ns1619  (Alomone Labs)


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    Name:
    NS 1619
    Description:
    NS 1619 is a potent and selective KCa1 1 BK slo Large conductance Ca2 activated K channel modulator enhancer NS 1619 was effective in eliciting and enhancing KCa1 1 channels in smooth muscle as well as in neurons with maximal effects at concentrations around 30 muM NS 1619 was used xenopus oocytes by intracarotid infusion and significantly enhanced blood tumor barrier permeability in the brain tumor area but not in normal brain tissue
    Catalog Number:
    N-105
    Price:
    76.0
    Category:
    Small Molecule
    Source:
    Synthetic
    Applications:
    0
    Purity:
    >95%
    Size:
    5 mg
    Format:
    Lyophilized/solid.
    Formula:
    C15H8F6N2O2
    Molecular Weight:
    362.2
    Molecule Name:
    11,3-Dihydro-1-[2-hydroxy-5-(trifluoromethyl)phenyl]-5-(trifluoromethyl)-2H-benzimidazol-2-one.
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    Structured Review

    Alomone Labs ns1619
    NS 1619
    NS 1619 is a potent and selective KCa1 1 BK slo Large conductance Ca2 activated K channel modulator enhancer NS 1619 was effective in eliciting and enhancing KCa1 1 channels in smooth muscle as well as in neurons with maximal effects at concentrations around 30 muM NS 1619 was used xenopus oocytes by intracarotid infusion and significantly enhanced blood tumor barrier permeability in the brain tumor area but not in normal brain tissue
    https://www.bioz.com/result/ns1619/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ns1619 - by Bioz Stars, 2021-09
    93/100 stars

    Images

    1) Product Images from "Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration"

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2020.00210

    Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).
    Figure Legend Snippet: Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).

    Techniques Used: Migration, Control Assay, Positive Control

    2) Product Images from "Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration"

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2020.00210

    Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).
    Figure Legend Snippet: Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).

    Techniques Used: Migration, Control Assay, Positive Control

    3) Product Images from "Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration"

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2020.00210

    Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).
    Figure Legend Snippet: Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).

    Techniques Used: Migration, Control Assay, Positive Control

    4) Product Images from "Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration"

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2020.00210

    Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).
    Figure Legend Snippet: Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).

    Techniques Used: Migration, Control Assay, Positive Control

    5) Product Images from "Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration"

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2020.00210

    Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).
    Figure Legend Snippet: Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).

    Techniques Used: Migration, Control Assay, Positive Control

    6) Product Images from "Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration"

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2020.00210

    Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).
    Figure Legend Snippet: Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).

    Techniques Used: Migration, Control Assay, Positive Control

    7) Product Images from "Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration"

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2020.00210

    Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).
    Figure Legend Snippet: Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).

    Techniques Used: Migration, Control Assay, Positive Control

    Related Articles

    Activation Assay:

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration
    Article Snippet: .. In addition, BK channel activation or inhibition using NS1619 or IBTX in the presence or absence of 5% PL did not affect cell viability ( ). ..

    Inhibition:

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration
    Article Snippet: .. In addition, BK channel activation or inhibition using NS1619 or IBTX in the presence or absence of 5% PL did not affect cell viability ( ). ..

    other:

    Article Title: Voltage‐dependent activation of Rac1 by Nav1.5 channels promotes cell migration, et al. Voltage‐dependent activation of Rac1 by Nav1.5 channels promotes cell migration
    Article Snippet: 2.1 ChemicalsIberiotoxin, NS‐1619, tetrodotoxin (TTX) and veratridine were purchased from Alomone Labs.

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration
    Article Snippet: The cells were then subjected to the following treatments after 16 h: IBTX 10 nM; NS1619 10 μM; 5% PL plus heparin (1% v/v); IBTX 10 nM + 5% PL plus heparin (1% v/v); and NS1619 10 μM + 5% PL plus heparin (1% v/v).

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration
    Article Snippet: Reagents The BK channel antagonist, Iberiotoxin (IBTX), and agonist, NS1619 (Alomone Labs, Jerusalem, Israel), were solubilized in water and dimethyl sulfoxide, respectively.

    Migration:

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration
    Article Snippet: .. Interestingly, rMSCs migration was enhanced by the co-treatment with 5% PL and NS1619 (1.47 ± 0.04 and 1.90 ± 0.07 for 5% PL vs. 5% PL + NS1619 10 μM, respectively; n = 5, p < 0.001; ) suggesting a synergistic action on BK channels between NS1619 (10 μM) and 5% PL. ..

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration
    Article Snippet: .. The effect was dose-dependent because cells treated with NS1619 3 μM did not show significant differences in migration versus control cells. ..

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  • 93
    Alomone Labs ns 1619
    Na v 1.5‐dependent membrane potential depolarization regulates lamellipodia formation. (a) Images of representative cells after treatment with TTX (30 μM) or <t>NS‐1619</t> (1 μM) for 3 hr. Cells were fixed and stained with phalloidin (red) and DAPI (blue). Lower row shows masks of cells in the upper row, from which the circularity was calculated. (b) Circularity ( n ≥ 61). (c) Feret's diameter (µm; n ≥ 57). (d) Number of MDA‐MB‐231 cells with a lamellipodium ( p
    Ns 1619, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ns 1619/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ns 1619 - by Bioz Stars, 2021-09
    93/100 stars
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    Na v 1.5‐dependent membrane potential depolarization regulates lamellipodia formation. (a) Images of representative cells after treatment with TTX (30 μM) or NS‐1619 (1 μM) for 3 hr. Cells were fixed and stained with phalloidin (red) and DAPI (blue). Lower row shows masks of cells in the upper row, from which the circularity was calculated. (b) Circularity ( n ≥ 61). (c) Feret's diameter (µm; n ≥ 57). (d) Number of MDA‐MB‐231 cells with a lamellipodium ( p

    Journal: Journal of Cellular Physiology

    Article Title: Voltage‐dependent activation of Rac1 by Nav1.5 channels promotes cell migration, et al. Voltage‐dependent activation of Rac1 by Nav1.5 channels promotes cell migration

    doi: 10.1002/jcp.29290

    Figure Lengend Snippet: Na v 1.5‐dependent membrane potential depolarization regulates lamellipodia formation. (a) Images of representative cells after treatment with TTX (30 μM) or NS‐1619 (1 μM) for 3 hr. Cells were fixed and stained with phalloidin (red) and DAPI (blue). Lower row shows masks of cells in the upper row, from which the circularity was calculated. (b) Circularity ( n ≥ 61). (c) Feret's diameter (µm; n ≥ 57). (d) Number of MDA‐MB‐231 cells with a lamellipodium ( p

    Article Snippet: 2.1 ChemicalsIberiotoxin, NS‐1619, tetrodotoxin (TTX) and veratridine were purchased from Alomone Labs.

    Techniques: Staining, Multiple Displacement Amplification

    Na v 1.5 and V m regulate Rac1‐GTP colocalization with phosphatidylserine. (a) Images of representative cells after treatment with TTX (30 µM) and NS‐1619 (1 µM) for 3 hr. Cells were labeled with Rac1‐GTP antibody (green), annexin V (red), and DAPI (blue). Dashed lines highlight regions of interest at the leading edge. (b) Cytofluorogram showing colocalization of annexin V and Rac1‐GTP staining in region of interest in control cell from (a), normalized to maximum in each channel. (c) Cytofluorogram showing colocalization of annexin V and Rac1‐GTP staining in region of interest in TTX cell from (a), normalized to maximum in each channel. (d) Cytofluorogram showing colocalization of annexin V and Rac1‐GTP staining in region of interest in NS‐1619 cell from (a), normalized to maximum in each channel. (e) Manders' corrected colocalization coefficients for annexin V and Rac1‐GTP staining in regions of interest of cells after treatment with TTX (30 µM) and NS‐1619 (1 µM) for 3 hr ( n = 30). (f) Li's intensity correlation quotient for Rac1‐GTP and annexin V colocalization ( n = 30). Data are mean and SEM . ** p

    Journal: Journal of Cellular Physiology

    Article Title: Voltage‐dependent activation of Rac1 by Nav1.5 channels promotes cell migration, et al. Voltage‐dependent activation of Rac1 by Nav1.5 channels promotes cell migration

    doi: 10.1002/jcp.29290

    Figure Lengend Snippet: Na v 1.5 and V m regulate Rac1‐GTP colocalization with phosphatidylserine. (a) Images of representative cells after treatment with TTX (30 µM) and NS‐1619 (1 µM) for 3 hr. Cells were labeled with Rac1‐GTP antibody (green), annexin V (red), and DAPI (blue). Dashed lines highlight regions of interest at the leading edge. (b) Cytofluorogram showing colocalization of annexin V and Rac1‐GTP staining in region of interest in control cell from (a), normalized to maximum in each channel. (c) Cytofluorogram showing colocalization of annexin V and Rac1‐GTP staining in region of interest in TTX cell from (a), normalized to maximum in each channel. (d) Cytofluorogram showing colocalization of annexin V and Rac1‐GTP staining in region of interest in NS‐1619 cell from (a), normalized to maximum in each channel. (e) Manders' corrected colocalization coefficients for annexin V and Rac1‐GTP staining in regions of interest of cells after treatment with TTX (30 µM) and NS‐1619 (1 µM) for 3 hr ( n = 30). (f) Li's intensity correlation quotient for Rac1‐GTP and annexin V colocalization ( n = 30). Data are mean and SEM . ** p

    Article Snippet: 2.1 ChemicalsIberiotoxin, NS‐1619, tetrodotoxin (TTX) and veratridine were purchased from Alomone Labs.

    Techniques: Labeling, Staining

    The large conductance Ca 2+ ‐activated K + channel K Ca 1.1 regulates the membrane potential but not intracellular Na + . (a) MDA‐MB‐231 cells labeled with K Ca 1.1 antibody (green), phalloidin to label the actin cytoskeleton (red), and DAPI to label the nucleus (blue). (b) Western blot of K Ca 1.1 in control MDA‐MB‐231 cells and cells in which Na v 1.5 has been knocked down with shRNA. Positive control = rat brain lysate. Loading control = α‐tubulin. (c) Representative perforated patch clamp recording showing activation of outward current using the K Ca 1.1 activator (NS‐1619; 1 µM) and inhibition with iberiotoxin (100 nM). The cell was held at −120 mV for 250 ms before depolarization to + 60 mV for 300 ms. (d) Current–voltage relationship of the K Ca 1.1 current. Cells were held at −120 mV for 250 ms before depolarization to voltages ranging from −60 to +90 mV in 10 mV steps for 300 ms ( n = 5). Data are fitted with single exponential functions. (e) Dose‐dependent effect of NS‐1619 on the steady‐state V m ( n ≥ 6). Data are fitted to a sigmoidal logistic function. (f) Effect of NS‐1619 (1 µM) on steady‐state V m ( n = 12). (g) Effect of NS‐1619 (1 µM, 5 min) on [Na + ] i ( n = 22). (h) V m recorded using intracellular solution with free [Ca 2+ ] buffered to 5.7 nM versus 100 nM ( n ≥ 10). Data are mean and SEM. ** p

    Journal: Journal of Cellular Physiology

    Article Title: Voltage‐dependent activation of Rac1 by Nav1.5 channels promotes cell migration, et al. Voltage‐dependent activation of Rac1 by Nav1.5 channels promotes cell migration

    doi: 10.1002/jcp.29290

    Figure Lengend Snippet: The large conductance Ca 2+ ‐activated K + channel K Ca 1.1 regulates the membrane potential but not intracellular Na + . (a) MDA‐MB‐231 cells labeled with K Ca 1.1 antibody (green), phalloidin to label the actin cytoskeleton (red), and DAPI to label the nucleus (blue). (b) Western blot of K Ca 1.1 in control MDA‐MB‐231 cells and cells in which Na v 1.5 has been knocked down with shRNA. Positive control = rat brain lysate. Loading control = α‐tubulin. (c) Representative perforated patch clamp recording showing activation of outward current using the K Ca 1.1 activator (NS‐1619; 1 µM) and inhibition with iberiotoxin (100 nM). The cell was held at −120 mV for 250 ms before depolarization to + 60 mV for 300 ms. (d) Current–voltage relationship of the K Ca 1.1 current. Cells were held at −120 mV for 250 ms before depolarization to voltages ranging from −60 to +90 mV in 10 mV steps for 300 ms ( n = 5). Data are fitted with single exponential functions. (e) Dose‐dependent effect of NS‐1619 on the steady‐state V m ( n ≥ 6). Data are fitted to a sigmoidal logistic function. (f) Effect of NS‐1619 (1 µM) on steady‐state V m ( n = 12). (g) Effect of NS‐1619 (1 µM, 5 min) on [Na + ] i ( n = 22). (h) V m recorded using intracellular solution with free [Ca 2+ ] buffered to 5.7 nM versus 100 nM ( n ≥ 10). Data are mean and SEM. ** p

    Article Snippet: 2.1 ChemicalsIberiotoxin, NS‐1619, tetrodotoxin (TTX) and veratridine were purchased from Alomone Labs.

    Techniques: Multiple Displacement Amplification, Labeling, Western Blot, shRNA, Positive Control, Patch Clamp, Activation Assay, Inhibition

    Na v 1.5 and V m regulate Rac1 activation/distribution. (a) Images of representative cells after treatment with TTX (30 µM) and NS‐1619 (1 µM) for 3 hr. Cells were labeled with Rac1‐GTP antibody (green), phalloidin (red), and DAPI (blue). Arrows in the Rac1‐GTP panels highlight the distribution or lack of expression at the leading edge. (b) Rac1‐GTP signal density, measured across 20 arcs, in 0.43 µm radius increments, within a quadrant mask region of interest at the leading edge, normalized to the first arc ( n ≥ 66). (c) Peak Rac1‐GTP signal density per cell from (b), normalized to the first arc ( n ≥ 66). (d) Total Rac1‐GTP quantified in whole‐cell lysates using colorimetric small GTPase activation assay ( n = 6). (e) Images of representative cells after treatment with TTX (30 µM) and NS‐1619 (1 µM) for 3 hr. Cells were labeled with Rac1‐GTP antibody (green), total Rac1 antibody (red), and DAPI (blue). Arrows in the Rac1‐GTP panels highlight the distribution or lack of expression at the leading edge. (f) Total Rac1 signal density, measured across 20 arcs, in 0.43 µm radius increments, within a quadrant mask region of interest at the leading edge, normalized to the first arc ( n ≥ 59). (g) Peak Rac1 signal density per cell from (f), normalized to the first arc ( n ≥ 59). (h) Ratio of Peak Rac1‐GTP/Peak total Rac1 for each experimental repeat, normalized to control ( n = 3). Data are mean and SEM . * p

    Journal: Journal of Cellular Physiology

    Article Title: Voltage‐dependent activation of Rac1 by Nav1.5 channels promotes cell migration, et al. Voltage‐dependent activation of Rac1 by Nav1.5 channels promotes cell migration

    doi: 10.1002/jcp.29290

    Figure Lengend Snippet: Na v 1.5 and V m regulate Rac1 activation/distribution. (a) Images of representative cells after treatment with TTX (30 µM) and NS‐1619 (1 µM) for 3 hr. Cells were labeled with Rac1‐GTP antibody (green), phalloidin (red), and DAPI (blue). Arrows in the Rac1‐GTP panels highlight the distribution or lack of expression at the leading edge. (b) Rac1‐GTP signal density, measured across 20 arcs, in 0.43 µm radius increments, within a quadrant mask region of interest at the leading edge, normalized to the first arc ( n ≥ 66). (c) Peak Rac1‐GTP signal density per cell from (b), normalized to the first arc ( n ≥ 66). (d) Total Rac1‐GTP quantified in whole‐cell lysates using colorimetric small GTPase activation assay ( n = 6). (e) Images of representative cells after treatment with TTX (30 µM) and NS‐1619 (1 µM) for 3 hr. Cells were labeled with Rac1‐GTP antibody (green), total Rac1 antibody (red), and DAPI (blue). Arrows in the Rac1‐GTP panels highlight the distribution or lack of expression at the leading edge. (f) Total Rac1 signal density, measured across 20 arcs, in 0.43 µm radius increments, within a quadrant mask region of interest at the leading edge, normalized to the first arc ( n ≥ 59). (g) Peak Rac1 signal density per cell from (f), normalized to the first arc ( n ≥ 59). (h) Ratio of Peak Rac1‐GTP/Peak total Rac1 for each experimental repeat, normalized to control ( n = 3). Data are mean and SEM . * p

    Article Snippet: 2.1 ChemicalsIberiotoxin, NS‐1619, tetrodotoxin (TTX) and veratridine were purchased from Alomone Labs.

    Techniques: Activation Assay, Labeling, Expressing

    Na v 1.5‐dependent membrane potential depolarization regulates cell migration. (a) Representative scratch wounds at 0 hr and 6 hr into a wound healing assay ± TTX (30 μM) or NS‐1619 (1 μM). Red dotted lines highlight wound edges. (b) Wound area during the migration assay (“gap remaining”), normalized to starting value ( n = 3). (c) t 1/2 of wound closure ( n ≥ 5). (d) Collective migration (µm/hr) of cells closing the wound ( n ≥ 5). (e) Instantaneous velocity (µm/s) of segmented cells ( n ≥ 2,662). (f) Polar histograms showing directionality of migrating cells at the leading edge of wounds ( p

    Journal: Journal of Cellular Physiology

    Article Title: Voltage‐dependent activation of Rac1 by Nav1.5 channels promotes cell migration, et al. Voltage‐dependent activation of Rac1 by Nav1.5 channels promotes cell migration

    doi: 10.1002/jcp.29290

    Figure Lengend Snippet: Na v 1.5‐dependent membrane potential depolarization regulates cell migration. (a) Representative scratch wounds at 0 hr and 6 hr into a wound healing assay ± TTX (30 μM) or NS‐1619 (1 μM). Red dotted lines highlight wound edges. (b) Wound area during the migration assay (“gap remaining”), normalized to starting value ( n = 3). (c) t 1/2 of wound closure ( n ≥ 5). (d) Collective migration (µm/hr) of cells closing the wound ( n ≥ 5). (e) Instantaneous velocity (µm/s) of segmented cells ( n ≥ 2,662). (f) Polar histograms showing directionality of migrating cells at the leading edge of wounds ( p

    Article Snippet: 2.1 ChemicalsIberiotoxin, NS‐1619, tetrodotoxin (TTX) and veratridine were purchased from Alomone Labs.

    Techniques: Migration, Wound Healing Assay

    Na v 1.5 and V m regulate Rac1-GTP colocalization with phosphatidylserine. (A) Images of representative cells after treatment with TTX (30 µM) and NS-1619 (1 µM) for 3 h. Cells were labeled with Rac1-GTP antibody (green), annexin V (red) and DAPI (blue). Dashed lines highlight regions of interest at the leading edge. (B) Cytofluorogram showing colocalization of annexin V and Rac1-GTP staining in region of interest in control cell from (A), normalized to maximum in each channel. (C) Cytofluorogram showing colocalization of annexin V and Rac1-GTP staining in region of interest in TTX cell from (A), normalized to maximum in each channel. (D) Cytofluorogram showing colocalization of annexin V and Rac1-GTP staining in region of interest in NS-1619 cell from (A), normalized to maximum in each channel. (E) Manders’ corrected colocalization coefficients for annexin V and Rac1-GTP staining in regions of interest of cells after treatment with TTX (30 µM) and NS-1619 (1 µM) for 3 h (n = 30). (F) Li’s intensity correlation quotient for Rac1-GTP and annexin V colocalization (n = 30). Data are mean and SEM. **P

    Journal: bioRxiv

    Article Title: Voltage-dependent activation of Rac1 by Nav1.5 channels promotes cell migration

    doi: 10.1101/597088

    Figure Lengend Snippet: Na v 1.5 and V m regulate Rac1-GTP colocalization with phosphatidylserine. (A) Images of representative cells after treatment with TTX (30 µM) and NS-1619 (1 µM) for 3 h. Cells were labeled with Rac1-GTP antibody (green), annexin V (red) and DAPI (blue). Dashed lines highlight regions of interest at the leading edge. (B) Cytofluorogram showing colocalization of annexin V and Rac1-GTP staining in region of interest in control cell from (A), normalized to maximum in each channel. (C) Cytofluorogram showing colocalization of annexin V and Rac1-GTP staining in region of interest in TTX cell from (A), normalized to maximum in each channel. (D) Cytofluorogram showing colocalization of annexin V and Rac1-GTP staining in region of interest in NS-1619 cell from (A), normalized to maximum in each channel. (E) Manders’ corrected colocalization coefficients for annexin V and Rac1-GTP staining in regions of interest of cells after treatment with TTX (30 µM) and NS-1619 (1 µM) for 3 h (n = 30). (F) Li’s intensity correlation quotient for Rac1-GTP and annexin V colocalization (n = 30). Data are mean and SEM. **P

    Article Snippet: ChemicalsIberiotoxin, NS-1619, tetrodotoxin (TTX) and veratridine were purchased from Alomone Labs.

    Techniques: Labeling, Staining

    Na v 1.5 and V m regulate Rac1 activation/distribution. (A) Images of representative cells after treatment with TTX (30 µM) and NS-1619 (1 µM) for 3 h. Cells were labeled with Rac1-GTP antibody (green), phalloidin (red) and DAPI (blue). Arrows in the Rac1-GTP panels highlight the distribution or lack of expression at the leading edge. (B) Rac1-GTP signal density, measured across 20 arcs, in 0.43 µm radius increments, within a quadrant mask region of interest at the leading edge, normalized to the first arc (n ≥ 66). (C) Peak Rac1-GTP signal density per cell from (B), normalized to the first arc (n ≥ 66). (D) Total Rac1-GTP quantified in whole cell lysates using colorimetric small GTPase activation assay (n = 6). (E) Images of representative cells after treatment with TTX (30 µM) and NS-1619 (1 µM) for 3 h. Cells were labeled with Rac1-GTP antibody (green), total Rac1 antibody (red), and DAPI (blue). Arrows in the Rac1-GTP panels highlight the distribution or lack of expression at the leading edge. (F) Total Rac1 signal density, measured across 20 arcs, in 0.43 µm radius increments, within a quadrant mask region of interest at the leading edge, normalized to the first arc (n ≥ 59). (G) Peak Rac1 signal density per cell from (F), normalized to the first arc (n ≥ 59). (H) Ratio of Peak Rac1-GTP/Peak total Rac1 for each experimental repeat, normalized to control (n = 3). Data are mean and SEM. *P

    Journal: bioRxiv

    Article Title: Voltage-dependent activation of Rac1 by Nav1.5 channels promotes cell migration

    doi: 10.1101/597088

    Figure Lengend Snippet: Na v 1.5 and V m regulate Rac1 activation/distribution. (A) Images of representative cells after treatment with TTX (30 µM) and NS-1619 (1 µM) for 3 h. Cells were labeled with Rac1-GTP antibody (green), phalloidin (red) and DAPI (blue). Arrows in the Rac1-GTP panels highlight the distribution or lack of expression at the leading edge. (B) Rac1-GTP signal density, measured across 20 arcs, in 0.43 µm radius increments, within a quadrant mask region of interest at the leading edge, normalized to the first arc (n ≥ 66). (C) Peak Rac1-GTP signal density per cell from (B), normalized to the first arc (n ≥ 66). (D) Total Rac1-GTP quantified in whole cell lysates using colorimetric small GTPase activation assay (n = 6). (E) Images of representative cells after treatment with TTX (30 µM) and NS-1619 (1 µM) for 3 h. Cells were labeled with Rac1-GTP antibody (green), total Rac1 antibody (red), and DAPI (blue). Arrows in the Rac1-GTP panels highlight the distribution or lack of expression at the leading edge. (F) Total Rac1 signal density, measured across 20 arcs, in 0.43 µm radius increments, within a quadrant mask region of interest at the leading edge, normalized to the first arc (n ≥ 59). (G) Peak Rac1 signal density per cell from (F), normalized to the first arc (n ≥ 59). (H) Ratio of Peak Rac1-GTP/Peak total Rac1 for each experimental repeat, normalized to control (n = 3). Data are mean and SEM. *P

    Article Snippet: ChemicalsIberiotoxin, NS-1619, tetrodotoxin (TTX) and veratridine were purchased from Alomone Labs.

    Techniques: Activation Assay, Labeling, Expressing

    Na v 1.5-dependent membrane potential depolarization regulates cell migration. (A) Representative scratch wounds at 0 h and 6 h into a wound healing assay ± TTX (30 μM) or NS-1619 (1 μM). Red dotted lines highlight wound edges. (B) Wound area during the migration assay (“gap remaining”), normalized to starting value (n = 3). (C) t 1/2 of wound closure (n ≥ 5). (D) Collective migration (µm/h) of cells closing the wound (n ≥ 5). (E) Instantaneous velocity (µm/s) of segmented cells (n ≥ 2662). (F) Polar histograms showing directionality of migrating cells at the leading edge of wounds (P

    Journal: bioRxiv

    Article Title: Voltage-dependent activation of Rac1 by Nav1.5 channels promotes cell migration

    doi: 10.1101/597088

    Figure Lengend Snippet: Na v 1.5-dependent membrane potential depolarization regulates cell migration. (A) Representative scratch wounds at 0 h and 6 h into a wound healing assay ± TTX (30 μM) or NS-1619 (1 μM). Red dotted lines highlight wound edges. (B) Wound area during the migration assay (“gap remaining”), normalized to starting value (n = 3). (C) t 1/2 of wound closure (n ≥ 5). (D) Collective migration (µm/h) of cells closing the wound (n ≥ 5). (E) Instantaneous velocity (µm/s) of segmented cells (n ≥ 2662). (F) Polar histograms showing directionality of migrating cells at the leading edge of wounds (P

    Article Snippet: ChemicalsIberiotoxin, NS-1619, tetrodotoxin (TTX) and veratridine were purchased from Alomone Labs.

    Techniques: Migration, Wound Healing Assay

    The large conductance Ca 2+ -activated K + channel K Ca 1.1 regulates the membrane potential but not intracellular Na + . (A) MDA-MB-231 cells labeled with K Ca 1.1 antibody (green), phalloidin to label the actin cytoskeleton (red), and DAPI to label the nucleus (blue). Western blot of K Ca 1.1 in control MDA-MB-231 cells and cells in which Na v 1.5 has been knocked down with shRNA. Positive control = rat brain lysate. Loading control = α -tubulin. Representative perforated patch clamp recording showing activation of outward current using the K Ca 1.1 activator (NS-1619; 1 µM) and inhibition with iberiotoxin (100 nM). The cell was held at −120 mV for 250 ms before depolarization to +60 mV for 300 ms. (D) Current-voltage relationship of the K Ca 1.1 current. Cells were held at −120 mV for 250 ms before depolarization to voltages ranging from −60 to +90 mV in 10 mV steps for 300 ms (n = 5). Data are fitted with single exponential functions. (E) Dose-dependent effect of NS-1619 on the steady-state V m (n ≥ 6). Data are fitted to a sigmoidal logistic function. (F) Effect of NS-1619 (1 µM) on steady-state V m (n = 12). (G) Effect of NS-1619 (1 µM, 5 min) on [Na + ] i (n = 22). (H) V m recorded using intracellular solution with free [Ca 2+ ] buffered to 5.7 nM vs. 100 nM (n ≥ 10). Data are mean and SEM. **P

    Journal: bioRxiv

    Article Title: Voltage-dependent activation of Rac1 by Nav1.5 channels promotes cell migration

    doi: 10.1101/597088

    Figure Lengend Snippet: The large conductance Ca 2+ -activated K + channel K Ca 1.1 regulates the membrane potential but not intracellular Na + . (A) MDA-MB-231 cells labeled with K Ca 1.1 antibody (green), phalloidin to label the actin cytoskeleton (red), and DAPI to label the nucleus (blue). Western blot of K Ca 1.1 in control MDA-MB-231 cells and cells in which Na v 1.5 has been knocked down with shRNA. Positive control = rat brain lysate. Loading control = α -tubulin. Representative perforated patch clamp recording showing activation of outward current using the K Ca 1.1 activator (NS-1619; 1 µM) and inhibition with iberiotoxin (100 nM). The cell was held at −120 mV for 250 ms before depolarization to +60 mV for 300 ms. (D) Current-voltage relationship of the K Ca 1.1 current. Cells were held at −120 mV for 250 ms before depolarization to voltages ranging from −60 to +90 mV in 10 mV steps for 300 ms (n = 5). Data are fitted with single exponential functions. (E) Dose-dependent effect of NS-1619 on the steady-state V m (n ≥ 6). Data are fitted to a sigmoidal logistic function. (F) Effect of NS-1619 (1 µM) on steady-state V m (n = 12). (G) Effect of NS-1619 (1 µM, 5 min) on [Na + ] i (n = 22). (H) V m recorded using intracellular solution with free [Ca 2+ ] buffered to 5.7 nM vs. 100 nM (n ≥ 10). Data are mean and SEM. **P

    Article Snippet: ChemicalsIberiotoxin, NS-1619, tetrodotoxin (TTX) and veratridine were purchased from Alomone Labs.

    Techniques: Multiple Displacement Amplification, Labeling, Western Blot, shRNA, Positive Control, Patch Clamp, Activation Assay, Inhibition

    Na v 1.5-dependent membrane potential depolarization regulates lamellipodia formation. (A) Images of representative cells after treatment with TTX (30 μM) or NS-1619 (1 μM) for 3 h. Cells were fixed and stained with phalloidin (red) and DAPI (blue). Lower row shows masks of cells in the upper row, from which the circularity was calculated. (B) Circularity (n ≥ 61). (C) Feret’s diameter (µm; n ≥ 57). (D) Number of MDA-MB-231 cells with a lamellipodium (P

    Journal: bioRxiv

    Article Title: Voltage-dependent activation of Rac1 by Nav1.5 channels promotes cell migration

    doi: 10.1101/597088

    Figure Lengend Snippet: Na v 1.5-dependent membrane potential depolarization regulates lamellipodia formation. (A) Images of representative cells after treatment with TTX (30 μM) or NS-1619 (1 μM) for 3 h. Cells were fixed and stained with phalloidin (red) and DAPI (blue). Lower row shows masks of cells in the upper row, from which the circularity was calculated. (B) Circularity (n ≥ 61). (C) Feret’s diameter (µm; n ≥ 57). (D) Number of MDA-MB-231 cells with a lamellipodium (P

    Article Snippet: ChemicalsIberiotoxin, NS-1619, tetrodotoxin (TTX) and veratridine were purchased from Alomone Labs.

    Techniques: Staining, Multiple Displacement Amplification

    Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).

    Journal: Frontiers in Physiology

    Article Title: Activation of BK Channel Contributes to PL-Induced Mesenchymal Stem Cell Migration

    doi: 10.3389/fphys.2020.00210

    Figure Lengend Snippet: Effect of PL in rMSC migration. (A) rMSCs monolayers after scratching at 0 and 24 h in control cells and after treatment with IBTX (10 nM) or NS1619 in presence and absence of 5% PL. (B) Number of cells counted in wound area after each treatment was divided by number of cells in wound area in control assay. (C) Effect of PL in cell viability after 24 h of treatment with IBTX or NS1619 in the presence and absence of 5% PL. Doxorubicin 30 μM was used as a positive control. Data were normalized to control cells without treatment and shown as mean ± SEM ( n = 5).

    Article Snippet: The cells were then subjected to the following treatments after 16 h: IBTX 10 nM; NS1619 10 μM; 5% PL plus heparin (1% v/v); IBTX 10 nM + 5% PL plus heparin (1% v/v); and NS1619 10 μM + 5% PL plus heparin (1% v/v).

    Techniques: Migration, Control Assay, Positive Control