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mgtx  (Alomone Labs)


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    Structured Review

    Alomone Labs mgtx
    ( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin <t>(MgTx;</t> Kv1.3 channel blocker) or <t>dendrotoxin</t> <t>(DTx;</t> Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.
    Mgtx, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 49 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 49 article reviews
    mgtx - by Bioz Stars, 2026-02
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    Images

    1) Product Images from "Striatal cholinergic interneuron pause response requires Kv1 channels, is absent in dyskinetic mice, and is restored by dopamine D5 receptor inverse agonism"

    Article Title: Striatal cholinergic interneuron pause response requires Kv1 channels, is absent in dyskinetic mice, and is restored by dopamine D5 receptor inverse agonism

    Journal: eLife

    doi: 10.7554/eLife.102184

    ( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin (MgTx; Kv1.3 channel blocker) or dendrotoxin (DTx; Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.
    Figure Legend Snippet: ( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin (MgTx; Kv1.3 channel blocker) or dendrotoxin (DTx; Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.

    Techniques Used: Activation Assay, Control, Concentration Assay



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    ( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin <t>(MgTx;</t> Kv1.3 channel blocker) or <t>dendrotoxin</t> <t>(DTx;</t> Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.
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    mgtx  (MedChemExpress)
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    ( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin <t>(MgTx;</t> Kv1.3 channel blocker) or <t>dendrotoxin</t> <t>(DTx;</t> Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.
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    ( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin <t>(MgTx;</t> Kv1.3 channel blocker) or <t>dendrotoxin</t> <t>(DTx;</t> Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.
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    margatoxin mrgx  (Alomone Labs)
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    ( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin <t>(MgTx;</t> Kv1.3 channel blocker) or <t>dendrotoxin</t> <t>(DTx;</t> Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.
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    ( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin <t>(MgTx;</t> Kv1.3 channel blocker) or <t>dendrotoxin</t> <t>(DTx;</t> Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.
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    Image Search Results


    ( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin (MgTx; Kv1.3 channel blocker) or dendrotoxin (DTx; Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.

    Journal: eLife

    Article Title: Striatal cholinergic interneuron pause response requires Kv1 channels, is absent in dyskinetic mice, and is restored by dopamine D5 receptor inverse agonism

    doi: 10.7554/eLife.102184

    Figure Lengend Snippet: ( A ) Schematic representation of the tested hypotheses. DP: depolarization; HP: hyperpolarization; Glu: glutamate; DA: dopamine. ( B ) Representative recordings of striatal cholinergic interneurons (SCINs) in response to optogenetic activation of thalamic terminals, with or without margatoxin (MgTx; Kv1.3 channel blocker) or dendrotoxin (DTx; Kv1.1 and Kv1.6 channels blocker) in the bath. ( C ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA interaction ns, treatment *p=0.0051; control-MgTx 30 nM: *p=0.0005; control-MgTx 3 nM: ns; control-DTX: *p=0.0462; MgTx 30 nM-MgTx 3 nM: *p<0.0001; MgTx 30 nM-DTX: ns; MgTx 3 nM-DTX: *p=0.0027). ( D ) Baseline ISI of SCINs recorded with or without MgTx 3 nM, 30 nM, or DTx (one-way ANOVA, ns). ( E ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without MgTx 3 nM, 30 nM, or DTx 100 nM, in the bath (two-way RM ANOVA, ns). ( F ) Representative recordings of SCINs in response to optogenetic activation of thalamic terminals, with or without Ba 2+ (10 µM; Kir2.2 channel blocker at this concentration) or XE 991 (10 µM; Kv7 channel blocker) in the bath. ( G ) Pause duration/baseline ISI of SCINs that responded with 1, 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, with or without 10 µM XE 991 or 10 µM Ba 2+ (two-way RM ANOVA, ns). ( H ) Baseline ISI of SCINs recorded with or without Ba 2+ or XE 991 (one-way ANOVA, ns). ( I ) Burst duration of SCINs that responded with 2, 3, or 4 spikes to optogenetic activation of thalamic terminals, for the above conditions (two-way RM ANOVA, ns). Mean ± SEM; n=7–16 cells per group, from >5 mice. Figure 2—source data 1. Contribution of the Kv1 current to the pause response.

    Article Snippet: The following stock solvents and final concentrations were used: distilled H 2 O for BaCl (10 μM), ZD7288 (30 μM), mecamylamine (10 μM, RBI), methiothepin (10 μM), quinpirole (1 μM, 10 μM), and sumanirole (10 μM); DMSO for CNQX (40 μM, Tocris), PIC (100 μM), SKF81297 (2 μM), SCH23390 (10 μM), sulpiride (10 μM, Santa Cruz Biotechnology), XE991 (10 μM), and clozapine (10 μM, Rospaw Laboratory); and the manufacturer’s recommended storage buffer (0.1% BSA, 100 mM NaCl, 10 mM Tris pH 7.5, 1 mM EDTA) for MgTx (3 nM and 30 nM, Alomone Labs) and g-DTx (100 nM, Alomone Labs).

    Techniques: Activation Assay, Control, Concentration Assay