cacna1b  (Alomone Labs)


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    Alomone Labs cacna1b
    Cacna1b, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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  • 94
    Alomone Labs bay k8644
    Effects of BIII 890CL on Ca 2+ responses triggered by VTD or Bay <t>K8644.</t> ( A ) Representative Fura-2 fluorescence kinetic traces illustrating Ca 2+ response induced by 10 µM of VTD, alone or co-injected with 1 µM of TTX or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. ( B ) Concentration–inhibition relationship of VTD-induced Ca 2+ responses by BIII 890CL, (IC50 = 1.47 ± 0.18 µM, Hill slope = 1.26 ± 0.23, R 2 = 0.94). ( C ) Representative Fura-2 fluorescence kinetics traces illustrating Ca 2+ response induced by 1 µM of Bay K8644, a specific L-type Ca V channel activator, alone or co-injected with 10 µM of nifedipine or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. Data represent the mean ± SEM ( n = 3) of recordings of two independent experiments.
    Bay K8644, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bay k8644/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bay k8644 - by Bioz Stars, 2022-10
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    94
    Alomone Labs anti cacna1a cav2 1 antibody
    a Representative confocal image of a nerve terminal arborization. Singly, dually, and innervated by three or more axons NMJs from YFP muscles and also images of the morphologic maturation (S1, the most inmature, and S4, almost fully differentiated, stages) of the postsynaptic clusters from P9 mice. The bar indicates 10 μm. b Confocal immunofluorescence location of α 1D L-, N-, and P/Q-type voltage-dependent calcium channels (VDCCs) at the NMJ. Triple labeling of VDCCs (green fluorescence) with syntaxin (blue fluorescence) and nAChR-α-bungarotoxin (red fluorescence) in merge images. Figure shows the presence of α 1D L-, <t>N-,</t> <t>and</t> <t>P/Q-type-VDCC</t> (in green) in the nerve terminal of P9 Levator auris longus (LAL) muscle endplates. The bar indicates 10 μm
    Anti Cacna1a Cav2 1 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti cacna1a cav2 1 antibody/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti cacna1a cav2 1 antibody - by Bioz Stars, 2022-10
    94/100 stars
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    95
    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
    https://www.bioz.com/result/ω conotoxin gvia/product/Alomone Labs
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ω conotoxin gvia - by Bioz Stars, 2022-10
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    Effects of BIII 890CL on Ca 2+ responses triggered by VTD or Bay K8644. ( A ) Representative Fura-2 fluorescence kinetic traces illustrating Ca 2+ response induced by 10 µM of VTD, alone or co-injected with 1 µM of TTX or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. ( B ) Concentration–inhibition relationship of VTD-induced Ca 2+ responses by BIII 890CL, (IC50 = 1.47 ± 0.18 µM, Hill slope = 1.26 ± 0.23, R 2 = 0.94). ( C ) Representative Fura-2 fluorescence kinetics traces illustrating Ca 2+ response induced by 1 µM of Bay K8644, a specific L-type Ca V channel activator, alone or co-injected with 10 µM of nifedipine or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. Data represent the mean ± SEM ( n = 3) of recordings of two independent experiments.

    Journal: International Journal of Molecular Sciences

    Article Title: Pharmacological Dissection of the Crosstalk between NaV and CaV Channels in GH3b6 Cells

    doi: 10.3390/ijms23020827

    Figure Lengend Snippet: Effects of BIII 890CL on Ca 2+ responses triggered by VTD or Bay K8644. ( A ) Representative Fura-2 fluorescence kinetic traces illustrating Ca 2+ response induced by 10 µM of VTD, alone or co-injected with 1 µM of TTX or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. ( B ) Concentration–inhibition relationship of VTD-induced Ca 2+ responses by BIII 890CL, (IC50 = 1.47 ± 0.18 µM, Hill slope = 1.26 ± 0.23, R 2 = 0.94). ( C ) Representative Fura-2 fluorescence kinetics traces illustrating Ca 2+ response induced by 1 µM of Bay K8644, a specific L-type Ca V channel activator, alone or co-injected with 10 µM of nifedipine or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. Data represent the mean ± SEM ( n = 3) of recordings of two independent experiments.

    Article Snippet: BIII 890 CL, such as BI 55 CL, was kindly provided by Boehringer Ingelheim (Biberach an der Riss, Germany) and Bay K8644 was from Alomone (Jerusalem, Israel).

    Techniques: Fluorescence, Injection, Negative Control, Concentration Assay, Inhibition

    a Representative confocal image of a nerve terminal arborization. Singly, dually, and innervated by three or more axons NMJs from YFP muscles and also images of the morphologic maturation (S1, the most inmature, and S4, almost fully differentiated, stages) of the postsynaptic clusters from P9 mice. The bar indicates 10 μm. b Confocal immunofluorescence location of α 1D L-, N-, and P/Q-type voltage-dependent calcium channels (VDCCs) at the NMJ. Triple labeling of VDCCs (green fluorescence) with syntaxin (blue fluorescence) and nAChR-α-bungarotoxin (red fluorescence) in merge images. Figure shows the presence of α 1D L-, N-, and P/Q-type-VDCC (in green) in the nerve terminal of P9 Levator auris longus (LAL) muscle endplates. The bar indicates 10 μm

    Journal: Molecular Neurobiology

    Article Title: Involvement of the Voltage-Gated Calcium Channels L- P/Q- and N-Types in Synapse Elimination During Neuromuscular Junction Development

    doi: 10.1007/s12035-022-02818-2

    Figure Lengend Snippet: a Representative confocal image of a nerve terminal arborization. Singly, dually, and innervated by three or more axons NMJs from YFP muscles and also images of the morphologic maturation (S1, the most inmature, and S4, almost fully differentiated, stages) of the postsynaptic clusters from P9 mice. The bar indicates 10 μm. b Confocal immunofluorescence location of α 1D L-, N-, and P/Q-type voltage-dependent calcium channels (VDCCs) at the NMJ. Triple labeling of VDCCs (green fluorescence) with syntaxin (blue fluorescence) and nAChR-α-bungarotoxin (red fluorescence) in merge images. Figure shows the presence of α 1D L-, N-, and P/Q-type-VDCC (in green) in the nerve terminal of P9 Levator auris longus (LAL) muscle endplates. The bar indicates 10 μm

    Article Snippet: Muscles were incubated overnight at 4 °C with anti-CaV 1.3 (CACNA1D) antibody voltage-dependent L-type calcium channel subunit α1D (1/100; ACC-005, Alomone Labs, Jerusalem, Israel); anti-CaV 2.1 (CACNA1A) antibody voltage-dependent P/Q-type calcium channel subunit α1A (1/100; ACC-001, Alomone Labs, Jerusalem, Israel); anti-CaV 2.2 (CACNA1B) antibody voltage-dependent N-type calcium channel subunit α1B (1/100; ACC1-002, Alomone Labs, Jerusalem, Israel), and anti-mouse syntaxin (1/1000, S066, Sigma, St Louis, MO, USA).

    Techniques: Mouse Assay, Immunofluorescence, Labeling, Fluorescence

    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

    Inhibition of presynaptic voltage-gated Ca 2+ channels prevents axonal but not dendritic BDNF transport defects. (A) Representative images of MAP2 and AβO immunocytochemistry. Pretreatment of tau −/− neurons with 50 μM ω-agatoxin IVA (P/Q-type channel blocker), 100 μM ω-conotoxin GVIA (N-type channel blocker), 10 μM nimodipine, or 1.5 mM EGTA did not prevent AβO binding. (B) Inhibition of P/Q- and N-type VGCCs prevented axonal BDNF transport defects independent of tau. Consistent with the absence of L-type Ca 2+ channels in axons, nimodipine pretreatment did not prevent AβO-induced transport defects. Extracellular Ca 2+ chelation with EGTA precluded FAT disruption. (C) By contrast, in dendrites, inhibition of P/Q- and N-type VGCCs failed to prevent AβO-induced transport defects. Pretreatment with nimodipine or EGTA also did not prevent AβO-induced transport defects. Graphs show means ± SEM. A minimum of 15 cells from three different cultures were analyzed per condition; *** p

    Journal: Molecular Biology of the Cell

    Article Title: Dendritic and axonal mechanisms of Ca2+ elevation impair BDNF transport in Aβ oligomer–treated hippocampal neurons

    doi: 10.1091/mbc.E14-12-1612

    Figure Lengend Snippet: Inhibition of presynaptic voltage-gated Ca 2+ channels prevents axonal but not dendritic BDNF transport defects. (A) Representative images of MAP2 and AβO immunocytochemistry. Pretreatment of tau −/− neurons with 50 μM ω-agatoxin IVA (P/Q-type channel blocker), 100 μM ω-conotoxin GVIA (N-type channel blocker), 10 μM nimodipine, or 1.5 mM EGTA did not prevent AβO binding. (B) Inhibition of P/Q- and N-type VGCCs prevented axonal BDNF transport defects independent of tau. Consistent with the absence of L-type Ca 2+ channels in axons, nimodipine pretreatment did not prevent AβO-induced transport defects. Extracellular Ca 2+ chelation with EGTA precluded FAT disruption. (C) By contrast, in dendrites, inhibition of P/Q- and N-type VGCCs failed to prevent AβO-induced transport defects. Pretreatment with nimodipine or EGTA also did not prevent AβO-induced transport defects. Graphs show means ± SEM. A minimum of 15 cells from three different cultures were analyzed per condition; *** p

    Article Snippet: For all VGCC inhibition experiments, cells were incubated with 100 μM conotoxin GVIA (Alomone Labs, Jerusalem, Israel), 50 μM agatoxin IVA (Alomone Labs), or 10 μM nimodipine (Tocris Bioscience, Bristol, United Kingdom) for 30 min before AβO treatments.

    Techniques: Inhibition, Immunocytochemistry, Binding Assay