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sk1  (Alomone Labs)


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    Alomone Labs sk1
    Apamin-sensitive SK2 channel-mediated mAHP currents may be linked to changes in neuronal spike frequency and adaptation at 24 h post-ketamine anesthesia. (A,B) Representative traces (A) and amplitudes (B) of the mAHP currents, treatment conditions as indicated. S1 slices from control (Ctrl) and ketamine-treated (Ket) rats were separately incubated and perfused with apamin (100 nM) or its vehicle. 22–25 neurons from 7–10 rats were used per condition. (C) Plots of spike frequency vs. current injected for layer II/III pyramidal neurons of S1. The significant differences in the spike frequency between the Ctrl and Ket groups (Ctrl: Vehicle vs. Ket: Vehicle, 80 pA, 100 pA and 110 pA, P < 0.01; 90 pA, P < 0.001) were eliminated after apamin treatment (Ctrl: Apamin vs. Ket: Apamin, P > 0.05). 20–22 neurons from 7–9 rats were recorded per condition. (D,E) Spikes in S1 layer II/III pyramidal neurons evoked for 3 s, 80 pA current injection (D) , and the adaptation index (E) was obtained by the algorithm mentioned above. 18–20 neurons from 7–9 rats were recorded per condition. (F) Quantitative analysis of <t>SK1-3</t> mRNA in S1 of P8 rats. 5 rats were used per condition. P > 0.05. (G,H) Immunoblots and quantitative analysis of total (G) and membrane-bound (H) SK1-3 levels in S1 of ketamine-treated rats, normalized to corresponding levels in control rats. 8–12 rats were used per condition. * P < 0.05, ** P < 0.01, *** P < 0.001; n.s ., not significant. Data were analyzed using the Mann-Whitney U test for (F,H) and unpaired two-tailed Student’s t-tests for the other panels. Data are shown as the mean ± SEM.
    Sk1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/apc-039/pmc13017914-81-6-8?v=Alomone+Labs
    Average 94 stars, based on 16 article reviews
    sk1 - by Bioz Stars, 2026-07
    94/100 stars

    Images

    1) Product Images from "Compensatory attenuation of cortical apoptosis by SK2 downregulation following ketamine anesthesia"

    Article Title: Compensatory attenuation of cortical apoptosis by SK2 downregulation following ketamine anesthesia

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2026.1761187

    Apamin-sensitive SK2 channel-mediated mAHP currents may be linked to changes in neuronal spike frequency and adaptation at 24 h post-ketamine anesthesia. (A,B) Representative traces (A) and amplitudes (B) of the mAHP currents, treatment conditions as indicated. S1 slices from control (Ctrl) and ketamine-treated (Ket) rats were separately incubated and perfused with apamin (100 nM) or its vehicle. 22–25 neurons from 7–10 rats were used per condition. (C) Plots of spike frequency vs. current injected for layer II/III pyramidal neurons of S1. The significant differences in the spike frequency between the Ctrl and Ket groups (Ctrl: Vehicle vs. Ket: Vehicle, 80 pA, 100 pA and 110 pA, P < 0.01; 90 pA, P < 0.001) were eliminated after apamin treatment (Ctrl: Apamin vs. Ket: Apamin, P > 0.05). 20–22 neurons from 7–9 rats were recorded per condition. (D,E) Spikes in S1 layer II/III pyramidal neurons evoked for 3 s, 80 pA current injection (D) , and the adaptation index (E) was obtained by the algorithm mentioned above. 18–20 neurons from 7–9 rats were recorded per condition. (F) Quantitative analysis of SK1-3 mRNA in S1 of P8 rats. 5 rats were used per condition. P > 0.05. (G,H) Immunoblots and quantitative analysis of total (G) and membrane-bound (H) SK1-3 levels in S1 of ketamine-treated rats, normalized to corresponding levels in control rats. 8–12 rats were used per condition. * P < 0.05, ** P < 0.01, *** P < 0.001; n.s ., not significant. Data were analyzed using the Mann-Whitney U test for (F,H) and unpaired two-tailed Student’s t-tests for the other panels. Data are shown as the mean ± SEM.
    Figure Legend Snippet: Apamin-sensitive SK2 channel-mediated mAHP currents may be linked to changes in neuronal spike frequency and adaptation at 24 h post-ketamine anesthesia. (A,B) Representative traces (A) and amplitudes (B) of the mAHP currents, treatment conditions as indicated. S1 slices from control (Ctrl) and ketamine-treated (Ket) rats were separately incubated and perfused with apamin (100 nM) or its vehicle. 22–25 neurons from 7–10 rats were used per condition. (C) Plots of spike frequency vs. current injected for layer II/III pyramidal neurons of S1. The significant differences in the spike frequency between the Ctrl and Ket groups (Ctrl: Vehicle vs. Ket: Vehicle, 80 pA, 100 pA and 110 pA, P < 0.01; 90 pA, P < 0.001) were eliminated after apamin treatment (Ctrl: Apamin vs. Ket: Apamin, P > 0.05). 20–22 neurons from 7–9 rats were recorded per condition. (D,E) Spikes in S1 layer II/III pyramidal neurons evoked for 3 s, 80 pA current injection (D) , and the adaptation index (E) was obtained by the algorithm mentioned above. 18–20 neurons from 7–9 rats were recorded per condition. (F) Quantitative analysis of SK1-3 mRNA in S1 of P8 rats. 5 rats were used per condition. P > 0.05. (G,H) Immunoblots and quantitative analysis of total (G) and membrane-bound (H) SK1-3 levels in S1 of ketamine-treated rats, normalized to corresponding levels in control rats. 8–12 rats were used per condition. * P < 0.05, ** P < 0.01, *** P < 0.001; n.s ., not significant. Data were analyzed using the Mann-Whitney U test for (F,H) and unpaired two-tailed Student’s t-tests for the other panels. Data are shown as the mean ± SEM.

    Techniques Used: Control, Incubation, Injection, Western Blot, Membrane, MANN-WHITNEY, Two Tailed Test



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    Apamin-sensitive SK2 channel-mediated mAHP currents may be linked to changes in neuronal spike frequency and adaptation at 24 h post-ketamine anesthesia. (A,B) Representative traces (A) and amplitudes (B) of the mAHP currents, treatment conditions as indicated. S1 slices from control (Ctrl) and ketamine-treated (Ket) rats were separately incubated and perfused with apamin (100 nM) or its vehicle. 22–25 neurons from 7–10 rats were used per condition. (C) Plots of spike frequency vs. current injected for layer II/III pyramidal neurons of S1. The significant differences in the spike frequency between the Ctrl and Ket groups (Ctrl: Vehicle vs. Ket: Vehicle, 80 pA, 100 pA and 110 pA, P < 0.01; 90 pA, P < 0.001) were eliminated after apamin treatment (Ctrl: Apamin vs. Ket: Apamin, P > 0.05). 20–22 neurons from 7–9 rats were recorded per condition. (D,E) Spikes in S1 layer II/III pyramidal neurons evoked for 3 s, 80 pA current injection (D) , and the adaptation index (E) was obtained by the algorithm mentioned above. 18–20 neurons from 7–9 rats were recorded per condition. (F) Quantitative analysis of <t>SK1-3</t> mRNA in S1 of P8 rats. 5 rats were used per condition. P > 0.05. (G,H) Immunoblots and quantitative analysis of total (G) and membrane-bound (H) SK1-3 levels in S1 of ketamine-treated rats, normalized to corresponding levels in control rats. 8–12 rats were used per condition. * P < 0.05, ** P < 0.01, *** P < 0.001; n.s ., not significant. Data were analyzed using the Mann-Whitney U test for (F,H) and unpaired two-tailed Student’s t-tests for the other panels. Data are shown as the mean ± SEM.
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    qRT-PCR and Western blotting results showing KCNN 1–3 mRNA levels and K Ca 2.1/2.2/2.3 proteins levels in the atria of SR controls (n=20) and AF patients (n=32). ( A ) mRNA levels of KCNN1, KCNN2, and KCNN3 in SR and AF. ( B ) mRNA expression differences of KCNN1, KCNN2, and KCNN3 in SR group. ( C ) mRNA expression differences of KCNN1, KCNN2, and KCNN3 in AF group. ( D ) K Ca 2.1–2.3 <t>(SK1–3)</t> proteins expression changes in SR (n=20) and AF (n=32). * P <0.05 vs. SR.
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    Image Search Results


    Apamin-sensitive SK2 channel-mediated mAHP currents may be linked to changes in neuronal spike frequency and adaptation at 24 h post-ketamine anesthesia. (A,B) Representative traces (A) and amplitudes (B) of the mAHP currents, treatment conditions as indicated. S1 slices from control (Ctrl) and ketamine-treated (Ket) rats were separately incubated and perfused with apamin (100 nM) or its vehicle. 22–25 neurons from 7–10 rats were used per condition. (C) Plots of spike frequency vs. current injected for layer II/III pyramidal neurons of S1. The significant differences in the spike frequency between the Ctrl and Ket groups (Ctrl: Vehicle vs. Ket: Vehicle, 80 pA, 100 pA and 110 pA, P < 0.01; 90 pA, P < 0.001) were eliminated after apamin treatment (Ctrl: Apamin vs. Ket: Apamin, P > 0.05). 20–22 neurons from 7–9 rats were recorded per condition. (D,E) Spikes in S1 layer II/III pyramidal neurons evoked for 3 s, 80 pA current injection (D) , and the adaptation index (E) was obtained by the algorithm mentioned above. 18–20 neurons from 7–9 rats were recorded per condition. (F) Quantitative analysis of SK1-3 mRNA in S1 of P8 rats. 5 rats were used per condition. P > 0.05. (G,H) Immunoblots and quantitative analysis of total (G) and membrane-bound (H) SK1-3 levels in S1 of ketamine-treated rats, normalized to corresponding levels in control rats. 8–12 rats were used per condition. * P < 0.05, ** P < 0.01, *** P < 0.001; n.s ., not significant. Data were analyzed using the Mann-Whitney U test for (F,H) and unpaired two-tailed Student’s t-tests for the other panels. Data are shown as the mean ± SEM.

    Journal: Frontiers in Pharmacology

    Article Title: Compensatory attenuation of cortical apoptosis by SK2 downregulation following ketamine anesthesia

    doi: 10.3389/fphar.2026.1761187

    Figure Lengend Snippet: Apamin-sensitive SK2 channel-mediated mAHP currents may be linked to changes in neuronal spike frequency and adaptation at 24 h post-ketamine anesthesia. (A,B) Representative traces (A) and amplitudes (B) of the mAHP currents, treatment conditions as indicated. S1 slices from control (Ctrl) and ketamine-treated (Ket) rats were separately incubated and perfused with apamin (100 nM) or its vehicle. 22–25 neurons from 7–10 rats were used per condition. (C) Plots of spike frequency vs. current injected for layer II/III pyramidal neurons of S1. The significant differences in the spike frequency between the Ctrl and Ket groups (Ctrl: Vehicle vs. Ket: Vehicle, 80 pA, 100 pA and 110 pA, P < 0.01; 90 pA, P < 0.001) were eliminated after apamin treatment (Ctrl: Apamin vs. Ket: Apamin, P > 0.05). 20–22 neurons from 7–9 rats were recorded per condition. (D,E) Spikes in S1 layer II/III pyramidal neurons evoked for 3 s, 80 pA current injection (D) , and the adaptation index (E) was obtained by the algorithm mentioned above. 18–20 neurons from 7–9 rats were recorded per condition. (F) Quantitative analysis of SK1-3 mRNA in S1 of P8 rats. 5 rats were used per condition. P > 0.05. (G,H) Immunoblots and quantitative analysis of total (G) and membrane-bound (H) SK1-3 levels in S1 of ketamine-treated rats, normalized to corresponding levels in control rats. 8–12 rats were used per condition. * P < 0.05, ** P < 0.01, *** P < 0.001; n.s ., not significant. Data were analyzed using the Mann-Whitney U test for (F,H) and unpaired two-tailed Student’s t-tests for the other panels. Data are shown as the mean ± SEM.

    Article Snippet: The following primary antibodies were used: SK1 (1:500, Alomone Labs, Cat# APC-039), SK2 (1:500, Alomone Labs, Cat# APC-028), SK3 (1:500, Alomone Labs, Cat# APC-025), β-actin (1:1,000, Millipore, Cat# A1978 ), and pan-cadherin (1:1,000, Sigma-Aldrich, Cat# SAB4500001 ).

    Techniques: Control, Incubation, Injection, Western Blot, Membrane, MANN-WHITNEY, Two Tailed Test

    qRT-PCR and Western blotting results showing KCNN 1–3 mRNA levels and K Ca 2.1/2.2/2.3 proteins levels in the atria of SR controls (n=20) and AF patients (n=32). ( A ) mRNA levels of KCNN1, KCNN2, and KCNN3 in SR and AF. ( B ) mRNA expression differences of KCNN1, KCNN2, and KCNN3 in SR group. ( C ) mRNA expression differences of KCNN1, KCNN2, and KCNN3 in AF group. ( D ) K Ca 2.1–2.3 (SK1–3) proteins expression changes in SR (n=20) and AF (n=32). * P <0.05 vs. SR.

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    Article Title: Ca 2+ /Calmodulin-Dependent Protein Kinase II (CaMKII) Increases Small-Conductance Ca 2+ -Activated K + Current in Patients with Chronic Atrial Fibrillation

    doi: 10.12659/MSM.909684

    Figure Lengend Snippet: qRT-PCR and Western blotting results showing KCNN 1–3 mRNA levels and K Ca 2.1/2.2/2.3 proteins levels in the atria of SR controls (n=20) and AF patients (n=32). ( A ) mRNA levels of KCNN1, KCNN2, and KCNN3 in SR and AF. ( B ) mRNA expression differences of KCNN1, KCNN2, and KCNN3 in SR group. ( C ) mRNA expression differences of KCNN1, KCNN2, and KCNN3 in AF group. ( D ) K Ca 2.1–2.3 (SK1–3) proteins expression changes in SR (n=20) and AF (n=32). * P <0.05 vs. SR.

    Article Snippet: The PVDF membrane was incubated with rabbit polyclonal anti-KCa 2.1 (SK1), anti-KCa 2.2 (SK2), anti-KCa 2.3 (SK3, Alomone Labs, Jerusalem, Israel) (dilution 1: 500), rabbit polyclonal anti-CaM (Santa Cruz Biotechnology, Santa Cruz, USA) (dilution 1: 1000), rabbit polyclonal anti-CaMKII (Abcam, Cambridge, UK) (dilution 1: 1000), rabbit polyclonal anti-pCaMKII (Thr 286 , Cell signaling, USA) (dilution 1: 1000), anti-pCaMKII (Thr 287 , Abcam, Cambridge, UK) (dilution 1: 1000), and rabbit polyclonal anti-GAPDH (Santa Cruz Biotechnology, Santa Cruz, USA) (dilution 1: 2000) overnight at 4ºC.

    Techniques: Quantitative RT-PCR, Western Blot, Expressing