apc101  (Alomone Labs)


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    Alomone Labs apc101
    Apc101, 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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    apc101 - by Bioz Stars, 2022-05
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    Alomone Labs xe991 dihydrochloride
    Kv7.4 is a regulation target of 5-HT 1A auto-inhibition. (A1) 5-HT 1A receptor agonist 8-OH-DPAT increased the Kv7 current in DRN 5-HT neurons of WT mice and the effect was reversed by <t>XE991.</t> (A2) Voltage clamping protocol and the corresponding traces recorded from (A1) . (A3) Summarized data for experiments shown in (A1) (paired samples test, ** P
    Xe991 Dihydrochloride, 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/xe991 dihydrochloride/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    xe991 dihydrochloride - by Bioz Stars, 2022-05
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    94
    Alomone Labs anti kv1 3
    Inhibition of mitochondrial <t>Kv1.3</t> kills PANC-1 cells. (A) PANC-1 cells were treated or left untreated with different membrane permeant Kv1.3 inhibitors (PAPTP 10 µM, PCARBTP 10 µM, and clofazimine 20 µM) for 24 h. Cell death was determined by staining with an Alexa568 coupled Annexin V by fluorescent microscopy. The images are representative of three different replicates. (B) Quantification of Annexin V-positive cells from the experiments shown in (A) : represented is the percentage of Annexin V-positive cells ± SEM ( n = 3; ** p
    Anti Kv1 3, 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 kv1 3/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
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    88
    Alomone Labs retigabine dihydrochloride
    KCNQ activation increases flurothyl-induced seizure latencies in Kcnq1 mice and decreases spontaneous seizure frequency in Kcna1 −/− mice. ( A ) Administration of RTG (10 mg·kg −1 , ip) had no significant effect on latency to flurothyl-induced myoclonic jerks (MJ) in Tac:N:NIHS-BC Kcna1 +/+ and Kcna1 −/− mice. However, RTG decreased latency to myoclonic jerk in Kcnq1 A340E/A340E mutant mice ( B ). ( C ) Administration of RTG (10 mg·kg −1 , ip) had no significant effect on latency to flurothyl-induced generalized tonic-clonic seizures (GTCS) in Tac:N:NIHS-BC Kcna1 +/+ and Kcna1 −/− mice. However, RTG significantly increased the latency to GTCS in Kcnq1 strain (C57BL/6) mice ( D ). ( E ) EEG traces showing representative spontaneous seizure activity in Kcna1 −/− mice after receiving either VEH or RTG (10 mg·kg −1 ). ( F ) Analysis of spontaneous seizure frequency in Kcna1 −/− mice (n = 6) showed a significant decrease after treatment with 10 mg·kg −1 RTG. ( G ) Average spontaneous seizure durations were similar in Kcna1 −/− mice that exhibited seizures after VEH and 10 mg·kg −1 RTG administration (n = 3). For ( A-D ): *, P ≤ 0.05; **, P ≤ 0.01 (two-tailed unpaired Student’s t -test; n = 6–11 per treatment). For ( F ) and ( G ): *, P ≤ 0.05 (two-tailed paired Student’s t -test). Abbreviations: LT, left temporal; VEH, vehicle; RTG, <t>retigabine;</t> NS, not significant compared to VEH control.
    Retigabine Dihydrochloride, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/retigabine dihydrochloride/product/Alomone Labs
    Average 88 stars, based on 1 article reviews
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    Kv7.4 is a regulation target of 5-HT 1A auto-inhibition. (A1) 5-HT 1A receptor agonist 8-OH-DPAT increased the Kv7 current in DRN 5-HT neurons of WT mice and the effect was reversed by XE991. (A2) Voltage clamping protocol and the corresponding traces recorded from (A1) . (A3) Summarized data for experiments shown in (A1) (paired samples test, ** P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Selective Modulation of K+ Channel Kv7.4 Significantly Affects the Excitability of DRN 5-HT Neurons

    doi: 10.3389/fncel.2017.00405

    Figure Lengend Snippet: Kv7.4 is a regulation target of 5-HT 1A auto-inhibition. (A1) 5-HT 1A receptor agonist 8-OH-DPAT increased the Kv7 current in DRN 5-HT neurons of WT mice and the effect was reversed by XE991. (A2) Voltage clamping protocol and the corresponding traces recorded from (A1) . (A3) Summarized data for experiments shown in (A1) (paired samples test, ** P

    Article Snippet: XE991 dihydrochloride was from the Alomone Labs (Jerusalem, Israel).

    Techniques: Inhibition, Mouse Assay

    Fasudil potently augments Kv7.4 currents in DRN 5-HT neurons. (A1) Sample time course shows that fasudil (30 μM) augments Kv7 current, which is completely blocked by XE991 (3 μM) in neurons from WT mice. (A2) Voltage clamping protocol and the corresponding current traces recorded from (A1) . (A3) Summarized data for the experiment shown in (A1) (Wilcoxon Singed Ranks Test, * P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Selective Modulation of K+ Channel Kv7.4 Significantly Affects the Excitability of DRN 5-HT Neurons

    doi: 10.3389/fncel.2017.00405

    Figure Lengend Snippet: Fasudil potently augments Kv7.4 currents in DRN 5-HT neurons. (A1) Sample time course shows that fasudil (30 μM) augments Kv7 current, which is completely blocked by XE991 (3 μM) in neurons from WT mice. (A2) Voltage clamping protocol and the corresponding current traces recorded from (A1) . (A3) Summarized data for the experiment shown in (A1) (Wilcoxon Singed Ranks Test, * P

    Article Snippet: XE991 dihydrochloride was from the Alomone Labs (Jerusalem, Israel).

    Techniques: Mouse Assay

    Kv7.4 activity modulates the excitability of the DRN 5-HT neurons. (A,B) Effects of fasudil on the elicited firing activity of DRN 5-HT neurons from WT mice and Kv7.4 −/− mice. (A1) Fasudil (30 μM) significantly hyperpolarized resting membrane potential (RMP) and the effect completely reversed by XE991 (3 μM) in WT mice. (A2) Typical traces with firing activity elicited by depolarizing 250 pA current injection, recorded from a neuron of WT mice. (A3) Summary of RMP in response to fasudil (30 μM) in WT DRN 5-HT neurons (paired samples test, *** P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Selective Modulation of K+ Channel Kv7.4 Significantly Affects the Excitability of DRN 5-HT Neurons

    doi: 10.3389/fncel.2017.00405

    Figure Lengend Snippet: Kv7.4 activity modulates the excitability of the DRN 5-HT neurons. (A,B) Effects of fasudil on the elicited firing activity of DRN 5-HT neurons from WT mice and Kv7.4 −/− mice. (A1) Fasudil (30 μM) significantly hyperpolarized resting membrane potential (RMP) and the effect completely reversed by XE991 (3 μM) in WT mice. (A2) Typical traces with firing activity elicited by depolarizing 250 pA current injection, recorded from a neuron of WT mice. (A3) Summary of RMP in response to fasudil (30 μM) in WT DRN 5-HT neurons (paired samples test, *** P

    Article Snippet: XE991 dihydrochloride was from the Alomone Labs (Jerusalem, Israel).

    Techniques: Activity Assay, Mouse Assay, Injection

    5-HT augments Kv7.4 currents in DRN 5-HT neurons. (A1) Sample time course shows that 5-HT (30 μM) induced a sharp augmentation of Kv7 current and the augmentation was completely reversed by XE991 (3 μM) in DRN 5-HT neurons of WT mice. (A2) Voltage clamping protocol and representative current traces recorded from (A1) . (A3) Summarized data for experiments shown in (A1) (Wilcoxon Signed Ranks Test, *** P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Selective Modulation of K+ Channel Kv7.4 Significantly Affects the Excitability of DRN 5-HT Neurons

    doi: 10.3389/fncel.2017.00405

    Figure Lengend Snippet: 5-HT augments Kv7.4 currents in DRN 5-HT neurons. (A1) Sample time course shows that 5-HT (30 μM) induced a sharp augmentation of Kv7 current and the augmentation was completely reversed by XE991 (3 μM) in DRN 5-HT neurons of WT mice. (A2) Voltage clamping protocol and representative current traces recorded from (A1) . (A3) Summarized data for experiments shown in (A1) (Wilcoxon Signed Ranks Test, *** P

    Article Snippet: XE991 dihydrochloride was from the Alomone Labs (Jerusalem, Israel).

    Techniques: Mouse Assay

    Inhibition of mitochondrial Kv1.3 kills PANC-1 cells. (A) PANC-1 cells were treated or left untreated with different membrane permeant Kv1.3 inhibitors (PAPTP 10 µM, PCARBTP 10 µM, and clofazimine 20 µM) for 24 h. Cell death was determined by staining with an Alexa568 coupled Annexin V by fluorescent microscopy. The images are representative of three different replicates. (B) Quantification of Annexin V-positive cells from the experiments shown in (A) : represented is the percentage of Annexin V-positive cells ± SEM ( n = 3; ** p

    Journal: Frontiers in Oncology

    Article Title: Regulation of Proliferation by a Mitochondrial Potassium Channel in Pancreatic Ductal Adenocarcinoma Cells

    doi: 10.3389/fonc.2017.00239

    Figure Lengend Snippet: Inhibition of mitochondrial Kv1.3 kills PANC-1 cells. (A) PANC-1 cells were treated or left untreated with different membrane permeant Kv1.3 inhibitors (PAPTP 10 µM, PCARBTP 10 µM, and clofazimine 20 µM) for 24 h. Cell death was determined by staining with an Alexa568 coupled Annexin V by fluorescent microscopy. The images are representative of three different replicates. (B) Quantification of Annexin V-positive cells from the experiments shown in (A) : represented is the percentage of Annexin V-positive cells ± SEM ( n = 3; ** p

    Article Snippet: After blocking with a 10% solution of defatted milk, the membranes were incubated overnight at 4°C with the following primary antibodies: anti-Kv1.3 (1:200, rabbit polyclonal; Alomone Labs APC-101); anti-GAPDH (1:1,000, mouse monoclonal; Millipore MAB374).

    Techniques: Inhibition, Staining, Microscopy

    Sublethal inhibition of mitochondrial Kv1.3 leads to cell cycle alterations. (A) FACS analysis of cell cycle of PANC-1 cells untreated or treated with clofazimine 1 µM and ShK 100 nM for 24 h. The distribution was determined by staining cells with 50 µg/mL Propidium Iodide and the acquisition was performed by a FACSantoII (Beckton Dickson). The plots are representative of three separated determinations. Light blue peaks represent apoptotic cells, while red peaks represent cells in G1 and G2/M phases. S phase is represented by the area with blue straight lines. A sub-G1 peak is due to dead cells. In the graph of untreated cells the labels and the arrows identify the different populations that are reported. (B) Cell cycle distribution in PANC-1 cells pretreated (lower panels) or not (upper panels) with 50 µM Mitotempo or 20 mM N-acetylcysteine (NAC) for 1 h, before the addition of mitochondrial Kv1.3 inhibitors PAPTP and PCARBTP (both at 100 nM) for 24 h. The experiment and the analysis have been performed as in (A) . The plots are representative of three separate measurements.

    Journal: Frontiers in Oncology

    Article Title: Regulation of Proliferation by a Mitochondrial Potassium Channel in Pancreatic Ductal Adenocarcinoma Cells

    doi: 10.3389/fonc.2017.00239

    Figure Lengend Snippet: Sublethal inhibition of mitochondrial Kv1.3 leads to cell cycle alterations. (A) FACS analysis of cell cycle of PANC-1 cells untreated or treated with clofazimine 1 µM and ShK 100 nM for 24 h. The distribution was determined by staining cells with 50 µg/mL Propidium Iodide and the acquisition was performed by a FACSantoII (Beckton Dickson). The plots are representative of three separated determinations. Light blue peaks represent apoptotic cells, while red peaks represent cells in G1 and G2/M phases. S phase is represented by the area with blue straight lines. A sub-G1 peak is due to dead cells. In the graph of untreated cells the labels and the arrows identify the different populations that are reported. (B) Cell cycle distribution in PANC-1 cells pretreated (lower panels) or not (upper panels) with 50 µM Mitotempo or 20 mM N-acetylcysteine (NAC) for 1 h, before the addition of mitochondrial Kv1.3 inhibitors PAPTP and PCARBTP (both at 100 nM) for 24 h. The experiment and the analysis have been performed as in (A) . The plots are representative of three separate measurements.

    Article Snippet: After blocking with a 10% solution of defatted milk, the membranes were incubated overnight at 4°C with the following primary antibodies: anti-Kv1.3 (1:200, rabbit polyclonal; Alomone Labs APC-101); anti-GAPDH (1:1,000, mouse monoclonal; Millipore MAB374).

    Techniques: Inhibition, FACS, Staining

    Potassium channel Kv1.3 is expressed in PANC-1 cells. (A) Kv1.3 expression was determined by Western Blot in PANC-1 cells. 60 µg of total protein extract were loaded into a SDS gel and blotted onto a polyvinylidene fluoride (PVDF) membrane. Kv1.3 band was evaluated by immunoblotting with a specific antibody. GAPDH was used as loading control. The blot is a representative image of three different observations. (B) Inhibition of mitochondrial Kv1.3 by different concentration of membrane permeant blockers resulted in a reduction of the MTS signal from PANC-1 cells. Values are reported as percentage respect to untreated sample ± SEM. All compounds were added for 24 h. Staurosporine was used as positive control ( n = 3; *** p

    Journal: Frontiers in Oncology

    Article Title: Regulation of Proliferation by a Mitochondrial Potassium Channel in Pancreatic Ductal Adenocarcinoma Cells

    doi: 10.3389/fonc.2017.00239

    Figure Lengend Snippet: Potassium channel Kv1.3 is expressed in PANC-1 cells. (A) Kv1.3 expression was determined by Western Blot in PANC-1 cells. 60 µg of total protein extract were loaded into a SDS gel and blotted onto a polyvinylidene fluoride (PVDF) membrane. Kv1.3 band was evaluated by immunoblotting with a specific antibody. GAPDH was used as loading control. The blot is a representative image of three different observations. (B) Inhibition of mitochondrial Kv1.3 by different concentration of membrane permeant blockers resulted in a reduction of the MTS signal from PANC-1 cells. Values are reported as percentage respect to untreated sample ± SEM. All compounds were added for 24 h. Staurosporine was used as positive control ( n = 3; *** p

    Article Snippet: After blocking with a 10% solution of defatted milk, the membranes were incubated overnight at 4°C with the following primary antibodies: anti-Kv1.3 (1:200, rabbit polyclonal; Alomone Labs APC-101); anti-GAPDH (1:1,000, mouse monoclonal; Millipore MAB374).

    Techniques: Expressing, Western Blot, SDS-Gel, Inhibition, Concentration Assay, Positive Control

    Characterization of the Kv1.3 and Kv1.5 mutant channels containing the YS segment. A , average normalized activation and inactivation curves are shown as conductance-voltage relationships for Kv1.3, Kv1.5, the truncated Kv1.3-YS channel, and the chimeras Kv1.5-YS 532 and Kv1.5-YS 613 . All datasets were fitted to Boltzmann functions. Each data point is the mean ± S.E. of 6–11 cells. B , confocal images of non-permeabilized cells transfected with Kv1.3-YS-Cherry, Kv1.5-YS 532 -EGFP, and Kv1.5-YS 613 -EGFP. An extracellular anti-Kv1.3 antibody was used to label Kv1.3-YS ( green ), whereas the extracellular anti-Kv1.5 antibody was used for Kv1.5-YS 532 and Kv1.5-YS 613 chimeras ( red ). Nuclei were stained by Hoechst ( blue ). C , proliferation rate of the indicated channels or GFP-transfected cells (control) was determined by measuring EdU incorporation. Significant differences when comparing to Kv1.3 (*) or to control (#) are indicated. Statistical analysis was performed with one-way ANOVA followed by a Tukey's HSD multiple comparison. Each bar is the average of 9–15 determinations from 5 different assays. D , the average peak current amplitude obtained in cell-attached experiments for Kv1.5 channels and all the Kv1.5 chimeras was plotted against the % of the channels expressed at the plasma membrane ( upper graph ) or their normalized effect on proliferation (taking 100% as the proliferation rate of GFP-transfected HEK cells, lower graph ). The correlation between expression and current was fit to a linear regression curve ( y = 18.54 + 0.0066x, R 2 = 0.85, p = 0.008), but there was no correlation between proliferation and current amplitude ( R 2 = 0.23, p = 0.19).

    Journal: The Journal of Biological Chemistry

    Article Title: Molecular Determinants of Kv1.3 Potassium Channels-induced Proliferation *

    doi: 10.1074/jbc.M115.678995

    Figure Lengend Snippet: Characterization of the Kv1.3 and Kv1.5 mutant channels containing the YS segment. A , average normalized activation and inactivation curves are shown as conductance-voltage relationships for Kv1.3, Kv1.5, the truncated Kv1.3-YS channel, and the chimeras Kv1.5-YS 532 and Kv1.5-YS 613 . All datasets were fitted to Boltzmann functions. Each data point is the mean ± S.E. of 6–11 cells. B , confocal images of non-permeabilized cells transfected with Kv1.3-YS-Cherry, Kv1.5-YS 532 -EGFP, and Kv1.5-YS 613 -EGFP. An extracellular anti-Kv1.3 antibody was used to label Kv1.3-YS ( green ), whereas the extracellular anti-Kv1.5 antibody was used for Kv1.5-YS 532 and Kv1.5-YS 613 chimeras ( red ). Nuclei were stained by Hoechst ( blue ). C , proliferation rate of the indicated channels or GFP-transfected cells (control) was determined by measuring EdU incorporation. Significant differences when comparing to Kv1.3 (*) or to control (#) are indicated. Statistical analysis was performed with one-way ANOVA followed by a Tukey's HSD multiple comparison. Each bar is the average of 9–15 determinations from 5 different assays. D , the average peak current amplitude obtained in cell-attached experiments for Kv1.5 channels and all the Kv1.5 chimeras was plotted against the % of the channels expressed at the plasma membrane ( upper graph ) or their normalized effect on proliferation (taking 100% as the proliferation rate of GFP-transfected HEK cells, lower graph ). The correlation between expression and current was fit to a linear regression curve ( y = 18.54 + 0.0066x, R 2 = 0.85, p = 0.008), but there was no correlation between proliferation and current amplitude ( R 2 = 0.23, p = 0.19).

    Article Snippet: Non-permeabilized cells were incubated with anti-Kv1.3 or anti Kv1.5 extracellular primary antibodies (APC101 or APC150, Alomone Labs), whereas permeabilized cells were incubated with anti-Kv1.3 COOH (75-009, NeuroMab) or anti-Kv1.5 COOH (APC004, Alomone Labs), all at a final concentration of 1:50.

    Techniques: Mutagenesis, Activation Assay, Transfection, Staining, Expressing

    KCNQ activation increases flurothyl-induced seizure latencies in Kcnq1 mice and decreases spontaneous seizure frequency in Kcna1 −/− mice. ( A ) Administration of RTG (10 mg·kg −1 , ip) had no significant effect on latency to flurothyl-induced myoclonic jerks (MJ) in Tac:N:NIHS-BC Kcna1 +/+ and Kcna1 −/− mice. However, RTG decreased latency to myoclonic jerk in Kcnq1 A340E/A340E mutant mice ( B ). ( C ) Administration of RTG (10 mg·kg −1 , ip) had no significant effect on latency to flurothyl-induced generalized tonic-clonic seizures (GTCS) in Tac:N:NIHS-BC Kcna1 +/+ and Kcna1 −/− mice. However, RTG significantly increased the latency to GTCS in Kcnq1 strain (C57BL/6) mice ( D ). ( E ) EEG traces showing representative spontaneous seizure activity in Kcna1 −/− mice after receiving either VEH or RTG (10 mg·kg −1 ). ( F ) Analysis of spontaneous seizure frequency in Kcna1 −/− mice (n = 6) showed a significant decrease after treatment with 10 mg·kg −1 RTG. ( G ) Average spontaneous seizure durations were similar in Kcna1 −/− mice that exhibited seizures after VEH and 10 mg·kg −1 RTG administration (n = 3). For ( A-D ): *, P ≤ 0.05; **, P ≤ 0.01 (two-tailed unpaired Student’s t -test; n = 6–11 per treatment). For ( F ) and ( G ): *, P ≤ 0.05 (two-tailed paired Student’s t -test). Abbreviations: LT, left temporal; VEH, vehicle; RTG, retigabine; NS, not significant compared to VEH control.

    Journal: Epilepsia

    Article Title: Pharmacogenetics of KCNQ channel activation in two potassium channelopathy mouse models of epilepsy

    doi: 10.1111/epi.13978

    Figure Lengend Snippet: KCNQ activation increases flurothyl-induced seizure latencies in Kcnq1 mice and decreases spontaneous seizure frequency in Kcna1 −/− mice. ( A ) Administration of RTG (10 mg·kg −1 , ip) had no significant effect on latency to flurothyl-induced myoclonic jerks (MJ) in Tac:N:NIHS-BC Kcna1 +/+ and Kcna1 −/− mice. However, RTG decreased latency to myoclonic jerk in Kcnq1 A340E/A340E mutant mice ( B ). ( C ) Administration of RTG (10 mg·kg −1 , ip) had no significant effect on latency to flurothyl-induced generalized tonic-clonic seizures (GTCS) in Tac:N:NIHS-BC Kcna1 +/+ and Kcna1 −/− mice. However, RTG significantly increased the latency to GTCS in Kcnq1 strain (C57BL/6) mice ( D ). ( E ) EEG traces showing representative spontaneous seizure activity in Kcna1 −/− mice after receiving either VEH or RTG (10 mg·kg −1 ). ( F ) Analysis of spontaneous seizure frequency in Kcna1 −/− mice (n = 6) showed a significant decrease after treatment with 10 mg·kg −1 RTG. ( G ) Average spontaneous seizure durations were similar in Kcna1 −/− mice that exhibited seizures after VEH and 10 mg·kg −1 RTG administration (n = 3). For ( A-D ): *, P ≤ 0.05; **, P ≤ 0.01 (two-tailed unpaired Student’s t -test; n = 6–11 per treatment). For ( F ) and ( G ): *, P ≤ 0.05 (two-tailed paired Student’s t -test). Abbreviations: LT, left temporal; VEH, vehicle; RTG, retigabine; NS, not significant compared to VEH control.

    Article Snippet: Retigabine dihydrochloride (RTG; Alomone Labs, Jerusalem, Israel) was administered at a concentration of 5, 10, or 20 mg·kg−1 , as specified in the text.

    Techniques: Activation Assay, Mouse Assay, Mutagenesis, Activity Assay, Two Tailed Test