margatoxin  (Alomone Labs)


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    Structured Review

    Alomone Labs margatoxin
    Current-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : representative traces of phasic action potentials recorded from the soma of dissociated postganglionic sympathetic neurons in the absence (control; black line) and presence <t>(MgTX;</t>
    Margatoxin, 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
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    Images

    1) Product Images from "Kv1.3 channels in postganglionic sympathetic neurons: expression, function, and modulation"

    Article Title: Kv1.3 channels in postganglionic sympathetic neurons: expression, function, and modulation

    Journal:

    doi: 10.1152/ajpregu.00077.2008

    Current-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : representative traces of phasic action potentials recorded from the soma of dissociated postganglionic sympathetic neurons in the absence (control; black line) and presence (MgTX;
    Figure Legend Snippet: Current-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : representative traces of phasic action potentials recorded from the soma of dissociated postganglionic sympathetic neurons in the absence (control; black line) and presence (MgTX;

    Techniques Used:

    Voltage-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : ionic current measured in untransfected dissociated sympathetic neurons in the absence (control; n = 18) and presence of 1 nM margatoxin (MgTX; n = 15). Current
    Figure Legend Snippet: Voltage-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : ionic current measured in untransfected dissociated sympathetic neurons in the absence (control; n = 18) and presence of 1 nM margatoxin (MgTX; n = 15). Current

    Techniques Used:

    2) Product Images from "Membrane Potential Distinctly Modulates Mobility and Signaling of IL-2 and IL-15 Receptors in T Cells"

    Article Title: Membrane Potential Distinctly Modulates Mobility and Signaling of IL-2 and IL-15 Receptors in T Cells

    Journal: Biophysical Journal

    doi: 10.1016/j.bpj.2018.04.038

    Signaling efficiency of IL-2 and -15 receptors. Flow cytometry was used to measure STAT5 phosphorylation on a cell-by-cell basis using Alexa647-anti-PSTAT mAbs. Control samples were incubated in HBSS, and depolarization was achieved either by K-HBSS buffer or by margatoxin (1.5 nM); hyperpolarization was induced by valinomycin (10 μ M). ( A ) K6 cells were stimulated with IL-2 (50 pM, 10 min, 37°C). ( B ) FT7.10 cells were treated with IL-15 (50 pM, 5 min, 37°C). Data from labeled samples were corrected with the mean fluorescence of the isotype controls (IC) and normalized to the intensities measured at resting MP. Autofluorescence (AF) is also shown. The third columns (ØIL-2, ØIL-15) display the normalized basal STAT5 phosphorylation in the absence of cytokine. Averages ± SEM of n = 6 independent measurements are presented. Statistically significant changes relative to the control sample are marked as ∗ p
    Figure Legend Snippet: Signaling efficiency of IL-2 and -15 receptors. Flow cytometry was used to measure STAT5 phosphorylation on a cell-by-cell basis using Alexa647-anti-PSTAT mAbs. Control samples were incubated in HBSS, and depolarization was achieved either by K-HBSS buffer or by margatoxin (1.5 nM); hyperpolarization was induced by valinomycin (10 μ M). ( A ) K6 cells were stimulated with IL-2 (50 pM, 10 min, 37°C). ( B ) FT7.10 cells were treated with IL-15 (50 pM, 5 min, 37°C). Data from labeled samples were corrected with the mean fluorescence of the isotype controls (IC) and normalized to the intensities measured at resting MP. Autofluorescence (AF) is also shown. The third columns (ØIL-2, ØIL-15) display the normalized basal STAT5 phosphorylation in the absence of cytokine. Averages ± SEM of n = 6 independent measurements are presented. Statistically significant changes relative to the control sample are marked as ∗ p

    Techniques Used: Flow Cytometry, Cytometry, Incubation, Labeling, Fluorescence

    Homoassociations ( A ) and heteroassociations of ( B ) of IL-2R α , IL-15R α , MHC I, and MHC II detected by flow cytometric FRET measurements on FT7.10 cells. Receptors were labeled with donor-tagged (Alexa 546) and acceptor-tagged (Alexa 647) mAbs. The average FRET efficiencies from three independent experiments are shown; in each experiment, > 10,000 cells were measured per treatment. Control samples were incubated in HBSS, and depolarization was achieved either by K-HBSS buffer or by margatoxin (1.5 nM); hyperpolarization was induced by valinomycin (10 μ M). Statistically significant changes relative to the control sample are marked as ∗ p .
    Figure Legend Snippet: Homoassociations ( A ) and heteroassociations of ( B ) of IL-2R α , IL-15R α , MHC I, and MHC II detected by flow cytometric FRET measurements on FT7.10 cells. Receptors were labeled with donor-tagged (Alexa 546) and acceptor-tagged (Alexa 647) mAbs. The average FRET efficiencies from three independent experiments are shown; in each experiment, > 10,000 cells were measured per treatment. Control samples were incubated in HBSS, and depolarization was achieved either by K-HBSS buffer or by margatoxin (1.5 nM); hyperpolarization was induced by valinomycin (10 μ M). Statistically significant changes relative to the control sample are marked as ∗ p .

    Techniques Used: Flow Cytometry, Labeling, Incubation

    3) Product Images from "Inhibition of Kv channel expression by NSAIDs depolarizes membrane potential and inhibits cell migration by disrupting calpain signaling"

    Article Title: Inhibition of Kv channel expression by NSAIDs depolarizes membrane potential and inhibits cell migration by disrupting calpain signaling

    Journal: Biochemical pharmacology

    doi: 10.1016/j.bcp.2015.10.017

    Effect of NSAIDs, 40 mM K + -containing media, or MgTx on calpain activity in IEC-6 cells. Cells were treated with control (A; 0.1% DMSO) or 100 μM NS-398 (B) for 48 h or control (C; PBS), 40 mM K + -containing media (D) or 10 nM MgTx (E) for 24 h prior to measurement of fluorescence of BOC-LM-CMAC using confocal microscopy. (F) Measurement of mean intensity of BOC-LM-CMAC fluorescence and calpain activity in confocal experiments ( n = 4 per treatment). * indicates a significant difference from non-targeting siRNA ( p
    Figure Legend Snippet: Effect of NSAIDs, 40 mM K + -containing media, or MgTx on calpain activity in IEC-6 cells. Cells were treated with control (A; 0.1% DMSO) or 100 μM NS-398 (B) for 48 h or control (C; PBS), 40 mM K + -containing media (D) or 10 nM MgTx (E) for 24 h prior to measurement of fluorescence of BOC-LM-CMAC using confocal microscopy. (F) Measurement of mean intensity of BOC-LM-CMAC fluorescence and calpain activity in confocal experiments ( n = 4 per treatment). * indicates a significant difference from non-targeting siRNA ( p

    Techniques Used: Activity Assay, Fluorescence, Confocal Microscopy

    IEC-6 cell migration is inhibited by pharmacological inhibition of K v 1.3 channels. Cells were treated with 10 nM MgTx for 24 h prior to wounding, and microphotographs of control (A) and MgTx-treated (B) cells were taken 6 h after wounding. (C) Percent migration of IEC-6 cells following treatment and wounding as determined by measuring the percentage of a standardized region of interest covered by cells ( n = 12 for each treatment group). * indicates a significant difference from control ( p
    Figure Legend Snippet: IEC-6 cell migration is inhibited by pharmacological inhibition of K v 1.3 channels. Cells were treated with 10 nM MgTx for 24 h prior to wounding, and microphotographs of control (A) and MgTx-treated (B) cells were taken 6 h after wounding. (C) Percent migration of IEC-6 cells following treatment and wounding as determined by measuring the percentage of a standardized region of interest covered by cells ( n = 12 for each treatment group). * indicates a significant difference from control ( p

    Techniques Used: Migration, Inhibition

    Depolarization of E m by K v channel siRNA, 40 mM K + -containing media, NSAIDs, or pharmacological inhibition of K v 1.3 with MgTx. (A) DiBAC 4 (3) fluorescence in IEC-6 cells nucleofected with non-targeting ( n = 10), K v 1.3 ( n = 12), K v 1.4 ( n = 12), or K v 1.6 ( n = 12) siRNA 48 h prior to E m measurement. Increased fluorescence indicates depolarization of E m . (B) Increased DiBAC 4 (3) fluorescence in IEC-6 cells treated with 40 mM K + -containing media ( n = 12) or 10 nM MgTx ( n = 12) for 24 h prior to E m measurement. (C and D) Increased DiBAC 4 (3) fluorescence in IEC-6 cells treated with varying concentrations of indomethacin or NS-398 ( n = 16 per concentration), respectively for 48 h. * indicates a significant difference from non-targeting siRNA ( p
    Figure Legend Snippet: Depolarization of E m by K v channel siRNA, 40 mM K + -containing media, NSAIDs, or pharmacological inhibition of K v 1.3 with MgTx. (A) DiBAC 4 (3) fluorescence in IEC-6 cells nucleofected with non-targeting ( n = 10), K v 1.3 ( n = 12), K v 1.4 ( n = 12), or K v 1.6 ( n = 12) siRNA 48 h prior to E m measurement. Increased fluorescence indicates depolarization of E m . (B) Increased DiBAC 4 (3) fluorescence in IEC-6 cells treated with 40 mM K + -containing media ( n = 12) or 10 nM MgTx ( n = 12) for 24 h prior to E m measurement. (C and D) Increased DiBAC 4 (3) fluorescence in IEC-6 cells treated with varying concentrations of indomethacin or NS-398 ( n = 16 per concentration), respectively for 48 h. * indicates a significant difference from non-targeting siRNA ( p

    Techniques Used: Inhibition, Fluorescence, Concentration Assay

    4) Product Images from "Blockade of Kv1.3 Potassium Channels Inhibits Differentiation and Granzyme B Secretion of Human CD8+ T Effector Memory Lymphocytes"

    Article Title: Blockade of Kv1.3 Potassium Channels Inhibits Differentiation and Granzyme B Secretion of Human CD8+ T Effector Memory Lymphocytes

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0054267

    Kv1.3 channel blocker attenuates GrB mediated neural cell toxicity. Freshly isolated human CD8+ T cells were simulated with anti-CD3 or anti-CD3/CD28 in the presence or absence of MgTx. Cultured supernatants were collected at 3 days after stimulation. (A). Human neural cells cultured on poly-D-lysine pre-coated 96 well plates were pretreated with supernatants from non-activated CD8 T cells (Unstim.), anti-CD3 or anti-CD3/CD28-activated CD8+ T cells without MgTx (none), and with MgTx (MgTx). After 24 hours of treatment, CellQuanti-blue dye was added in each well for 30 minutes. Fluorescence was then detected using a plate reader. Cell viability was quantified by fluorescence intensity. (B). MgTx (30 nM) was added to culture media and incubated for 3 days. Human NPCs were treated with supernatants without MgTx (Ctrl), MgTx contained sups with vehicle treatment, with GrB alone (GrB) or MgTx containing sups plus GrB treatment (GrB/MgTx sups). Neurotoxicity was evaluated by cell viability quantified by fluorescence intensity. The fluorescence intensity in each group is plotted as percent relative to that in non-activated cells (Unstim.) or control cells (Ctrl). Data are mean of triplicate ± SD of one representative of three independent experiments. Values that are significantly different from that of vehicle treated control are indicated as *, p
    Figure Legend Snippet: Kv1.3 channel blocker attenuates GrB mediated neural cell toxicity. Freshly isolated human CD8+ T cells were simulated with anti-CD3 or anti-CD3/CD28 in the presence or absence of MgTx. Cultured supernatants were collected at 3 days after stimulation. (A). Human neural cells cultured on poly-D-lysine pre-coated 96 well plates were pretreated with supernatants from non-activated CD8 T cells (Unstim.), anti-CD3 or anti-CD3/CD28-activated CD8+ T cells without MgTx (none), and with MgTx (MgTx). After 24 hours of treatment, CellQuanti-blue dye was added in each well for 30 minutes. Fluorescence was then detected using a plate reader. Cell viability was quantified by fluorescence intensity. (B). MgTx (30 nM) was added to culture media and incubated for 3 days. Human NPCs were treated with supernatants without MgTx (Ctrl), MgTx contained sups with vehicle treatment, with GrB alone (GrB) or MgTx containing sups plus GrB treatment (GrB/MgTx sups). Neurotoxicity was evaluated by cell viability quantified by fluorescence intensity. The fluorescence intensity in each group is plotted as percent relative to that in non-activated cells (Unstim.) or control cells (Ctrl). Data are mean of triplicate ± SD of one representative of three independent experiments. Values that are significantly different from that of vehicle treated control are indicated as *, p

    Techniques Used: Isolation, Cell Culture, Fluorescence, Incubation

    K+ channel blockers inhibit GrB production by activated CD8+ T cells. Freshly isolated CD8+ T cells were pretreated with a Kv1.3 channel blocker, ShK at various concentrations (A) or with ShK (10 nM), MgTX (30 nM), ChTX (50 nM) and TRAM-34 (500 nM) (B) for 3 h, followed by stimulation with anti-CD3/CD28 or anti-CD3 alone. The levels of GrB were measured in cell supernatants by ELISA at 6 h (A) and indicated times (B and C). Data are mean of triplicate ± SD of one representative of three independent and reproducible experiments. Values that are significantly different from that of non-blocker vehicle treated control are indicated as follows: *, p
    Figure Legend Snippet: K+ channel blockers inhibit GrB production by activated CD8+ T cells. Freshly isolated CD8+ T cells were pretreated with a Kv1.3 channel blocker, ShK at various concentrations (A) or with ShK (10 nM), MgTX (30 nM), ChTX (50 nM) and TRAM-34 (500 nM) (B) for 3 h, followed by stimulation with anti-CD3/CD28 or anti-CD3 alone. The levels of GrB were measured in cell supernatants by ELISA at 6 h (A) and indicated times (B and C). Data are mean of triplicate ± SD of one representative of three independent and reproducible experiments. Values that are significantly different from that of non-blocker vehicle treated control are indicated as follows: *, p

    Techniques Used: Isolation, Enzyme-linked Immunosorbent Assay

    Kv1.3 blockade suppresses proliferation and differentiation of anti-CD3 stimulated CD8+ T cells. ( A) Freshly isolated CD8+ T cells were pretreated with Kv channel blockers, ShK (10 nM), MgTx (30 nM) and ChTx (50 nM), for 3 hours, then stimulated with anti-CD3 alone or anti-CD3/CD28. After 4 days of culture, proliferation was measured by [3H] thymidine uptake. Data show the mean ± SD of three experiments. Significant differences are marked as follows: (*, p
    Figure Legend Snippet: Kv1.3 blockade suppresses proliferation and differentiation of anti-CD3 stimulated CD8+ T cells. ( A) Freshly isolated CD8+ T cells were pretreated with Kv channel blockers, ShK (10 nM), MgTx (30 nM) and ChTx (50 nM), for 3 hours, then stimulated with anti-CD3 alone or anti-CD3/CD28. After 4 days of culture, proliferation was measured by [3H] thymidine uptake. Data show the mean ± SD of three experiments. Significant differences are marked as follows: (*, p

    Techniques Used: Isolation

    K+ channel blockers do not affect CD107a expression on activated CD8+ T cells. (A) Freshly isolated CD8+ T cells were stimulated with anti-CD3/CD28 or anti-CD3 for 24 hours. Cells were then stained with a CD107a-specific mAb, or an IgG1 isotype control (filled histogram) at the indicated times. (B). CD8+ T cells were pretreated with ShK (10 nM), MgTX (30 nM), ChTX (50 nM) and TRAM-34 (500 nM) for 3 h, followed by stimulation with anti-CD3/CD28 or anti-CD3 alone for 6 hours. Surface expression levels of CD107a were then analyzed by flow cytometry. FACS plots shown are representative data from three separate experiments.
    Figure Legend Snippet: K+ channel blockers do not affect CD107a expression on activated CD8+ T cells. (A) Freshly isolated CD8+ T cells were stimulated with anti-CD3/CD28 or anti-CD3 for 24 hours. Cells were then stained with a CD107a-specific mAb, or an IgG1 isotype control (filled histogram) at the indicated times. (B). CD8+ T cells were pretreated with ShK (10 nM), MgTX (30 nM), ChTX (50 nM) and TRAM-34 (500 nM) for 3 h, followed by stimulation with anti-CD3/CD28 or anti-CD3 alone for 6 hours. Surface expression levels of CD107a were then analyzed by flow cytometry. FACS plots shown are representative data from three separate experiments.

    Techniques Used: Expressing, Isolation, Staining, Flow Cytometry, Cytometry, FACS

    5) Product Images from "Activated T cells Inhibit Neurogenesis by Releasing Granzyme B: Rescue by Kv1.3 blockers"

    Article Title: Activated T cells Inhibit Neurogenesis by Releasing Granzyme B: Rescue by Kv1.3 blockers

    Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

    doi: 10.1523/JNEUROSCI.0311-10.2010

    MgTX protects NPC against GrB-induced effects in rat dentate gyrus Eight weeks old female rats were stereotaxically injected in the dentate gyrus (DG) with GrB (1 ug), MgTX (10 ng) +GrB (1 ug) or vehicle control (PBS). After seven days, the rats received BrdU (100 mg/kg, i.p.) two hours before being euthanized. Serial sections of the hippocampus and DG were analyzed by quantitative immunohistochemistry. Sections were immunostained with anti-BrdU (red), and anti-NeuN (green) or anti-Kv1.3 (green). DAPI (blue) was used for nuclear staining. BrdU positive cells in the subgranular zone (SGZ) of every sixth section were counted in a blinded fashion, and normalized to the volume of each granule cell layer (GCL). (A) Representative immunostained sections are shown from each of the treated groups. (B) Quantitative analysis shows decreased numbers of BrdU staining cells with GrB and restoration with MgTX (C) Kv1.3 (green) fluorescence immunohistochemistry shows GrB increases Kv1.3 expression in the dentate gyrus compared to vehicle control. The cellular localization of Kv1.3 (green) was characterized by co-localization studies with BrdU (red).
    Figure Legend Snippet: MgTX protects NPC against GrB-induced effects in rat dentate gyrus Eight weeks old female rats were stereotaxically injected in the dentate gyrus (DG) with GrB (1 ug), MgTX (10 ng) +GrB (1 ug) or vehicle control (PBS). After seven days, the rats received BrdU (100 mg/kg, i.p.) two hours before being euthanized. Serial sections of the hippocampus and DG were analyzed by quantitative immunohistochemistry. Sections were immunostained with anti-BrdU (red), and anti-NeuN (green) or anti-Kv1.3 (green). DAPI (blue) was used for nuclear staining. BrdU positive cells in the subgranular zone (SGZ) of every sixth section were counted in a blinded fashion, and normalized to the volume of each granule cell layer (GCL). (A) Representative immunostained sections are shown from each of the treated groups. (B) Quantitative analysis shows decreased numbers of BrdU staining cells with GrB and restoration with MgTX (C) Kv1.3 (green) fluorescence immunohistochemistry shows GrB increases Kv1.3 expression in the dentate gyrus compared to vehicle control. The cellular localization of Kv1.3 (green) was characterized by co-localization studies with BrdU (red).

    Techniques Used: Injection, Immunohistochemistry, Staining, BrdU Staining, Fluorescence, Expressing

    Kv1.3 mediates effect of GrB on NPC neurogenesis To monitor NPC neurogenesis NPC cultures were cultured in differentiating media for 4-7 days. Cells were immunostained with anti-beta-III tubulin antibody (red) and anti-GFAP antiserum (green). Beta-III tubulin positive neurons were counted in each well and the cell numbers were expressed as percentage of total cells. Cells in 5 pre-assigned fields (approx 200 cells/field) were counted on each cover slip and three cover slips were counted in every group. Data represents mean ± SEM from three experiments. (A) Kv1.3 selective blocker MgTX (10 nM) prevented the effects of GrB (4 nM) on NPC neurogenesis. (B) MgTX also attenuated the effect of supernatants from activated T cells (Ac-T) on NPC neurogenesis. (C) Transfection of Kv1.3 siRNA (25 nM final concentration) but not nonspecific control (NSi) into NPC blocked the effects of GrB (4 nM) on NPC neurogenesis. (D) Representative photomicrographs immunostaining for beta-III tubulin.
    Figure Legend Snippet: Kv1.3 mediates effect of GrB on NPC neurogenesis To monitor NPC neurogenesis NPC cultures were cultured in differentiating media for 4-7 days. Cells were immunostained with anti-beta-III tubulin antibody (red) and anti-GFAP antiserum (green). Beta-III tubulin positive neurons were counted in each well and the cell numbers were expressed as percentage of total cells. Cells in 5 pre-assigned fields (approx 200 cells/field) were counted on each cover slip and three cover slips were counted in every group. Data represents mean ± SEM from three experiments. (A) Kv1.3 selective blocker MgTX (10 nM) prevented the effects of GrB (4 nM) on NPC neurogenesis. (B) MgTX also attenuated the effect of supernatants from activated T cells (Ac-T) on NPC neurogenesis. (C) Transfection of Kv1.3 siRNA (25 nM final concentration) but not nonspecific control (NSi) into NPC blocked the effects of GrB (4 nM) on NPC neurogenesis. (D) Representative photomicrographs immunostaining for beta-III tubulin.

    Techniques Used: Cell Culture, Transfection, Concentration Assay, Immunostaining

    6) Product Images from "Electrical Remodeling of Preoptic GABAergic Neurons Involves the Kv1.5 Subunit"

    Article Title: Electrical Remodeling of Preoptic GABAergic Neurons Involves the Kv1.5 Subunit

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0096643

    Differential sensitivity to K + channel blockers of I DR recorded in GAD65-GFP and Kv4.2−/−;GAD65-GFP preoptic GABAergic neurons. A. Hongotoxin-1 (0.3 nM) -sensitive component of I DR . Representative currents from a GAD65-GFP (left) and a Kv4.2−/−;GAD65-GFP (right) neuron. B. DPO-1 (0.5 µM) - sensitive component of I DR . Representative currents from a GAD65-GFP (left) and a Kv4.2−/−;GAD65-GFP (right) neuron. C. Margatoxin (5 nM) - sensitive component of I DR . Representative currents from a GAD65-GFP (left) and a Kv4.2−/−;GAD65-GFP (right) neuron. A-C. The currents were elicited by the same voltage step protocol depicted in the inset. TTX (1 µM) was present in all extracellular solutions. D. Bar chart summarizing the current density of the hongotoxin-1 (0.3 nM, n = 13 and n = 16 neurons, respectively)-sensitive, DPO-1 (0.5 µM, n = 23 and n = 26 neurons, respectively)-sensitive, dendrotoxin-K (50 nM, n = 5 and n = 6 neurons, respectively)-sensitive, and margatoxin (5 nM, n = 7 and n = 6 neurons, respectively)-sensitive in GAD65-GFP and Kv4.2−/−;GAD65-GFP neurons. Bars represent averages + S.D. The current densities were calculated using the I DR amplitude at the end of the depolarizing step to 0 mV. ** represents significant differences between GAD65-GFP and Kv4.2−/−;GAD65-GFP groups P
    Figure Legend Snippet: Differential sensitivity to K + channel blockers of I DR recorded in GAD65-GFP and Kv4.2−/−;GAD65-GFP preoptic GABAergic neurons. A. Hongotoxin-1 (0.3 nM) -sensitive component of I DR . Representative currents from a GAD65-GFP (left) and a Kv4.2−/−;GAD65-GFP (right) neuron. B. DPO-1 (0.5 µM) - sensitive component of I DR . Representative currents from a GAD65-GFP (left) and a Kv4.2−/−;GAD65-GFP (right) neuron. C. Margatoxin (5 nM) - sensitive component of I DR . Representative currents from a GAD65-GFP (left) and a Kv4.2−/−;GAD65-GFP (right) neuron. A-C. The currents were elicited by the same voltage step protocol depicted in the inset. TTX (1 µM) was present in all extracellular solutions. D. Bar chart summarizing the current density of the hongotoxin-1 (0.3 nM, n = 13 and n = 16 neurons, respectively)-sensitive, DPO-1 (0.5 µM, n = 23 and n = 26 neurons, respectively)-sensitive, dendrotoxin-K (50 nM, n = 5 and n = 6 neurons, respectively)-sensitive, and margatoxin (5 nM, n = 7 and n = 6 neurons, respectively)-sensitive in GAD65-GFP and Kv4.2−/−;GAD65-GFP neurons. Bars represent averages + S.D. The current densities were calculated using the I DR amplitude at the end of the depolarizing step to 0 mV. ** represents significant differences between GAD65-GFP and Kv4.2−/−;GAD65-GFP groups P

    Techniques Used:

    7) Product Images from "Kv1.3 channels in postganglionic sympathetic neurons: expression, function, and modulation"

    Article Title: Kv1.3 channels in postganglionic sympathetic neurons: expression, function, and modulation

    Journal:

    doi: 10.1152/ajpregu.00077.2008

    Current-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : representative traces of phasic action potentials recorded from the soma of dissociated postganglionic sympathetic neurons in the absence (control; black line) and presence (MgTX;
    Figure Legend Snippet: Current-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : representative traces of phasic action potentials recorded from the soma of dissociated postganglionic sympathetic neurons in the absence (control; black line) and presence (MgTX;

    Techniques Used:

    Voltage-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : ionic current measured in untransfected dissociated sympathetic neurons in the absence (control; n = 18) and presence of 1 nM margatoxin (MgTX; n = 15). Current
    Figure Legend Snippet: Voltage-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : ionic current measured in untransfected dissociated sympathetic neurons in the absence (control; n = 18) and presence of 1 nM margatoxin (MgTX; n = 15). Current

    Techniques Used:

    8) Product Images from "Activated T cells Inhibit Neurogenesis by Releasing Granzyme B: Rescue by Kv1.3 blockers"

    Article Title: Activated T cells Inhibit Neurogenesis by Releasing Granzyme B: Rescue by Kv1.3 blockers

    Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

    doi: 10.1523/JNEUROSCI.0311-10.2010

    MgTX protects NPC against GrB-induced effects in rat dentate gyrus Eight weeks old female rats were stereotaxically injected in the dentate gyrus (DG) with GrB (1 ug), MgTX (10 ng) +GrB (1 ug) or vehicle control (PBS). After seven days, the rats received BrdU (100 mg/kg, i.p.) two hours before being euthanized. Serial sections of the hippocampus and DG were analyzed by quantitative immunohistochemistry. Sections were immunostained with anti-BrdU (red), and anti-NeuN (green) or anti-Kv1.3 (green). DAPI (blue) was used for nuclear staining. BrdU positive cells in the subgranular zone (SGZ) of every sixth section were counted in a blinded fashion, and normalized to the volume of each granule cell layer (GCL). (A) Representative immunostained sections are shown from each of the treated groups. (B) Quantitative analysis shows decreased numbers of BrdU staining cells with GrB and restoration with MgTX (C) Kv1.3 (green) fluorescence immunohistochemistry shows GrB increases Kv1.3 expression in the dentate gyrus compared to vehicle control. The cellular localization of Kv1.3 (green) was characterized by co-localization studies with BrdU (red).
    Figure Legend Snippet: MgTX protects NPC against GrB-induced effects in rat dentate gyrus Eight weeks old female rats were stereotaxically injected in the dentate gyrus (DG) with GrB (1 ug), MgTX (10 ng) +GrB (1 ug) or vehicle control (PBS). After seven days, the rats received BrdU (100 mg/kg, i.p.) two hours before being euthanized. Serial sections of the hippocampus and DG were analyzed by quantitative immunohistochemistry. Sections were immunostained with anti-BrdU (red), and anti-NeuN (green) or anti-Kv1.3 (green). DAPI (blue) was used for nuclear staining. BrdU positive cells in the subgranular zone (SGZ) of every sixth section were counted in a blinded fashion, and normalized to the volume of each granule cell layer (GCL). (A) Representative immunostained sections are shown from each of the treated groups. (B) Quantitative analysis shows decreased numbers of BrdU staining cells with GrB and restoration with MgTX (C) Kv1.3 (green) fluorescence immunohistochemistry shows GrB increases Kv1.3 expression in the dentate gyrus compared to vehicle control. The cellular localization of Kv1.3 (green) was characterized by co-localization studies with BrdU (red).

    Techniques Used: Injection, Immunohistochemistry, Staining, BrdU Staining, Fluorescence, Expressing

    Kv1.3 mediates effect of GrB on NPC neurogenesis To monitor NPC neurogenesis NPC cultures were cultured in differentiating media for 4-7 days. Cells were immunostained with anti-beta-III tubulin antibody (red) and anti-GFAP antiserum (green). Beta-III tubulin positive neurons were counted in each well and the cell numbers were expressed as percentage of total cells. Cells in 5 pre-assigned fields (approx 200 cells/field) were counted on each cover slip and three cover slips were counted in every group. Data represents mean ± SEM from three experiments. (A) Kv1.3 selective blocker MgTX (10 nM) prevented the effects of GrB (4 nM) on NPC neurogenesis. (B) MgTX also attenuated the effect of supernatants from activated T cells (Ac-T) on NPC neurogenesis. (C) Transfection of Kv1.3 siRNA (25 nM final concentration) but not nonspecific control (NSi) into NPC blocked the effects of GrB (4 nM) on NPC neurogenesis. (D) Representative photomicrographs immunostaining for beta-III tubulin.
    Figure Legend Snippet: Kv1.3 mediates effect of GrB on NPC neurogenesis To monitor NPC neurogenesis NPC cultures were cultured in differentiating media for 4-7 days. Cells were immunostained with anti-beta-III tubulin antibody (red) and anti-GFAP antiserum (green). Beta-III tubulin positive neurons were counted in each well and the cell numbers were expressed as percentage of total cells. Cells in 5 pre-assigned fields (approx 200 cells/field) were counted on each cover slip and three cover slips were counted in every group. Data represents mean ± SEM from three experiments. (A) Kv1.3 selective blocker MgTX (10 nM) prevented the effects of GrB (4 nM) on NPC neurogenesis. (B) MgTX also attenuated the effect of supernatants from activated T cells (Ac-T) on NPC neurogenesis. (C) Transfection of Kv1.3 siRNA (25 nM final concentration) but not nonspecific control (NSi) into NPC blocked the effects of GrB (4 nM) on NPC neurogenesis. (D) Representative photomicrographs immunostaining for beta-III tubulin.

    Techniques Used: Cell Culture, Transfection, Concentration Assay, Immunostaining

    9) Product Images from "Potent Suppression of Kv1.3 Potassium Channel and IL-2 Secretion by Diphenyl Phosphine Oxide-1 in Human T Cells"

    Article Title: Potent Suppression of Kv1.3 Potassium Channel and IL-2 Secretion by Diphenyl Phosphine Oxide-1 in Human T Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0064629

    Inhibitory effect of DPO-1 and potassium channel blockers on IL-2 production in activated Jurkat cells. Jurkat cells were activated with PHA (5 µg/mL) and PMA (80 nM) for 24 h. DPO-1 (3 and 10 µM), MgTX (10 nM) and ChTX (100 nM) were added simultaneously. *** P
    Figure Legend Snippet: Inhibitory effect of DPO-1 and potassium channel blockers on IL-2 production in activated Jurkat cells. Jurkat cells were activated with PHA (5 µg/mL) and PMA (80 nM) for 24 h. DPO-1 (3 and 10 µM), MgTX (10 nM) and ChTX (100 nM) were added simultaneously. *** P

    Techniques Used:

    Jurkat cells and human peripheral blood T cells (PBTC) express Kv1.3 currents. Original current traces were elicited by 300 ms depolarizing pulses from a holding potential of −80 mV to test potentials between −80 mV and +60 mV, with 10 mV steps in Jurkat cells ( A ), in peripheral blood T cells ( B ) and after application of 10 nM MgTX ( C ), a Kv1.3 blocker in Jurkat cells.
    Figure Legend Snippet: Jurkat cells and human peripheral blood T cells (PBTC) express Kv1.3 currents. Original current traces were elicited by 300 ms depolarizing pulses from a holding potential of −80 mV to test potentials between −80 mV and +60 mV, with 10 mV steps in Jurkat cells ( A ), in peripheral blood T cells ( B ) and after application of 10 nM MgTX ( C ), a Kv1.3 blocker in Jurkat cells.

    Techniques Used: Mass Spectrometry

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    Alomone Labs margatoxin
    Current-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : representative traces of phasic action potentials recorded from the soma of dissociated postganglionic sympathetic neurons in the absence (control; black line) and presence <t>(MgTX;</t>
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    Current-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : representative traces of phasic action potentials recorded from the soma of dissociated postganglionic sympathetic neurons in the absence (control; black line) and presence (MgTX;

    Journal:

    Article Title: Kv1.3 channels in postganglionic sympathetic neurons: expression, function, and modulation

    doi: 10.1152/ajpregu.00077.2008

    Figure Lengend Snippet: Current-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : representative traces of phasic action potentials recorded from the soma of dissociated postganglionic sympathetic neurons in the absence (control; black line) and presence (MgTX;

    Article Snippet: Pharmacological agents were applied at the following concentrations: 1 nM margatoxin (MgTX; Alomone Labs), 100 nM α-dendrotoxin (DTX; Research Biochemicals International), and 100 μM bethanechol (BeCh; Sigma).

    Techniques:

    Voltage-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : ionic current measured in untransfected dissociated sympathetic neurons in the absence (control; n = 18) and presence of 1 nM margatoxin (MgTX; n = 15). Current

    Journal:

    Article Title: Kv1.3 channels in postganglionic sympathetic neurons: expression, function, and modulation

    doi: 10.1152/ajpregu.00077.2008

    Figure Lengend Snippet: Voltage-clamp analyses of Kv1.3 in postganglionic sympathetic neurons. A : ionic current measured in untransfected dissociated sympathetic neurons in the absence (control; n = 18) and presence of 1 nM margatoxin (MgTX; n = 15). Current

    Article Snippet: Pharmacological agents were applied at the following concentrations: 1 nM margatoxin (MgTX; Alomone Labs), 100 nM α-dendrotoxin (DTX; Research Biochemicals International), and 100 μM bethanechol (BeCh; Sigma).

    Techniques:

    Signaling efficiency of IL-2 and -15 receptors. Flow cytometry was used to measure STAT5 phosphorylation on a cell-by-cell basis using Alexa647-anti-PSTAT mAbs. Control samples were incubated in HBSS, and depolarization was achieved either by K-HBSS buffer or by margatoxin (1.5 nM); hyperpolarization was induced by valinomycin (10 μ M). ( A ) K6 cells were stimulated with IL-2 (50 pM, 10 min, 37°C). ( B ) FT7.10 cells were treated with IL-15 (50 pM, 5 min, 37°C). Data from labeled samples were corrected with the mean fluorescence of the isotype controls (IC) and normalized to the intensities measured at resting MP. Autofluorescence (AF) is also shown. The third columns (ØIL-2, ØIL-15) display the normalized basal STAT5 phosphorylation in the absence of cytokine. Averages ± SEM of n = 6 independent measurements are presented. Statistically significant changes relative to the control sample are marked as ∗ p

    Journal: Biophysical Journal

    Article Title: Membrane Potential Distinctly Modulates Mobility and Signaling of IL-2 and IL-15 Receptors in T Cells

    doi: 10.1016/j.bpj.2018.04.038

    Figure Lengend Snippet: Signaling efficiency of IL-2 and -15 receptors. Flow cytometry was used to measure STAT5 phosphorylation on a cell-by-cell basis using Alexa647-anti-PSTAT mAbs. Control samples were incubated in HBSS, and depolarization was achieved either by K-HBSS buffer or by margatoxin (1.5 nM); hyperpolarization was induced by valinomycin (10 μ M). ( A ) K6 cells were stimulated with IL-2 (50 pM, 10 min, 37°C). ( B ) FT7.10 cells were treated with IL-15 (50 pM, 5 min, 37°C). Data from labeled samples were corrected with the mean fluorescence of the isotype controls (IC) and normalized to the intensities measured at resting MP. Autofluorescence (AF) is also shown. The third columns (ØIL-2, ØIL-15) display the normalized basal STAT5 phosphorylation in the absence of cytokine. Averages ± SEM of n = 6 independent measurements are presented. Statistically significant changes relative to the control sample are marked as ∗ p

    Article Snippet: Alternatively, we used margatoxin (MgTx; Alomone Labs, Jerusalem, Israel) , a Kv1.3 channel blocker (Kd : 30 pM) at a concentration of 1.5 nM for fluorescence experiments and 250 pM for patch clamp experiments.

    Techniques: Flow Cytometry, Cytometry, Incubation, Labeling, Fluorescence

    Homoassociations ( A ) and heteroassociations of ( B ) of IL-2R α , IL-15R α , MHC I, and MHC II detected by flow cytometric FRET measurements on FT7.10 cells. Receptors were labeled with donor-tagged (Alexa 546) and acceptor-tagged (Alexa 647) mAbs. The average FRET efficiencies from three independent experiments are shown; in each experiment, > 10,000 cells were measured per treatment. Control samples were incubated in HBSS, and depolarization was achieved either by K-HBSS buffer or by margatoxin (1.5 nM); hyperpolarization was induced by valinomycin (10 μ M). Statistically significant changes relative to the control sample are marked as ∗ p .

    Journal: Biophysical Journal

    Article Title: Membrane Potential Distinctly Modulates Mobility and Signaling of IL-2 and IL-15 Receptors in T Cells

    doi: 10.1016/j.bpj.2018.04.038

    Figure Lengend Snippet: Homoassociations ( A ) and heteroassociations of ( B ) of IL-2R α , IL-15R α , MHC I, and MHC II detected by flow cytometric FRET measurements on FT7.10 cells. Receptors were labeled with donor-tagged (Alexa 546) and acceptor-tagged (Alexa 647) mAbs. The average FRET efficiencies from three independent experiments are shown; in each experiment, > 10,000 cells were measured per treatment. Control samples were incubated in HBSS, and depolarization was achieved either by K-HBSS buffer or by margatoxin (1.5 nM); hyperpolarization was induced by valinomycin (10 μ M). Statistically significant changes relative to the control sample are marked as ∗ p .

    Article Snippet: Alternatively, we used margatoxin (MgTx; Alomone Labs, Jerusalem, Israel) , a Kv1.3 channel blocker (Kd : 30 pM) at a concentration of 1.5 nM for fluorescence experiments and 250 pM for patch clamp experiments.

    Techniques: Flow Cytometry, Labeling, Incubation