snx482  (Alomone Labs)


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    Structured Review

    Alomone Labs snx482
    F-ATPase/Ca v 2.3 functional complexes regulate ERK 1/2 phosphorylation and ROS production after fMLP activation of neutrophils. a. A representative western blot is presented to show the effect of F-ATPase/Ca v 2.3 functional complexes on ERK 1/2 phosphorylation. Neutrophils were pretreated with 400 nM <t>SNX482</t> and 50 μg/ml oligomycin A in Ca 2+ -containing HBSS for 30 min, followed by 1 min of 100 nM fMLP activation. Cells in Ca 2+ -containing HBSS or Ca 2+ -free HBSS incubated with or without fMLP were used as positive or negative controls, respectively. b. The effect of F-ATPase/Ca v 2.3 functional complexes on ROS production was assessed by flow cytometry. DHR123-loaded neutrophils were pretreated with 400 nM SNX482 and 50 μg/ml oligomycin A in Ca 2+ -containing HBSS for 30 min, followed by 30 min of 100 nM fMLP incubation. Cells in Ca 2+ -containing HBSS or Ca 2+ -free HBSS incubated with or without fMLP were used as positive or negative controls, respectively
    Snx482, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 3 article reviews
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    Images

    1) Product Images from "F0F1 ATP synthase regulates extracellular calcium influx in human neutrophils by interacting with Cav2.3 and modulates neutrophil accumulation in the lipopolysaccharide-challenged lung"

    Article Title: F0F1 ATP synthase regulates extracellular calcium influx in human neutrophils by interacting with Cav2.3 and modulates neutrophil accumulation in the lipopolysaccharide-challenged lung

    Journal: Cell Communication and Signaling : CCS

    doi: 10.1186/s12964-020-0515-3

    F-ATPase/Ca v 2.3 functional complexes regulate ERK 1/2 phosphorylation and ROS production after fMLP activation of neutrophils. a. A representative western blot is presented to show the effect of F-ATPase/Ca v 2.3 functional complexes on ERK 1/2 phosphorylation. Neutrophils were pretreated with 400 nM SNX482 and 50 μg/ml oligomycin A in Ca 2+ -containing HBSS for 30 min, followed by 1 min of 100 nM fMLP activation. Cells in Ca 2+ -containing HBSS or Ca 2+ -free HBSS incubated with or without fMLP were used as positive or negative controls, respectively. b. The effect of F-ATPase/Ca v 2.3 functional complexes on ROS production was assessed by flow cytometry. DHR123-loaded neutrophils were pretreated with 400 nM SNX482 and 50 μg/ml oligomycin A in Ca 2+ -containing HBSS for 30 min, followed by 30 min of 100 nM fMLP incubation. Cells in Ca 2+ -containing HBSS or Ca 2+ -free HBSS incubated with or without fMLP were used as positive or negative controls, respectively
    Figure Legend Snippet: F-ATPase/Ca v 2.3 functional complexes regulate ERK 1/2 phosphorylation and ROS production after fMLP activation of neutrophils. a. A representative western blot is presented to show the effect of F-ATPase/Ca v 2.3 functional complexes on ERK 1/2 phosphorylation. Neutrophils were pretreated with 400 nM SNX482 and 50 μg/ml oligomycin A in Ca 2+ -containing HBSS for 30 min, followed by 1 min of 100 nM fMLP activation. Cells in Ca 2+ -containing HBSS or Ca 2+ -free HBSS incubated with or without fMLP were used as positive or negative controls, respectively. b. The effect of F-ATPase/Ca v 2.3 functional complexes on ROS production was assessed by flow cytometry. DHR123-loaded neutrophils were pretreated with 400 nM SNX482 and 50 μg/ml oligomycin A in Ca 2+ -containing HBSS for 30 min, followed by 30 min of 100 nM fMLP incubation. Cells in Ca 2+ -containing HBSS or Ca 2+ -free HBSS incubated with or without fMLP were used as positive or negative controls, respectively

    Techniques Used: Functional Assay, Activation Assay, Western Blot, Incubation, Flow Cytometry

    F-ATPase/Ca v 2.3 complexes modulate extracellular Ca 2+ influx. ( a /left panel) Representative relative fluorescence intensity (RFI, Ex/Em = 488/525 nm) of Fluo-4-loaded neutrophils incubated in Ca 2+ -containing HBSS, with 0.1% DMSO used as a control, 400 nM SNX482 or 50 μg/ml oligomycin A used as an F-ATPase/Ca v 2.3 complex inhibitor and 100 μM thenoyltrifluoroacetone (TTFA) used as a mitochondrial metabolic inhibitor (upper panel). The arrows indicate when 100 nM fMLP was applied. NS/*/*** - P > 0.05/
    Figure Legend Snippet: F-ATPase/Ca v 2.3 complexes modulate extracellular Ca 2+ influx. ( a /left panel) Representative relative fluorescence intensity (RFI, Ex/Em = 488/525 nm) of Fluo-4-loaded neutrophils incubated in Ca 2+ -containing HBSS, with 0.1% DMSO used as a control, 400 nM SNX482 or 50 μg/ml oligomycin A used as an F-ATPase/Ca v 2.3 complex inhibitor and 100 μM thenoyltrifluoroacetone (TTFA) used as a mitochondrial metabolic inhibitor (upper panel). The arrows indicate when 100 nM fMLP was applied. NS/*/*** - P > 0.05/

    Techniques Used: Fluorescence, Incubation

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    Alomone Labs snx 482
    Glutamatergic transmission in the NL is predominantly triggered by Ca 2+ entry through N-type VGCCs. A : Both the ipsilateral (open circles) and the contralateral (filled circles) EPSCs recorded from the same NL neuron were largely and irreversibly blocked by the N-type blocker ω-Conotoxin-GVIA (ω-CTx-GVIA, 2.5 μM), with nearly identical time courses. Averaged traces under control (thin traces) and drug (thick traces) conditions are shown on the right. Stimulus artifacts are truncated for clarity. B-C : No inhibition of EPSCs was produced by the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga-IVA, 0.1 μM) or the L-type blocker nimodipine (10 μM). D: A small and reversible inhibition of the EPSCs by the R-type blocker <t>SNX-482</t> (50 nM) was observed. The different time courses of the EPSCs observed in the sampled neurons may be due to different locations of the neurons along the tonotopic frequency axis. E : Summary of the effects of different VGCC blockers on EPSCs of NL neurons. ω-CTx-GVIA inhibited the ipsilateral and the contralateral EPSCs by 88% and 86%, respectively. Blockers for P/Q- and L-type VGCCs had no effects on EPSCs. SNX-482 produced a small inhibition with a large variation among cells. No differences in the percent inhibition by either drug were detected between the ipsilateral and the contralateral EPSCs. Error bars represent standard deviations. n.s.: non-significant (paired t-test, p > 0.05; the number of cells is indicated in parentheses).
    Snx 482, 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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    Average 93 stars, based on 1 article reviews
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    Alomone Labs ω conotoxin gvia
    GHSR1a activity modulates native Ca V 2 currents in hypothalamic neurons from GHSR-eGFP reporter mice. (A) Representative I Ba traces and averaged I Ba before (control) and after (+ghrelin) 500-nM ghrelin application in hypothalamic GHSR1a− and GHSR1a+ neurons. (B) Averaged peak I Ba –voltage (I-V) relationships (evoked from a holding of −80 mV), reversal (V rev ), and activation (V 1/2 ) potential midpoints (calculated by Boltzmann linear function) obtained from GHSR1a− and GHSR1a+ neurons. (C) I Ba time courses of application of 1 µM <t>ω-conotoxin-GVIA</t> (conoTx) and 0.2 µM ω-agatoxin-IVA (agaTx) with or without previous 500-nM ghrelin application from hypothalamic GHSR1a− (top) and GHSR1a+ neurons (middle and bottom; left). Averaged percentage of I Ba sensitive to agaTx and conoTx from GHSR1a− and GHSR1a+ neurons, with (+ghrelin) or without 500-nM ghrelin application (right). (D) Representative and averaged I Na from GHSR1a− and GHSR1a+ neurons. Paired (A) or two-sample (B and D) Student’s t test and ANOVA with Dunnett’s post-test (C). *, P
    ω Conotoxin Gvia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 95 stars, based on 1 article reviews
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    Glutamatergic transmission in the NL is predominantly triggered by Ca 2+ entry through N-type VGCCs. A : Both the ipsilateral (open circles) and the contralateral (filled circles) EPSCs recorded from the same NL neuron were largely and irreversibly blocked by the N-type blocker ω-Conotoxin-GVIA (ω-CTx-GVIA, 2.5 μM), with nearly identical time courses. Averaged traces under control (thin traces) and drug (thick traces) conditions are shown on the right. Stimulus artifacts are truncated for clarity. B-C : No inhibition of EPSCs was produced by the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga-IVA, 0.1 μM) or the L-type blocker nimodipine (10 μM). D: A small and reversible inhibition of the EPSCs by the R-type blocker SNX-482 (50 nM) was observed. The different time courses of the EPSCs observed in the sampled neurons may be due to different locations of the neurons along the tonotopic frequency axis. E : Summary of the effects of different VGCC blockers on EPSCs of NL neurons. ω-CTx-GVIA inhibited the ipsilateral and the contralateral EPSCs by 88% and 86%, respectively. Blockers for P/Q- and L-type VGCCs had no effects on EPSCs. SNX-482 produced a small inhibition with a large variation among cells. No differences in the percent inhibition by either drug were detected between the ipsilateral and the contralateral EPSCs. Error bars represent standard deviations. n.s.: non-significant (paired t-test, p > 0.05; the number of cells is indicated in parentheses).

    Journal: Neuroscience

    Article Title: Regulation of glutamatergic and GABAergic neurotransmission in the chick nucleus laminaris: role of N-type calcium channels

    doi: 10.1016/j.neuroscience.2009.09.013

    Figure Lengend Snippet: Glutamatergic transmission in the NL is predominantly triggered by Ca 2+ entry through N-type VGCCs. A : Both the ipsilateral (open circles) and the contralateral (filled circles) EPSCs recorded from the same NL neuron were largely and irreversibly blocked by the N-type blocker ω-Conotoxin-GVIA (ω-CTx-GVIA, 2.5 μM), with nearly identical time courses. Averaged traces under control (thin traces) and drug (thick traces) conditions are shown on the right. Stimulus artifacts are truncated for clarity. B-C : No inhibition of EPSCs was produced by the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga-IVA, 0.1 μM) or the L-type blocker nimodipine (10 μM). D: A small and reversible inhibition of the EPSCs by the R-type blocker SNX-482 (50 nM) was observed. The different time courses of the EPSCs observed in the sampled neurons may be due to different locations of the neurons along the tonotopic frequency axis. E : Summary of the effects of different VGCC blockers on EPSCs of NL neurons. ω-CTx-GVIA inhibited the ipsilateral and the contralateral EPSCs by 88% and 86%, respectively. Blockers for P/Q- and L-type VGCCs had no effects on EPSCs. SNX-482 produced a small inhibition with a large variation among cells. No differences in the percent inhibition by either drug were detected between the ipsilateral and the contralateral EPSCs. Error bars represent standard deviations. n.s.: non-significant (paired t-test, p > 0.05; the number of cells is indicated in parentheses).

    Article Snippet: All chemicals and drugs were obtained from Sigma (Saint Louis, MO), except for SNX-482, ω-Conotoxin-GVIA (ω-CTx-GVIA) and tACPD, which were obtained from Peptide International (Louisville, KY), Alomone Labs (Jerusalem, Israel), and Tocris (Ballwin, MO), respectively.

    Techniques: Transmission Assay, Inhibition, Produced

    SNX-482 inhibition of non-L-type I Ca in cultured midbrain DA neurons. A. Representative traces illustrating the inhibition of non-L-type I Ca by 100 nM SNX-482 (red). Cells were initially perfused with a bath solution containing 3 μM isradipine (ISR, black). Full block was obtained using 2 μM Cd 2+ (blue). Square pulses (50 ms) were applied to 0 mV from a holding potential of −70 mV (top) B. Current amplitude values plotted as a function of time. After stabilization of I Ca with ISR (black circles), 100 nM SNX-482 was applied. The remaining currents was blocked by 2 μM Cd 2+ . C. SNX-482 inhibition expressed as % of control I Ca after LTCC block using 3 μM ISR. D. Mean current amplitude at the end of ISR application and at the end of SNX-482 application. Data represent the means ± SEM for the indicated number of experiments (N=4). Statistical significance was determined using paired Student’s t-test: *** p

    Journal: bioRxiv

    Article Title: Alternative splicing of auxiliary β2-subunits stabilizes Cav2.3 Ca2+ channel activity in continuously active midbrain dopamine neurons

    doi: 10.1101/2021.02.10.430224

    Figure Lengend Snippet: SNX-482 inhibition of non-L-type I Ca in cultured midbrain DA neurons. A. Representative traces illustrating the inhibition of non-L-type I Ca by 100 nM SNX-482 (red). Cells were initially perfused with a bath solution containing 3 μM isradipine (ISR, black). Full block was obtained using 2 μM Cd 2+ (blue). Square pulses (50 ms) were applied to 0 mV from a holding potential of −70 mV (top) B. Current amplitude values plotted as a function of time. After stabilization of I Ca with ISR (black circles), 100 nM SNX-482 was applied. The remaining currents was blocked by 2 μM Cd 2+ . C. SNX-482 inhibition expressed as % of control I Ca after LTCC block using 3 μM ISR. D. Mean current amplitude at the end of ISR application and at the end of SNX-482 application. Data represent the means ± SEM for the indicated number of experiments (N=4). Statistical significance was determined using paired Student’s t-test: *** p

    Article Snippet: For inhibition experiments, 100 nM SNX-482 (Alomone, Cat # RTS-500 dissolved in ACSF) or 10 µM nifedipine (Alomone, Cat # N-120 diluted into ACSF from a freshly prepared 10 mM stock solution in DMSO) was bath applied (in ACSF).

    Techniques: Inhibition, Cell Culture, Blocking Assay

    SNX-482 effects on pacemaking of cultured mouse midbrain DA neurons. A. Representative recording of spontaneous firing activity of cultured midbrain dopaminergic neurons before, during and after the application (wash-out) of 100 nM SNX-482. Inset (bottom right): overlay of one single AP before (control) and during the application of 100 nM SNX-482. B. Firing frequency [Hz], coefficient of variation of the interspike interval [%], and AHP peak [mV] before (control) and during the application of 100 nM SNX-482. Data represent the means ± SEM for the indicated number of experiments (N=3). Statistical significance was determined using paired Student’s t-test.: *** p

    Journal: bioRxiv

    Article Title: Alternative splicing of auxiliary β2-subunits stabilizes Cav2.3 Ca2+ channel activity in continuously active midbrain dopamine neurons

    doi: 10.1101/2021.02.10.430224

    Figure Lengend Snippet: SNX-482 effects on pacemaking of cultured mouse midbrain DA neurons. A. Representative recording of spontaneous firing activity of cultured midbrain dopaminergic neurons before, during and after the application (wash-out) of 100 nM SNX-482. Inset (bottom right): overlay of one single AP before (control) and during the application of 100 nM SNX-482. B. Firing frequency [Hz], coefficient of variation of the interspike interval [%], and AHP peak [mV] before (control) and during the application of 100 nM SNX-482. Data represent the means ± SEM for the indicated number of experiments (N=3). Statistical significance was determined using paired Student’s t-test.: *** p

    Article Snippet: For inhibition experiments, 100 nM SNX-482 (Alomone, Cat # RTS-500 dissolved in ACSF) or 10 µM nifedipine (Alomone, Cat # N-120 diluted into ACSF from a freshly prepared 10 mM stock solution in DMSO) was bath applied (in ACSF).

    Techniques: Cell Culture, Activity Assay

    Application of the selective R-type calcium channel blocker SNX-482 does not alter fictive locomotor-like activity. A : paired extracellular recordings from iL2 and iL5 in an isolated whole-cord preparation with cocktail (3–10 μM NMDA,

    Journal: Journal of Neurophysiology

    Article Title: Low-threshold calcium currents contribute to locomotor-like activity in neonatal mice

    doi: 10.1152/jn.00583.2011

    Figure Lengend Snippet: Application of the selective R-type calcium channel blocker SNX-482 does not alter fictive locomotor-like activity. A : paired extracellular recordings from iL2 and iL5 in an isolated whole-cord preparation with cocktail (3–10 μM NMDA,

    Article Snippet: The cycle frequency was not significantly affected by SNX-482 (control, mean = 0.24 ± 0.04 Hz; SNX-482, mean = 0.23 ± 0.02 Hz; n = 3; t = 0.39; P = 0.72; ).

    Techniques: Activity Assay, Isolation

    GHSR1a activity modulates native Ca V 2 currents in hypothalamic neurons from GHSR-eGFP reporter mice. (A) Representative I Ba traces and averaged I Ba before (control) and after (+ghrelin) 500-nM ghrelin application in hypothalamic GHSR1a− and GHSR1a+ neurons. (B) Averaged peak I Ba –voltage (I-V) relationships (evoked from a holding of −80 mV), reversal (V rev ), and activation (V 1/2 ) potential midpoints (calculated by Boltzmann linear function) obtained from GHSR1a− and GHSR1a+ neurons. (C) I Ba time courses of application of 1 µM ω-conotoxin-GVIA (conoTx) and 0.2 µM ω-agatoxin-IVA (agaTx) with or without previous 500-nM ghrelin application from hypothalamic GHSR1a− (top) and GHSR1a+ neurons (middle and bottom; left). Averaged percentage of I Ba sensitive to agaTx and conoTx from GHSR1a− and GHSR1a+ neurons, with (+ghrelin) or without 500-nM ghrelin application (right). (D) Representative and averaged I Na from GHSR1a− and GHSR1a+ neurons. Paired (A) or two-sample (B and D) Student’s t test and ANOVA with Dunnett’s post-test (C). *, P

    Journal: The Journal of General Physiology

    Article Title: Constitutive and ghrelin-dependent GHSR1a activation impairs CaV2.1 and CaV2.2 currents in hypothalamic neurons

    doi: 10.1085/jgp.201511383

    Figure Lengend Snippet: GHSR1a activity modulates native Ca V 2 currents in hypothalamic neurons from GHSR-eGFP reporter mice. (A) Representative I Ba traces and averaged I Ba before (control) and after (+ghrelin) 500-nM ghrelin application in hypothalamic GHSR1a− and GHSR1a+ neurons. (B) Averaged peak I Ba –voltage (I-V) relationships (evoked from a holding of −80 mV), reversal (V rev ), and activation (V 1/2 ) potential midpoints (calculated by Boltzmann linear function) obtained from GHSR1a− and GHSR1a+ neurons. (C) I Ba time courses of application of 1 µM ω-conotoxin-GVIA (conoTx) and 0.2 µM ω-agatoxin-IVA (agaTx) with or without previous 500-nM ghrelin application from hypothalamic GHSR1a− (top) and GHSR1a+ neurons (middle and bottom; left). Averaged percentage of I Ba sensitive to agaTx and conoTx from GHSR1a− and GHSR1a+ neurons, with (+ghrelin) or without 500-nM ghrelin application (right). (D) Representative and averaged I Na from GHSR1a− and GHSR1a+ neurons. Paired (A) or two-sample (B and D) Student’s t test and ANOVA with Dunnett’s post-test (C). *, P

    Article Snippet: We used ghrelin esterified with n -octanoic acid (Global Peptide); a GHSR1a inverse agonist, [d -Arg1,d -Phe5,d -Trp7,9,Leu11]–substance P (SPA; Santa Cruz Biotechnology, Inc.); the inhibitor of Gs protein, cholera toxin (ChTx; Sigma Aldrich); a specific inhibitor of Gi/o protein, pertussis toxin (PTx; Sigma-Aldrich); the CaV 2.1 blocker, ω-agatoxin-IVA (Peptides International); and the CaV2.2 blocker, ω-conotoxin-GVIA (Alomone Labs).

    Techniques: Activity Assay, Mouse Assay, Activation Assay

    GHSR1a activity inhibits native Ca V 2 currents from rat hypothalamic neurons. (A) Representative and averaged I Ba from nontransfected (nt) and GFP-, GHSR1a-YFP–, and GHSR1a-A204E-YFP–transfected neurons. (B) Normalized I Ba traces before (control) and after (+ghrelin) 500-nM ghrelin application, and averaged percentage of I Ba inhibition by ghrelin in each condition. (C) I Ba time courses of application of 1 µM ω-conotoxin-GVIA (conoTx) and 0.2 µM ω-agatoxin-IVA (agaTx) with or without previous 500-nM ghrelin application from GFP-, GHSR1a-, and GHSR1a-A204E–transfected neurons (left). Averaged percentage of I Ba sensitive to agaTx and conoTx from nontransfected (nt), GFP-, GHSR1a-, and GHSR1a-A204E–transfected neurons, with (+ghrelin) or without 500-nM ghrelin application (right). (D) Representative and averaged I Na from nontransfected (nt) and GFP-, GHSR1a-, and GHSR1a-A204E–transfected neurons. ANOVA with Dunnett’s post-test (A–D). *, P

    Journal: The Journal of General Physiology

    Article Title: Constitutive and ghrelin-dependent GHSR1a activation impairs CaV2.1 and CaV2.2 currents in hypothalamic neurons

    doi: 10.1085/jgp.201511383

    Figure Lengend Snippet: GHSR1a activity inhibits native Ca V 2 currents from rat hypothalamic neurons. (A) Representative and averaged I Ba from nontransfected (nt) and GFP-, GHSR1a-YFP–, and GHSR1a-A204E-YFP–transfected neurons. (B) Normalized I Ba traces before (control) and after (+ghrelin) 500-nM ghrelin application, and averaged percentage of I Ba inhibition by ghrelin in each condition. (C) I Ba time courses of application of 1 µM ω-conotoxin-GVIA (conoTx) and 0.2 µM ω-agatoxin-IVA (agaTx) with or without previous 500-nM ghrelin application from GFP-, GHSR1a-, and GHSR1a-A204E–transfected neurons (left). Averaged percentage of I Ba sensitive to agaTx and conoTx from nontransfected (nt), GFP-, GHSR1a-, and GHSR1a-A204E–transfected neurons, with (+ghrelin) or without 500-nM ghrelin application (right). (D) Representative and averaged I Na from nontransfected (nt) and GFP-, GHSR1a-, and GHSR1a-A204E–transfected neurons. ANOVA with Dunnett’s post-test (A–D). *, P

    Article Snippet: We used ghrelin esterified with n -octanoic acid (Global Peptide); a GHSR1a inverse agonist, [d -Arg1,d -Phe5,d -Trp7,9,Leu11]–substance P (SPA; Santa Cruz Biotechnology, Inc.); the inhibitor of Gs protein, cholera toxin (ChTx; Sigma Aldrich); a specific inhibitor of Gi/o protein, pertussis toxin (PTx; Sigma-Aldrich); the CaV 2.1 blocker, ω-agatoxin-IVA (Peptides International); and the CaV2.2 blocker, ω-conotoxin-GVIA (Alomone Labs).

    Techniques: Activity Assay, Transfection, Inhibition