ω conotoxin mviic  (Alomone Labs)


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    Alomone Labs ω conotoxin mviic
    ω Conotoxin Mviic, 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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    ω conotoxin mviic - by Bioz Stars, 2023-09
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    ω conotoxin mviic  (Alomone Labs)


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    Alomone Labs ω conotoxin mviic
    Spontaneous calcium transients and growth cone turning are sensitive to blockage of store-operated channels . (A) Individual control morphant growth cones exhibited sparse spontaneous calcium transients, occurring at a rate of approximately one transient per three minutes. (B) Homer1 morphant growth cones exhibited significantly greater frequency, at a rate of at least one spontaneous transient per minute. (C) A trace from a single Homer1 morphant growth cone showed a decrease in spontaneous calcium transient frequency in the presence of bath applied SKF-96365. (D) Quantification of spontaneous calcium transient frequencies in Homer1 morphant growth cones. Removing calcium from the media (Ca free) or bath application of La 3+ (La) or SKF-96365 (SKF) reduced spontaneous transient frequencies in Homer1 morphant growth cones to control (ctrl) levels. Bath application of a voltage-gated calcium channel (VGCC) inhibitor cocktail or nifedipine alone had little effect on the frequency of spontaneous calcium transients in Homer1 morphant growth cones. (E) Calcium-dependent brain derived neurotrophic factor (BDNF)-induced turning is mediated through store-operated channels. BDNF attraction was abolished when TRPC channels were inactivated with bath application of SKF-96365 or La 3+ . Inhibition of VGCCs with nifedipine <t>or</t> <t>ω-conotoxin-MVIIC</t> had no effect on control and Homer1 morphant growth cone turning. (F) Inhibition of store-operated channels did not alter axon extension rates. Error bars indicate standard error of the mean. Cocktail = nifedipine, ω-conotoxin-MVIIC plus Ni ++ . The scale bar in (C) applies also to (A, B).
    ω Conotoxin Mviic, 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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    ω conotoxin mviic - by Bioz Stars, 2023-09
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    1) Product Images from "Homer regulates calcium signalling in growth cone turning"

    Article Title: Homer regulates calcium signalling in growth cone turning

    Journal: Neural Development

    doi: 10.1186/1749-8104-4-29

    Spontaneous calcium transients and growth cone turning are sensitive to blockage of store-operated channels . (A) Individual control morphant growth cones exhibited sparse spontaneous calcium transients, occurring at a rate of approximately one transient per three minutes. (B) Homer1 morphant growth cones exhibited significantly greater frequency, at a rate of at least one spontaneous transient per minute. (C) A trace from a single Homer1 morphant growth cone showed a decrease in spontaneous calcium transient frequency in the presence of bath applied SKF-96365. (D) Quantification of spontaneous calcium transient frequencies in Homer1 morphant growth cones. Removing calcium from the media (Ca free) or bath application of La 3+ (La) or SKF-96365 (SKF) reduced spontaneous transient frequencies in Homer1 morphant growth cones to control (ctrl) levels. Bath application of a voltage-gated calcium channel (VGCC) inhibitor cocktail or nifedipine alone had little effect on the frequency of spontaneous calcium transients in Homer1 morphant growth cones. (E) Calcium-dependent brain derived neurotrophic factor (BDNF)-induced turning is mediated through store-operated channels. BDNF attraction was abolished when TRPC channels were inactivated with bath application of SKF-96365 or La 3+ . Inhibition of VGCCs with nifedipine or ω-conotoxin-MVIIC had no effect on control and Homer1 morphant growth cone turning. (F) Inhibition of store-operated channels did not alter axon extension rates. Error bars indicate standard error of the mean. Cocktail = nifedipine, ω-conotoxin-MVIIC plus Ni ++ . The scale bar in (C) applies also to (A, B).
    Figure Legend Snippet: Spontaneous calcium transients and growth cone turning are sensitive to blockage of store-operated channels . (A) Individual control morphant growth cones exhibited sparse spontaneous calcium transients, occurring at a rate of approximately one transient per three minutes. (B) Homer1 morphant growth cones exhibited significantly greater frequency, at a rate of at least one spontaneous transient per minute. (C) A trace from a single Homer1 morphant growth cone showed a decrease in spontaneous calcium transient frequency in the presence of bath applied SKF-96365. (D) Quantification of spontaneous calcium transient frequencies in Homer1 morphant growth cones. Removing calcium from the media (Ca free) or bath application of La 3+ (La) or SKF-96365 (SKF) reduced spontaneous transient frequencies in Homer1 morphant growth cones to control (ctrl) levels. Bath application of a voltage-gated calcium channel (VGCC) inhibitor cocktail or nifedipine alone had little effect on the frequency of spontaneous calcium transients in Homer1 morphant growth cones. (E) Calcium-dependent brain derived neurotrophic factor (BDNF)-induced turning is mediated through store-operated channels. BDNF attraction was abolished when TRPC channels were inactivated with bath application of SKF-96365 or La 3+ . Inhibition of VGCCs with nifedipine or ω-conotoxin-MVIIC had no effect on control and Homer1 morphant growth cone turning. (F) Inhibition of store-operated channels did not alter axon extension rates. Error bars indicate standard error of the mean. Cocktail = nifedipine, ω-conotoxin-MVIIC plus Ni ++ . The scale bar in (C) applies also to (A, B).

    Techniques Used: Derivative Assay, Inhibition

    ω conotoxin mviic  (Alomone Labs)


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    Alomone Labs ω conotoxin mviic
    ω Conotoxin Mviic, 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
    https://www.bioz.com/result/ω conotoxin mviic/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
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    93/100 stars

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    w conotoxin mviic 2  (Alomone Labs)


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    Alomone Labs w conotoxin mviic 2
    W Conotoxin Mviic 2, 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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    protein kinase c inhibitor k252a  (Alomone Labs)


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    Alomone Labs protein kinase c inhibitor k252a
    Protein Kinase C Inhibitor K252a, 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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    protein kinase c inhibitor k252a  (Alomone Labs)


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    Alomone Labs protein kinase c inhibitor k252a
    Protein Kinase C Inhibitor K252a, 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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    ω conotoxin mviic  (Alomone Labs)


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    Alomone Labs ω conotoxin mviic
    ω Conotoxin Mviic, 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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    ω conotoxin mviic  (Alomone Labs)


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    Alomone Labs ω conotoxin mviic
    Calcium influx through Ca V 1.2 induces PKA-II activity during depolarization. (A) Expression pattern of VGCC α subunits in overnight cultures of rat and mouse DRG determined by RNA-seq . TPM, transcripts per kilobase million. (B) Expression pattern of VGCC α subunits in mouse DRG neuron subgroups determined by single-cell RNA-seq . (C) Time course of pRII intensity in KCl-depolarized rat sensory neurons after pretreatment (10 min) with the NMDA receptor antagonist D-AP5 (10 µM), the Cav3.1-3.3 blocker TTA-P2 (1 µM), and a combination of the Cav2.1/2.2 blocker ω-agatoxin IVA (100 nM), <t>ω-conotoxin</t> <t>MVIIC</t> (200 nM), and ω-conotoxin GVIA (1 µM). (D) Inhibitory effect of verapamil (20 or 200 µM, 10-min pretreatment) on the pRII increase induced by KCl depolarization. (E) Dose–response curve showing the effect of verapamil (0–200 µM; IC 50 = 16 µM) on pRII signals induced by KCl depolarization (3 min). (F) Inhibitory effect of diltiazem (100 µM, 10 min) on the KCl-induced pRII increase. (G) Dose–response curve showing the inhibition of KCl-induced pRII signals by diltiazem (0–200 µM; IC 50 = 37 µM). (H) Reinforcing effect of the Ca V 1 agonist (S)-(-)-Bay K 8644 (2 µM, 10 min) on pRII signals induced by a low dose of KCl (10 mM). (I) Dose–response curve showing the reinforcing effect of Bay K 8644 (0–5 µM; EC 50 = 80 nM) on pRII signals induced by KCl (10 mM, 3 min). (J) Chelation of extracellular calcium with EGTA (2.5 mM, 30-min prestimulation) abolished the pRII response to KCl-depolarization. (K) Effect of the cell-permeable calcium chelator BAPTA-AM (100 µM, 60 min) on pRII signals induced by KCl depolarization (compound effect: F 1,28 = 10.9, P < 0.003). Values in C–K represent means ± SEM; n = 3–4 experiments; >2,000 neurons/condition; two-way ANOVA with Bonferroni’s test; § , P < 0.05; §§ , P < 0.01; §§§ , P < 0.001 indicate significance levels between KCl-induced pRII signals in the absence or presence of an agonist/antagonist.
    ω Conotoxin Mviic, 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
    https://www.bioz.com/result/ω conotoxin mviic/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ω conotoxin mviic - by Bioz Stars, 2023-09
    93/100 stars

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    1) Product Images from "Depolarization induces nociceptor sensitization by Ca V 1.2-mediated PKA-II activation"

    Article Title: Depolarization induces nociceptor sensitization by Ca V 1.2-mediated PKA-II activation

    Journal: The Journal of Cell Biology

    doi: 10.1083/jcb.202002083

    Calcium influx through Ca V 1.2 induces PKA-II activity during depolarization. (A) Expression pattern of VGCC α subunits in overnight cultures of rat and mouse DRG determined by RNA-seq . TPM, transcripts per kilobase million. (B) Expression pattern of VGCC α subunits in mouse DRG neuron subgroups determined by single-cell RNA-seq . (C) Time course of pRII intensity in KCl-depolarized rat sensory neurons after pretreatment (10 min) with the NMDA receptor antagonist D-AP5 (10 µM), the Cav3.1-3.3 blocker TTA-P2 (1 µM), and a combination of the Cav2.1/2.2 blocker ω-agatoxin IVA (100 nM), ω-conotoxin MVIIC (200 nM), and ω-conotoxin GVIA (1 µM). (D) Inhibitory effect of verapamil (20 or 200 µM, 10-min pretreatment) on the pRII increase induced by KCl depolarization. (E) Dose–response curve showing the effect of verapamil (0–200 µM; IC 50 = 16 µM) on pRII signals induced by KCl depolarization (3 min). (F) Inhibitory effect of diltiazem (100 µM, 10 min) on the KCl-induced pRII increase. (G) Dose–response curve showing the inhibition of KCl-induced pRII signals by diltiazem (0–200 µM; IC 50 = 37 µM). (H) Reinforcing effect of the Ca V 1 agonist (S)-(-)-Bay K 8644 (2 µM, 10 min) on pRII signals induced by a low dose of KCl (10 mM). (I) Dose–response curve showing the reinforcing effect of Bay K 8644 (0–5 µM; EC 50 = 80 nM) on pRII signals induced by KCl (10 mM, 3 min). (J) Chelation of extracellular calcium with EGTA (2.5 mM, 30-min prestimulation) abolished the pRII response to KCl-depolarization. (K) Effect of the cell-permeable calcium chelator BAPTA-AM (100 µM, 60 min) on pRII signals induced by KCl depolarization (compound effect: F 1,28 = 10.9, P < 0.003). Values in C–K represent means ± SEM; n = 3–4 experiments; >2,000 neurons/condition; two-way ANOVA with Bonferroni’s test; § , P < 0.05; §§ , P < 0.01; §§§ , P < 0.001 indicate significance levels between KCl-induced pRII signals in the absence or presence of an agonist/antagonist.
    Figure Legend Snippet: Calcium influx through Ca V 1.2 induces PKA-II activity during depolarization. (A) Expression pattern of VGCC α subunits in overnight cultures of rat and mouse DRG determined by RNA-seq . TPM, transcripts per kilobase million. (B) Expression pattern of VGCC α subunits in mouse DRG neuron subgroups determined by single-cell RNA-seq . (C) Time course of pRII intensity in KCl-depolarized rat sensory neurons after pretreatment (10 min) with the NMDA receptor antagonist D-AP5 (10 µM), the Cav3.1-3.3 blocker TTA-P2 (1 µM), and a combination of the Cav2.1/2.2 blocker ω-agatoxin IVA (100 nM), ω-conotoxin MVIIC (200 nM), and ω-conotoxin GVIA (1 µM). (D) Inhibitory effect of verapamil (20 or 200 µM, 10-min pretreatment) on the pRII increase induced by KCl depolarization. (E) Dose–response curve showing the effect of verapamil (0–200 µM; IC 50 = 16 µM) on pRII signals induced by KCl depolarization (3 min). (F) Inhibitory effect of diltiazem (100 µM, 10 min) on the KCl-induced pRII increase. (G) Dose–response curve showing the inhibition of KCl-induced pRII signals by diltiazem (0–200 µM; IC 50 = 37 µM). (H) Reinforcing effect of the Ca V 1 agonist (S)-(-)-Bay K 8644 (2 µM, 10 min) on pRII signals induced by a low dose of KCl (10 mM). (I) Dose–response curve showing the reinforcing effect of Bay K 8644 (0–5 µM; EC 50 = 80 nM) on pRII signals induced by KCl (10 mM, 3 min). (J) Chelation of extracellular calcium with EGTA (2.5 mM, 30-min prestimulation) abolished the pRII response to KCl-depolarization. (K) Effect of the cell-permeable calcium chelator BAPTA-AM (100 µM, 60 min) on pRII signals induced by KCl depolarization (compound effect: F 1,28 = 10.9, P < 0.003). Values in C–K represent means ± SEM; n = 3–4 experiments; >2,000 neurons/condition; two-way ANOVA with Bonferroni’s test; § , P < 0.05; §§ , P < 0.01; §§§ , P < 0.001 indicate significance levels between KCl-induced pRII signals in the absence or presence of an agonist/antagonist.

    Techniques Used: Activity Assay, Expressing, RNA Sequencing Assay, Inhibition

    ω conotoxin mviic  (Alomone Labs)


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    Alomone Labs ω conotoxin mviic
    ω Conotoxin Mviic, 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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    ω conotoxin mviic  (Alomone Labs)


    Bioz Verified Symbol Alomone Labs is a verified supplier
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    Alomone Labs ω conotoxin mviic
    ω Conotoxin Mviic, 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
    https://www.bioz.com/result/ω conotoxin mviic/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
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    Alomone Labs ω conotoxin mviic
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    w conotoxin mviic 2  (Alomone Labs)
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    W Conotoxin Mviic 2, 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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    protein kinase c inhibitor k252a  (Alomone Labs)
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    Alomone Labs protein kinase c inhibitor k252a
    Protein Kinase C Inhibitor K252a, 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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