arbor, MI), which inhibits myosin motor activity and thus CSK tension ; 10 nM jasplakinolide (Cayman Chemical), which enhances actin polymerization ; and 200 nM cytochalasin D (Tocris bioscience, Bristol, UK), which blocks actin polymerization , were supplemented to cell growth medium for 2 hr prior to cell stretch assays. .. Dosages of the inhibitors were optimized by titration to minimize their off-target effects on cell area, focal adhesion (FA) size, CSK tension, and actin CSK architecture ( ).

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    Cayman Chemical latrunculin a
    Multiplexed SIFTER detects subpopulations of cells with altered cytoskeletal protein complexes in response to F-actin destabilization. a) Schematic of the cell cytoskeleton composed of F-actin, intermediate filaments (IF) and microtubules (MT), and the unknown effects of <t>Latrunculin</t> A (LatA) on IF and MT. (b) Representative false-color fluorescence micrographs and intensity profiles from SIFTER. Monomeric proteins (e.g., β-Tubulin, β-Tub) are electrophoresed left of the microwell while F-actin, MT and IF are electrophoresed to the right of the microwell. Protein quantification is performed by peak area integration. Scale bar is 100 μm. (c) Heat maps with dendrograms from agglomerative hierarchical clustering with Euclidean distance metric and Ward linkage for U2OS cells incubated in DMSO (n = 92 cells, four SIFTER gels) or 2 μM Latrunculin A (LatA, n = 134 cells, four SIFTER gels). Distinct sub-lineages used as bait groups A-F for CellFishing are shown with colored bars. Heatmap is standardized by row (mean at 0, and color gradations at units of standard deviation). (d) Spectral clustering projections and heatmaps depicting LatA treatment bait group cells (blue), DMSO control cells (grey) and fished out DMSO control cells (yellow).
    Latrunculin A, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/latrunculin a/product/Cayman Chemical
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    latrunculin a - by Bioz Stars, 2021-07
    94/100 stars
      Buy from Supplier

    95
    Cayman Chemical jasplakinolide
    Ultrastructural analysis of non-small cell lung cancer (NSCLC) A549 cell spheroids. Representative images of NSCLC A549 cells showing cell surface architecture in a 2D adhesive culture dish ( left panel ) and a 3D poly-HEMA-coated dish ( right panel ). The images were taken after 3 days of culturing. The cells in the 2D monolayer culture were treated with 1 µM <t>jasplakinolide</t> for 1 h. Then, the cells were cultured on 2D tissue culture dishes or poly-HEMA-coated dishes. Upper panel: The representative transmission electron microscopy images of NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. Middle panel: The representative scanning electron microscopy images of NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. Lower panel: The phase-contrast micrographs showing the morphologies of human NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. White arrowhead indicates tight junction; Black arrowhead indicates protrusion. Note the adherens junctions and protrusions. Original magnification: ×1000. Scale bar: 200 μm.
    Jasplakinolide, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/jasplakinolide/product/Cayman Chemical
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    jasplakinolide - by Bioz Stars, 2021-07
    95/100 stars
      Buy from Supplier

    N/A
    Jasplakinolide is a natural macrocyclic peptide first isolated from a marine sponge It potently inhibits the proliferation of PC3 prostate carcinoma cells IC 35 nM by binding F actin KD
      Buy from Supplier

    Image Search Results


    Multiplexed SIFTER detects subpopulations of cells with altered cytoskeletal protein complexes in response to F-actin destabilization. a) Schematic of the cell cytoskeleton composed of F-actin, intermediate filaments (IF) and microtubules (MT), and the unknown effects of Latrunculin A (LatA) on IF and MT. (b) Representative false-color fluorescence micrographs and intensity profiles from SIFTER. Monomeric proteins (e.g., β-Tubulin, β-Tub) are electrophoresed left of the microwell while F-actin, MT and IF are electrophoresed to the right of the microwell. Protein quantification is performed by peak area integration. Scale bar is 100 μm. (c) Heat maps with dendrograms from agglomerative hierarchical clustering with Euclidean distance metric and Ward linkage for U2OS cells incubated in DMSO (n = 92 cells, four SIFTER gels) or 2 μM Latrunculin A (LatA, n = 134 cells, four SIFTER gels). Distinct sub-lineages used as bait groups A-F for CellFishing are shown with colored bars. Heatmap is standardized by row (mean at 0, and color gradations at units of standard deviation). (d) Spectral clustering projections and heatmaps depicting LatA treatment bait group cells (blue), DMSO control cells (grey) and fished out DMSO control cells (yellow).

    Journal: bioRxiv

    Article Title: Quantifying cytoskeletal heterogeneity via single-cell protein-complex fractionation

    doi: 10.1101/2020.09.12.294801

    Figure Lengend Snippet: Multiplexed SIFTER detects subpopulations of cells with altered cytoskeletal protein complexes in response to F-actin destabilization. a) Schematic of the cell cytoskeleton composed of F-actin, intermediate filaments (IF) and microtubules (MT), and the unknown effects of Latrunculin A (LatA) on IF and MT. (b) Representative false-color fluorescence micrographs and intensity profiles from SIFTER. Monomeric proteins (e.g., β-Tubulin, β-Tub) are electrophoresed left of the microwell while F-actin, MT and IF are electrophoresed to the right of the microwell. Protein quantification is performed by peak area integration. Scale bar is 100 μm. (c) Heat maps with dendrograms from agglomerative hierarchical clustering with Euclidean distance metric and Ward linkage for U2OS cells incubated in DMSO (n = 92 cells, four SIFTER gels) or 2 μM Latrunculin A (LatA, n = 134 cells, four SIFTER gels). Distinct sub-lineages used as bait groups A-F for CellFishing are shown with colored bars. Heatmap is standardized by row (mean at 0, and color gradations at units of standard deviation). (d) Spectral clustering projections and heatmaps depicting LatA treatment bait group cells (blue), DMSO control cells (grey) and fished out DMSO control cells (yellow).

    Article Snippet: F-actin cell staining with phalloidin and Latrunculin A and Jasplakinolide drug treatmentLatrunculin A (Cayman Chemicals 10010630) was dissolved in DMSO as a 2 mM stock solution and stored at −20 °C until use.

    Techniques: Fluorescence, Incubation, Standard Deviation

    Ultrastructural analysis of non-small cell lung cancer (NSCLC) A549 cell spheroids. Representative images of NSCLC A549 cells showing cell surface architecture in a 2D adhesive culture dish ( left panel ) and a 3D poly-HEMA-coated dish ( right panel ). The images were taken after 3 days of culturing. The cells in the 2D monolayer culture were treated with 1 µM jasplakinolide for 1 h. Then, the cells were cultured on 2D tissue culture dishes or poly-HEMA-coated dishes. Upper panel: The representative transmission electron microscopy images of NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. Middle panel: The representative scanning electron microscopy images of NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. Lower panel: The phase-contrast micrographs showing the morphologies of human NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. White arrowhead indicates tight junction; Black arrowhead indicates protrusion. Note the adherens junctions and protrusions. Original magnification: ×1000. Scale bar: 200 μm.

    Journal: International Journal of Molecular Sciences

    Article Title: AQP3 Increases Intercellular Cohesion in NSCLC A549 Cell Spheroids through Exploratory Cell Protrusions

    doi: 10.3390/ijms22084287

    Figure Lengend Snippet: Ultrastructural analysis of non-small cell lung cancer (NSCLC) A549 cell spheroids. Representative images of NSCLC A549 cells showing cell surface architecture in a 2D adhesive culture dish ( left panel ) and a 3D poly-HEMA-coated dish ( right panel ). The images were taken after 3 days of culturing. The cells in the 2D monolayer culture were treated with 1 µM jasplakinolide for 1 h. Then, the cells were cultured on 2D tissue culture dishes or poly-HEMA-coated dishes. Upper panel: The representative transmission electron microscopy images of NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. Middle panel: The representative scanning electron microscopy images of NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. Lower panel: The phase-contrast micrographs showing the morphologies of human NSCLC A549 cells grown in 2D ( left ) and 3D ( right ) cultures. White arrowhead indicates tight junction; Black arrowhead indicates protrusion. Note the adherens junctions and protrusions. Original magnification: ×1000. Scale bar: 200 μm.

    Article Snippet: Jasplakinolide and Y-27632 (Cayman Chemical, Ann Arbor, MI, USA) dissolved in dimethyl sulfoxide (Sigma-Aldrich, St. Louis, MO, USA) to reach a concentration of 1 mM.

    Techniques: Cell Culture, Transmission Assay, Electron Microscopy

    Protrusion controls migration and invasion of A549 cancer cells. ( A ) The phase-contrast micrograph of the migration of NSCLC A549 cells (left) and quantification (right) in the Transwell assay. The quantification of migrated cells treated with jasplakinolide represents three independent experiments, and the values represent the mean ± SEM of triplicate samples. The differences in expression levels were evaluated for significance using unpaired two-tailed t-test. * p

    Journal: International Journal of Molecular Sciences

    Article Title: AQP3 Increases Intercellular Cohesion in NSCLC A549 Cell Spheroids through Exploratory Cell Protrusions

    doi: 10.3390/ijms22084287

    Figure Lengend Snippet: Protrusion controls migration and invasion of A549 cancer cells. ( A ) The phase-contrast micrograph of the migration of NSCLC A549 cells (left) and quantification (right) in the Transwell assay. The quantification of migrated cells treated with jasplakinolide represents three independent experiments, and the values represent the mean ± SEM of triplicate samples. The differences in expression levels were evaluated for significance using unpaired two-tailed t-test. * p

    Article Snippet: Jasplakinolide and Y-27632 (Cayman Chemical, Ann Arbor, MI, USA) dissolved in dimethyl sulfoxide (Sigma-Aldrich, St. Louis, MO, USA) to reach a concentration of 1 mM.

    Techniques: Migration, Transwell Assay, Expressing, Two Tailed Test

    KRIT1 is required for myosin II contraction–induced epithelial barrier regulation. A ) TER of the monomeric actin–binding drug latrunculin A (LatA; 0.5 μM) treated control (blue diamonds) and KRIT1 knockdown monolayers (red diamonds). Results of 3 independent experiments are shown. Data points from the same individual experiments are connected by gray lines. B ) TER of actin polymerization inducer jasplakinolide (jas; 2 μM) treated control (blue diamonds) and KRIT1 knockdown monolayers. Results of 3 independent experiments are shown. Data points from the same individual experiments are connected by gray lines. C ) TER of myosin II motor inhibitor blebbistatin (blebb; 50 μM) treated control (blue diamonds) and KRIT1 knockdown (red diamonds) monolayers. Results of 4 independent experiments are shown. Data points from the same individual experiments are connected by gray lines. D ) Relative TER of blebbistatin (blebb; 50 μM) treated KRIT1 knockdown monolayers stably transfected with Tet-inducible EGFP-KRIT1 plasmid with (green diamonds) or without (red diamonds) doxycycline-induced EGFP-KRIT1 expression. Results of 4 independent experiments are shown. Data points from the same individual experiments are connect by gray lines. E , F ) Immunofluorescent microscopy of apical F-actin (green) and ZO-1 (red) in control and KRIT1 knockdown monolayers. X-y presentation. Scale bar, 10 μm ( E ). X-z presentation. Scale bar, 5 μm ( F ). G ) Quantification of distance between the tip of the apical actin cytoskeleton and the plane of the tight junction, as marked by ZO-1. Sixty cells from multiple fields were measured for each condition. β-gal, β-galactosidase; NS, not significant ( P > 0.05). # P ≤ 0.01.

    Journal: The FASEB Journal

    Article Title: The cerebral cavernous malformation disease causing gene KRIT1 participates in intestinal epithelial barrier maintenance and regulation

    doi: 10.1096/fj.201800343R

    Figure Lengend Snippet: KRIT1 is required for myosin II contraction–induced epithelial barrier regulation. A ) TER of the monomeric actin–binding drug latrunculin A (LatA; 0.5 μM) treated control (blue diamonds) and KRIT1 knockdown monolayers (red diamonds). Results of 3 independent experiments are shown. Data points from the same individual experiments are connected by gray lines. B ) TER of actin polymerization inducer jasplakinolide (jas; 2 μM) treated control (blue diamonds) and KRIT1 knockdown monolayers. Results of 3 independent experiments are shown. Data points from the same individual experiments are connected by gray lines. C ) TER of myosin II motor inhibitor blebbistatin (blebb; 50 μM) treated control (blue diamonds) and KRIT1 knockdown (red diamonds) monolayers. Results of 4 independent experiments are shown. Data points from the same individual experiments are connected by gray lines. D ) Relative TER of blebbistatin (blebb; 50 μM) treated KRIT1 knockdown monolayers stably transfected with Tet-inducible EGFP-KRIT1 plasmid with (green diamonds) or without (red diamonds) doxycycline-induced EGFP-KRIT1 expression. Results of 4 independent experiments are shown. Data points from the same individual experiments are connect by gray lines. E , F ) Immunofluorescent microscopy of apical F-actin (green) and ZO-1 (red) in control and KRIT1 knockdown monolayers. X-y presentation. Scale bar, 10 μm ( E ). X-z presentation. Scale bar, 5 μm ( F ). G ) Quantification of distance between the tip of the apical actin cytoskeleton and the plane of the tight junction, as marked by ZO-1. Sixty cells from multiple fields were measured for each condition. β-gal, β-galactosidase; NS, not significant ( P > 0.05). # P ≤ 0.01.

    Article Snippet: Treatment with latrunculin A (Cayman Chemicals, Ann Arbor, MI, USA) and jasplakinolide (Cayman Chemicals) was performed bilaterally in HBSS ( , ).

    Techniques: Binding Assay, Stable Transfection, Transfection, Plasmid Preparation, Expressing, Microscopy