phrixotoxin 1  (Alomone Labs)


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    Alomone Labs phrixotoxin 1
    Influences of voltage-gated potassium (K v ) channel inhibition on progenitor c ell proliferation . Proliferation of hNPCs was analyzed via BrdU incorporation assay. (A): Progenitor cell proliferation was measured colorimetrically after 72 h of K v channel inhibition and normalized to control values without addition of inhibitor. Electrophysiologically determined inhibitory doses (IC 50 /IC 80 ) of 4-aminopyridine (4-AP), <t>phrixotoxin-1</t> (PTX), ammonium chloride (NH 4 Cl), tetraethylammonium chloride (TEA), quinidine (QND) and α-dendrotoxin (DTX) were applied. Progenitor cell proliferation was significantly reduced by inhibition of I A with 4-AP, PTX, NH 4 Cl as well as by unspecific blockers like TEA and higher doses of QND. In contrast, the I K antagonist DTX increased proliferation of hNPCs (n≥4, 3 tissue preparations; one-way ANOVA, followed by Tukey's post-hoc test, *p
    Phrixotoxin 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phrixotoxin 1/product/Alomone Labs
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    phrixotoxin 1 - by Bioz Stars, 2021-12
    91/100 stars

    Images

    1) Product Images from "Characterization of Voltage-Gated Potassium Channels in Human Neural Progenitor Cells"

    Article Title: Characterization of Voltage-Gated Potassium Channels in Human Neural Progenitor Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0006168

    Influences of voltage-gated potassium (K v ) channel inhibition on progenitor c ell proliferation . Proliferation of hNPCs was analyzed via BrdU incorporation assay. (A): Progenitor cell proliferation was measured colorimetrically after 72 h of K v channel inhibition and normalized to control values without addition of inhibitor. Electrophysiologically determined inhibitory doses (IC 50 /IC 80 ) of 4-aminopyridine (4-AP), phrixotoxin-1 (PTX), ammonium chloride (NH 4 Cl), tetraethylammonium chloride (TEA), quinidine (QND) and α-dendrotoxin (DTX) were applied. Progenitor cell proliferation was significantly reduced by inhibition of I A with 4-AP, PTX, NH 4 Cl as well as by unspecific blockers like TEA and higher doses of QND. In contrast, the I K antagonist DTX increased proliferation of hNPCs (n≥4, 3 tissue preparations; one-way ANOVA, followed by Tukey's post-hoc test, *p
    Figure Legend Snippet: Influences of voltage-gated potassium (K v ) channel inhibition on progenitor c ell proliferation . Proliferation of hNPCs was analyzed via BrdU incorporation assay. (A): Progenitor cell proliferation was measured colorimetrically after 72 h of K v channel inhibition and normalized to control values without addition of inhibitor. Electrophysiologically determined inhibitory doses (IC 50 /IC 80 ) of 4-aminopyridine (4-AP), phrixotoxin-1 (PTX), ammonium chloride (NH 4 Cl), tetraethylammonium chloride (TEA), quinidine (QND) and α-dendrotoxin (DTX) were applied. Progenitor cell proliferation was significantly reduced by inhibition of I A with 4-AP, PTX, NH 4 Cl as well as by unspecific blockers like TEA and higher doses of QND. In contrast, the I K antagonist DTX increased proliferation of hNPCs (n≥4, 3 tissue preparations; one-way ANOVA, followed by Tukey's post-hoc test, *p

    Techniques Used: Inhibition, BrdU Incorporation Assay

    Cell viability after inhibition of voltage-gated potassium (K v ) channels. Determination of cell viability in proliferating hNPCs via 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium salt (MTT) assay. (A): Cell viability was measured colorimetrically after 72 h of K v channel inhibition with different concentrations of 4-aminopyridine (4-AP), phrixotoxin-1 (PTX), ammonium chloride (NH 4 Cl), tetraethylammonium chloride (TEA), quinidine (QND) and α-dendrotoxin (DTX) and normalized to control values without addition of inhibitor. (B): Viability of hNPCs was significantly reduced by electrophysiologically determined inhibitory doses (IC 50 /IC 80 ) of 4-AP, PTX and NH 4 Cl, which specifically blocked I A , as well as by TEA and higher doses of QND, which inhibited both current components (n≥4, 3 tissue preparations; one-way ANOVA, followed by Tukey's post-hoc test, ***p
    Figure Legend Snippet: Cell viability after inhibition of voltage-gated potassium (K v ) channels. Determination of cell viability in proliferating hNPCs via 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium salt (MTT) assay. (A): Cell viability was measured colorimetrically after 72 h of K v channel inhibition with different concentrations of 4-aminopyridine (4-AP), phrixotoxin-1 (PTX), ammonium chloride (NH 4 Cl), tetraethylammonium chloride (TEA), quinidine (QND) and α-dendrotoxin (DTX) and normalized to control values without addition of inhibitor. (B): Viability of hNPCs was significantly reduced by electrophysiologically determined inhibitory doses (IC 50 /IC 80 ) of 4-AP, PTX and NH 4 Cl, which specifically blocked I A , as well as by TEA and higher doses of QND, which inhibited both current components (n≥4, 3 tissue preparations; one-way ANOVA, followed by Tukey's post-hoc test, ***p

    Techniques Used: Inhibition, MTT Assay

    Pharmacological inhibition of K v currents in hNPCs. Biophysically separated A-type (I A ) and delayed-rectifying (I K ) K v currents in proliferating hNPCs were differentially inhibited by the 4-aminopyridine (4-AP, i), phrixotoxin-1 (PTX, ii), ammonium chloride (NH 4 Cl, iii), tetraethylammonium chloride (TEA, iv), quinidine (QND, v) and α-dendrotoxin (DTX, vi). (A): Peak amplitudes of I A were measured during a depolarizing voltage step from −130 mV to 0 mV between 0 and 20 ms (inset). (B): I K was determined between 280 and 300 ms of a 100 mV depolarization step following a −40 mV prepulse during the application of different antagonist concentrations (insets). (C): Both current values were normalized to the non-inhibited peak amplitudes. Dose-response relationships were fitted with the Hill equation and IC 50 values were determined (see Tab. 2 ). Note that PTX selectively and 4-AP preferentially inhibited I A , while DTX selectively blocked I K .
    Figure Legend Snippet: Pharmacological inhibition of K v currents in hNPCs. Biophysically separated A-type (I A ) and delayed-rectifying (I K ) K v currents in proliferating hNPCs were differentially inhibited by the 4-aminopyridine (4-AP, i), phrixotoxin-1 (PTX, ii), ammonium chloride (NH 4 Cl, iii), tetraethylammonium chloride (TEA, iv), quinidine (QND, v) and α-dendrotoxin (DTX, vi). (A): Peak amplitudes of I A were measured during a depolarizing voltage step from −130 mV to 0 mV between 0 and 20 ms (inset). (B): I K was determined between 280 and 300 ms of a 100 mV depolarization step following a −40 mV prepulse during the application of different antagonist concentrations (insets). (C): Both current values were normalized to the non-inhibited peak amplitudes. Dose-response relationships were fitted with the Hill equation and IC 50 values were determined (see Tab. 2 ). Note that PTX selectively and 4-AP preferentially inhibited I A , while DTX selectively blocked I K .

    Techniques Used: Inhibition, Mass Spectrometry

    2) Product Images from "BK Channels Mediate Dopamine Inhibition of Firing in a Subpopulation of Core Nucleus Accumbens Medium Spiny Neurons"

    Article Title: BK Channels Mediate Dopamine Inhibition of Firing in a Subpopulation of Core Nucleus Accumbens Medium Spiny Neurons

    Journal: Brain research

    doi: 10.1016/j.brainres.2014.09.015

    I A ion channel blocker phrixotoxin-1 does not alter MSNs firing pattern. A. Stability of MSNs RMP, Rin and firing frequency. Voltage traces in response to hyperpolarizing (−110 pA) and depolarizing (+250 pA) current pulses (800 ms) recorded at
    Figure Legend Snippet: I A ion channel blocker phrixotoxin-1 does not alter MSNs firing pattern. A. Stability of MSNs RMP, Rin and firing frequency. Voltage traces in response to hyperpolarizing (−110 pA) and depolarizing (+250 pA) current pulses (800 ms) recorded at

    Techniques Used: Mass Spectrometry

    3) Product Images from "BK Channels Mediate Dopamine Inhibition of Firing in a Subpopulation of Core Nucleus Accumbens Medium Spiny Neurons"

    Article Title: BK Channels Mediate Dopamine Inhibition of Firing in a Subpopulation of Core Nucleus Accumbens Medium Spiny Neurons

    Journal: Brain research

    doi: 10.1016/j.brainres.2014.09.015

    I A ion channel blocker phrixotoxin-1 does not alter MSNs firing pattern. A. Stability of MSNs RMP, Rin and firing frequency. Voltage traces in response to hyperpolarizing (−110 pA) and depolarizing (+250 pA) current pulses (800 ms) recorded at
    Figure Legend Snippet: I A ion channel blocker phrixotoxin-1 does not alter MSNs firing pattern. A. Stability of MSNs RMP, Rin and firing frequency. Voltage traces in response to hyperpolarizing (−110 pA) and depolarizing (+250 pA) current pulses (800 ms) recorded at

    Techniques Used: Mass Spectrometry

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    Alomone Labs phrixotoxin 1
    Influences of voltage-gated potassium (K v ) channel inhibition on progenitor c ell proliferation . Proliferation of hNPCs was analyzed via BrdU incorporation assay. (A): Progenitor cell proliferation was measured colorimetrically after 72 h of K v channel inhibition and normalized to control values without addition of inhibitor. Electrophysiologically determined inhibitory doses (IC 50 /IC 80 ) of 4-aminopyridine (4-AP), <t>phrixotoxin-1</t> (PTX), ammonium chloride (NH 4 Cl), tetraethylammonium chloride (TEA), quinidine (QND) and α-dendrotoxin (DTX) were applied. Progenitor cell proliferation was significantly reduced by inhibition of I A with 4-AP, PTX, NH 4 Cl as well as by unspecific blockers like TEA and higher doses of QND. In contrast, the I K antagonist DTX increased proliferation of hNPCs (n≥4, 3 tissue preparations; one-way ANOVA, followed by Tukey's post-hoc test, *p
    Phrixotoxin 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phrixotoxin 1/product/Alomone Labs
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    phrixotoxin 1 - by Bioz Stars, 2021-12
    91/100 stars
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    Influences of voltage-gated potassium (K v ) channel inhibition on progenitor c ell proliferation . Proliferation of hNPCs was analyzed via BrdU incorporation assay. (A): Progenitor cell proliferation was measured colorimetrically after 72 h of K v channel inhibition and normalized to control values without addition of inhibitor. Electrophysiologically determined inhibitory doses (IC 50 /IC 80 ) of 4-aminopyridine (4-AP), phrixotoxin-1 (PTX), ammonium chloride (NH 4 Cl), tetraethylammonium chloride (TEA), quinidine (QND) and α-dendrotoxin (DTX) were applied. Progenitor cell proliferation was significantly reduced by inhibition of I A with 4-AP, PTX, NH 4 Cl as well as by unspecific blockers like TEA and higher doses of QND. In contrast, the I K antagonist DTX increased proliferation of hNPCs (n≥4, 3 tissue preparations; one-way ANOVA, followed by Tukey's post-hoc test, *p

    Journal: PLoS ONE

    Article Title: Characterization of Voltage-Gated Potassium Channels in Human Neural Progenitor Cells

    doi: 10.1371/journal.pone.0006168

    Figure Lengend Snippet: Influences of voltage-gated potassium (K v ) channel inhibition on progenitor c ell proliferation . Proliferation of hNPCs was analyzed via BrdU incorporation assay. (A): Progenitor cell proliferation was measured colorimetrically after 72 h of K v channel inhibition and normalized to control values without addition of inhibitor. Electrophysiologically determined inhibitory doses (IC 50 /IC 80 ) of 4-aminopyridine (4-AP), phrixotoxin-1 (PTX), ammonium chloride (NH 4 Cl), tetraethylammonium chloride (TEA), quinidine (QND) and α-dendrotoxin (DTX) were applied. Progenitor cell proliferation was significantly reduced by inhibition of I A with 4-AP, PTX, NH 4 Cl as well as by unspecific blockers like TEA and higher doses of QND. In contrast, the I K antagonist DTX increased proliferation of hNPCs (n≥4, 3 tissue preparations; one-way ANOVA, followed by Tukey's post-hoc test, *p

    Article Snippet: Different antagonists (all from Sigma-Aldrich GmbH if not stated otherwise) were dissolved in this bathing solution: 4-aminopyridine (4-AP, 0.1–10 mM), phrixotoxin-1 (PTX, 1–1000 nM, Alomone Labs, Jerusalem, Israel), ammonium chloride (NH4 Cl, 1–100 mM), quinidine (QND, 0.1–100 µM), α-dendrotoxin (DTX, 1–1000 nM), margatoxin (MTX, 0.1–50 nM) and tetraethylammonium chloride (TEA, 1–100 mM).

    Techniques: Inhibition, BrdU Incorporation Assay

    Cell viability after inhibition of voltage-gated potassium (K v ) channels. Determination of cell viability in proliferating hNPCs via 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium salt (MTT) assay. (A): Cell viability was measured colorimetrically after 72 h of K v channel inhibition with different concentrations of 4-aminopyridine (4-AP), phrixotoxin-1 (PTX), ammonium chloride (NH 4 Cl), tetraethylammonium chloride (TEA), quinidine (QND) and α-dendrotoxin (DTX) and normalized to control values without addition of inhibitor. (B): Viability of hNPCs was significantly reduced by electrophysiologically determined inhibitory doses (IC 50 /IC 80 ) of 4-AP, PTX and NH 4 Cl, which specifically blocked I A , as well as by TEA and higher doses of QND, which inhibited both current components (n≥4, 3 tissue preparations; one-way ANOVA, followed by Tukey's post-hoc test, ***p

    Journal: PLoS ONE

    Article Title: Characterization of Voltage-Gated Potassium Channels in Human Neural Progenitor Cells

    doi: 10.1371/journal.pone.0006168

    Figure Lengend Snippet: Cell viability after inhibition of voltage-gated potassium (K v ) channels. Determination of cell viability in proliferating hNPCs via 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium salt (MTT) assay. (A): Cell viability was measured colorimetrically after 72 h of K v channel inhibition with different concentrations of 4-aminopyridine (4-AP), phrixotoxin-1 (PTX), ammonium chloride (NH 4 Cl), tetraethylammonium chloride (TEA), quinidine (QND) and α-dendrotoxin (DTX) and normalized to control values without addition of inhibitor. (B): Viability of hNPCs was significantly reduced by electrophysiologically determined inhibitory doses (IC 50 /IC 80 ) of 4-AP, PTX and NH 4 Cl, which specifically blocked I A , as well as by TEA and higher doses of QND, which inhibited both current components (n≥4, 3 tissue preparations; one-way ANOVA, followed by Tukey's post-hoc test, ***p

    Article Snippet: Different antagonists (all from Sigma-Aldrich GmbH if not stated otherwise) were dissolved in this bathing solution: 4-aminopyridine (4-AP, 0.1–10 mM), phrixotoxin-1 (PTX, 1–1000 nM, Alomone Labs, Jerusalem, Israel), ammonium chloride (NH4 Cl, 1–100 mM), quinidine (QND, 0.1–100 µM), α-dendrotoxin (DTX, 1–1000 nM), margatoxin (MTX, 0.1–50 nM) and tetraethylammonium chloride (TEA, 1–100 mM).

    Techniques: Inhibition, MTT Assay

    Pharmacological inhibition of K v currents in hNPCs. Biophysically separated A-type (I A ) and delayed-rectifying (I K ) K v currents in proliferating hNPCs were differentially inhibited by the 4-aminopyridine (4-AP, i), phrixotoxin-1 (PTX, ii), ammonium chloride (NH 4 Cl, iii), tetraethylammonium chloride (TEA, iv), quinidine (QND, v) and α-dendrotoxin (DTX, vi). (A): Peak amplitudes of I A were measured during a depolarizing voltage step from −130 mV to 0 mV between 0 and 20 ms (inset). (B): I K was determined between 280 and 300 ms of a 100 mV depolarization step following a −40 mV prepulse during the application of different antagonist concentrations (insets). (C): Both current values were normalized to the non-inhibited peak amplitudes. Dose-response relationships were fitted with the Hill equation and IC 50 values were determined (see Tab. 2 ). Note that PTX selectively and 4-AP preferentially inhibited I A , while DTX selectively blocked I K .

    Journal: PLoS ONE

    Article Title: Characterization of Voltage-Gated Potassium Channels in Human Neural Progenitor Cells

    doi: 10.1371/journal.pone.0006168

    Figure Lengend Snippet: Pharmacological inhibition of K v currents in hNPCs. Biophysically separated A-type (I A ) and delayed-rectifying (I K ) K v currents in proliferating hNPCs were differentially inhibited by the 4-aminopyridine (4-AP, i), phrixotoxin-1 (PTX, ii), ammonium chloride (NH 4 Cl, iii), tetraethylammonium chloride (TEA, iv), quinidine (QND, v) and α-dendrotoxin (DTX, vi). (A): Peak amplitudes of I A were measured during a depolarizing voltage step from −130 mV to 0 mV between 0 and 20 ms (inset). (B): I K was determined between 280 and 300 ms of a 100 mV depolarization step following a −40 mV prepulse during the application of different antagonist concentrations (insets). (C): Both current values were normalized to the non-inhibited peak amplitudes. Dose-response relationships were fitted with the Hill equation and IC 50 values were determined (see Tab. 2 ). Note that PTX selectively and 4-AP preferentially inhibited I A , while DTX selectively blocked I K .

    Article Snippet: Different antagonists (all from Sigma-Aldrich GmbH if not stated otherwise) were dissolved in this bathing solution: 4-aminopyridine (4-AP, 0.1–10 mM), phrixotoxin-1 (PTX, 1–1000 nM, Alomone Labs, Jerusalem, Israel), ammonium chloride (NH4 Cl, 1–100 mM), quinidine (QND, 0.1–100 µM), α-dendrotoxin (DTX, 1–1000 nM), margatoxin (MTX, 0.1–50 nM) and tetraethylammonium chloride (TEA, 1–100 mM).

    Techniques: Inhibition, Mass Spectrometry

    I A ion channel blocker phrixotoxin-1 does not alter MSNs firing pattern. A. Stability of MSNs RMP, Rin and firing frequency. Voltage traces in response to hyperpolarizing (−110 pA) and depolarizing (+250 pA) current pulses (800 ms) recorded at

    Journal: Brain research

    Article Title: BK Channels Mediate Dopamine Inhibition of Firing in a Subpopulation of Core Nucleus Accumbens Medium Spiny Neurons

    doi: 10.1016/j.brainres.2014.09.015

    Figure Lengend Snippet: I A ion channel blocker phrixotoxin-1 does not alter MSNs firing pattern. A. Stability of MSNs RMP, Rin and firing frequency. Voltage traces in response to hyperpolarizing (−110 pA) and depolarizing (+250 pA) current pulses (800 ms) recorded at

    Article Snippet: [ ] Chagot B, Escoubas P, Villegas E, Bernard C, Ferrat G, Corzo G, Lazdunski M, Darbon H. Solution structure of Phrixotoxin 1, a specific peptide inhibitor of Kv4 potassium channels from the venom of the theraphosid spider Phrixotrichus auratus.

    Techniques: Mass Spectrometry