mviia  (Alomone Labs)


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    Alomone Labs mviia
    Potency of Ca V 2.2 channel inhibition and side effects of intraplantar administration of <t>ω-conotoxins.</t> ( A ) Representative concentration response curves for inhibition of KCl evoked Ca V 2.2 response in SH-SY5Y cells. Potency of GVIA (IC 50 11.2 ± 3.3 nM), <t>MVIIA</t> (IC 50 6.8 ± 2.1 nM), and CVIF (IC 50 10.0 ± 3.1 nM) determined from three independent experiments each conducted in triplicate. ( B , C ) Intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF ( n = 6 per group) in naïve C57BL6/J mice did not significantly change mechanical and thermal PWTs compared to healthy control group ( n = 18) ( p > 0.05). ( D – F ) Intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF ( n = 6 per group) in naïve C57BL6/J mice did not significantly change foot slips, distance covered, and ataxia index in the parallel rod floor test compared with healthy control mice ( n = 18) ( p > 0.05). All data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA with Dunnett’s post-test.
    Mviia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mviia/product/Alomone Labs
    Average 86 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    mviia - by Bioz Stars, 2022-08
    86/100 stars

    Images

    1) Product Images from "Subcutaneous ω-Conotoxins Alleviate Mechanical Pain in Rodent Models of Acute Peripheral Neuropathy"

    Article Title: Subcutaneous ω-Conotoxins Alleviate Mechanical Pain in Rodent Models of Acute Peripheral Neuropathy

    Journal: Marine Drugs

    doi: 10.3390/md19020106

    Potency of Ca V 2.2 channel inhibition and side effects of intraplantar administration of ω-conotoxins. ( A ) Representative concentration response curves for inhibition of KCl evoked Ca V 2.2 response in SH-SY5Y cells. Potency of GVIA (IC 50 11.2 ± 3.3 nM), MVIIA (IC 50 6.8 ± 2.1 nM), and CVIF (IC 50 10.0 ± 3.1 nM) determined from three independent experiments each conducted in triplicate. ( B , C ) Intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF ( n = 6 per group) in naïve C57BL6/J mice did not significantly change mechanical and thermal PWTs compared to healthy control group ( n = 18) ( p > 0.05). ( D – F ) Intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF ( n = 6 per group) in naïve C57BL6/J mice did not significantly change foot slips, distance covered, and ataxia index in the parallel rod floor test compared with healthy control mice ( n = 18) ( p > 0.05). All data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA with Dunnett’s post-test.
    Figure Legend Snippet: Potency of Ca V 2.2 channel inhibition and side effects of intraplantar administration of ω-conotoxins. ( A ) Representative concentration response curves for inhibition of KCl evoked Ca V 2.2 response in SH-SY5Y cells. Potency of GVIA (IC 50 11.2 ± 3.3 nM), MVIIA (IC 50 6.8 ± 2.1 nM), and CVIF (IC 50 10.0 ± 3.1 nM) determined from three independent experiments each conducted in triplicate. ( B , C ) Intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF ( n = 6 per group) in naïve C57BL6/J mice did not significantly change mechanical and thermal PWTs compared to healthy control group ( n = 18) ( p > 0.05). ( D – F ) Intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF ( n = 6 per group) in naïve C57BL6/J mice did not significantly change foot slips, distance covered, and ataxia index in the parallel rod floor test compared with healthy control mice ( n = 18) ( p > 0.05). All data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA with Dunnett’s post-test.

    Techniques Used: Inhibition, Concentration Assay, Injection, Mouse Assay

    2) Product Images from "Cell-Based Reporter Release Assay to Determine the Activity of Calcium-Dependent Neurotoxins and Neuroactive Pharmaceuticals"

    Article Title: Cell-Based Reporter Release Assay to Determine the Activity of Calcium-Dependent Neurotoxins and Neuroactive Pharmaceuticals

    Journal: Toxins

    doi: 10.3390/toxins13040247

    Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin MVIIA for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer without ω-conotoxins: c:
    Figure Legend Snippet: Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin MVIIA for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer without ω-conotoxins: c:

    Techniques Used: Inhibition, Luciferase, Stable Transfection, Expressing, Cell Culture, Incubation, Activity Assay

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    Alomone Labs mviia
    Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin <t>MVIIA</t> for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer without <t>ω-conotoxins:</t> c:
    Mviia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mviia/product/Alomone Labs
    Average 85 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mviia - by Bioz Stars, 2022-08
    85/100 stars
    		  Buy from Supplier
    n type ca2 channel blocker conotoxin mviia  (Alomone Labs)
    86
    Alomone Labs n type ca2 channel blocker conotoxin mviia
    Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin <t>MVIIA</t> for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer without <t>ω-conotoxins:</t> c:
    N Type Ca2 Channel Blocker Conotoxin Mviia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/n type ca2 channel blocker conotoxin mviia/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    n type ca2 channel blocker conotoxin mviia - by Bioz Stars, 2022-08
    86/100 stars
    		  Buy from Supplier

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    Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin MVIIA for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer without ω-conotoxins: c:

    Journal: Toxins

    Article Title: Cell-Based Reporter Release Assay to Determine the Activity of Calcium-Dependent Neurotoxins and Neuroactive Pharmaceuticals

    doi: 10.3390/toxins13040247

    Figure Lengend Snippet: Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin MVIIA for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer without ω-conotoxins: c:

    Article Snippet: Neurotoxins and neuroactive pharmaceuticals used: carbachol, atropine, verapamil, nifedipine, thrimethadione and zonisamide were from Sigma-Aldrich (Taufkirchen, Germany); α-Latrotoxin (ALX-630-027) was from Enzo Life Science (Lörrach, Germany); ω-conotoxins GVIA and MVIIA were from Alamone labs (Jerusalem, Israel); agatoxin and SNX-482 were from tebu-bio (Offenbach, Germany).

    Techniques: Inhibition, Luciferase, Stable Transfection, Expressing, Cell Culture, Incubation, Activity Assay