anti hcn2 antibody Search Results


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  • 95
    Alomone Labs aa 147 161 crossing to mouse
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    Alomone Labs rb anti hcn2
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    Alomone Labs anti hcn2 antibody
    (A) Structural model of the CNBD of HCN channels. The 2 key residues R591 (yellow) and T592 (pink) that are crucial for binding of cAMP are highlighted. (B) Horizontal brain slices of WT and HCN2EA mice. The position of the dLGN (red) and the VB (blue) is indicated. (C) Detection of <t>HCN2</t> and HCN4 in Western blot analysis of punched dLGN and VB regions. Images are representatives of n = 3/group. (D) Western blot analysis of membrane preparations of HCN2EA and WT mice probed for HCN2 and a loading control (Na+/K+-ATPase). Images are representatives of n = 3/group. (E) Quantification of HCN2 expression level in relation to the Na+/K+-ATPase (n = 3).
    Anti Hcn2 Antibody, 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
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    Image Search Results


    (A) Structural model of the CNBD of HCN channels. The 2 key residues R591 (yellow) and T592 (pink) that are crucial for binding of cAMP are highlighted. (B) Horizontal brain slices of WT and HCN2EA mice. The position of the dLGN (red) and the VB (blue) is indicated. (C) Detection of HCN2 and HCN4 in Western blot analysis of punched dLGN and VB regions. Images are representatives of n = 3/group. (D) Western blot analysis of membrane preparations of HCN2EA and WT mice probed for HCN2 and a loading control (Na+/K+-ATPase). Images are representatives of n = 3/group. (E) Quantification of HCN2 expression level in relation to the Na+/K+-ATPase (n = 3).

    Journal: JCI Insight

    Article Title: Abolishing cAMP sensitivity in HCN2 pacemaker channels induces generalized seizures

    doi: 10.1172/jci.insight.126418

    Figure Lengend Snippet: (A) Structural model of the CNBD of HCN channels. The 2 key residues R591 (yellow) and T592 (pink) that are crucial for binding of cAMP are highlighted. (B) Horizontal brain slices of WT and HCN2EA mice. The position of the dLGN (red) and the VB (blue) is indicated. (C) Detection of HCN2 and HCN4 in Western blot analysis of punched dLGN and VB regions. Images are representatives of n = 3/group. (D) Western blot analysis of membrane preparations of HCN2EA and WT mice probed for HCN2 and a loading control (Na+/K+-ATPase). Images are representatives of n = 3/group. (E) Quantification of HCN2 expression level in relation to the Na+/K+-ATPase (n = 3).

    Article Snippet: Co-IPs were performed with anti-HCN2 antibody (Alomone, APC-030), anti-HCN4 (Alomone, APC-052), or anti-Trip8b (N212/7, Neuromab) using Novex Protein G magnetic beads (Thermo Fisher Scientific) according to the manufacturer’s protocol. qRT-PCR.

    Techniques: Binding Assay, Western Blot, Expressing

    (A) Distribution of HCN2 and HCN4 in the VB region of mouse thalamus. Scale bar: 200 μm. (B) Overlay of anti-HCN2 (green), anti-HCN4 (red), and Hoechst (blue). Scale bars: 200 μm. Upper: Single channels for HCN2 (green) and HCN4 (red) staining. Lower: Magnification (scale bars: 25 μm) of the dLGN (left) and VB (middle). (C) Magnified HCN2 stainings of WT (upper), HCN2EA litters (middle), and HCN2-KO mice (lower panel) in the VB region. Scale bars: 20 μm. (D) Analysis of the mean intensity of the HCN2 fluorescence in WT and HCN2EA soma and dendrites (WT: gray squares, soma [n = 20], dendrites [n = 26]; EA: blue squares, soma [n = 17], dendrites [n = 26]). (E) Magnified HCN4 stainings of WT (upper) and HCN2EA litters (middle). Staining in the absence of primary antibody is shown in the bottom panels. Scale bars: 20 μm. (F) Analysis of the mean intensity of the HCN4 fluorescence in WT and HCN2EA soma and dendrites (WT: gray circles, soma [n = 23], dendrites [n = 25]; EA: orange circles, soma [n = 25], dendrites [n = 25]) ***P < 0.001 by 1-way ANOVA with Bonferroni’s post hoc test. NS, not significant.

    Journal: JCI Insight

    Article Title: Abolishing cAMP sensitivity in HCN2 pacemaker channels induces generalized seizures

    doi: 10.1172/jci.insight.126418

    Figure Lengend Snippet: (A) Distribution of HCN2 and HCN4 in the VB region of mouse thalamus. Scale bar: 200 μm. (B) Overlay of anti-HCN2 (green), anti-HCN4 (red), and Hoechst (blue). Scale bars: 200 μm. Upper: Single channels for HCN2 (green) and HCN4 (red) staining. Lower: Magnification (scale bars: 25 μm) of the dLGN (left) and VB (middle). (C) Magnified HCN2 stainings of WT (upper), HCN2EA litters (middle), and HCN2-KO mice (lower panel) in the VB region. Scale bars: 20 μm. (D) Analysis of the mean intensity of the HCN2 fluorescence in WT and HCN2EA soma and dendrites (WT: gray squares, soma [n = 20], dendrites [n = 26]; EA: blue squares, soma [n = 17], dendrites [n = 26]). (E) Magnified HCN4 stainings of WT (upper) and HCN2EA litters (middle). Staining in the absence of primary antibody is shown in the bottom panels. Scale bars: 20 μm. (F) Analysis of the mean intensity of the HCN4 fluorescence in WT and HCN2EA soma and dendrites (WT: gray circles, soma [n = 23], dendrites [n = 25]; EA: orange circles, soma [n = 25], dendrites [n = 25]) ***P < 0.001 by 1-way ANOVA with Bonferroni’s post hoc test. NS, not significant.

    Article Snippet: Co-IPs were performed with anti-HCN2 antibody (Alomone, APC-030), anti-HCN4 (Alomone, APC-052), or anti-Trip8b (N212/7, Neuromab) using Novex Protein G magnetic beads (Thermo Fisher Scientific) according to the manufacturer’s protocol. qRT-PCR.

    Techniques: Staining, Fluorescence

    (A) EEG traces of WT (left), HCN2EA (middle), and global HCN2-KO mice (right panel). Spike and wave discharges (SWDs) in the EEG of HCN2EA and global HCN2-KO are marked by asterisks. SWDs concur with episodes of low activity in the EMG. Higher magnifications of SWD traces are displayed below the EEG of HCN2EA and HCN2-KO mice. Representative traces of animals analyzed in B. (B) SWD characteristics of HCN2EA (light blue, n = 5) and global HCN2-KO (dark blue, n = 6) animals compared with WT traces (gray, n = 6) regarding the time between 2 SDWs (left), mean SWD duration (middle), and the time per day in SWDs (right). NS, not significant (1-way ANOVA, Bonferroni’s post hoc test). (C) Time spent in different vigilance states (wake, NREM and REM sleep) during light and dark conditions (HCN2EA, blue; WT, gray; n = 7). (D) Power spectra of NREM sleep in HCN2EA (blue, n = 7) and WT animals (gray, n = 7). **P < 0.01 by 2-way ANOVA. (E) Mean sigma power in HCN2EA (blue, n = 7) and WT animals (gray, n = 7). *P = 0.0175 by Mann-Whitney test.

    Journal: JCI Insight

    Article Title: Abolishing cAMP sensitivity in HCN2 pacemaker channels induces generalized seizures

    doi: 10.1172/jci.insight.126418

    Figure Lengend Snippet: (A) EEG traces of WT (left), HCN2EA (middle), and global HCN2-KO mice (right panel). Spike and wave discharges (SWDs) in the EEG of HCN2EA and global HCN2-KO are marked by asterisks. SWDs concur with episodes of low activity in the EMG. Higher magnifications of SWD traces are displayed below the EEG of HCN2EA and HCN2-KO mice. Representative traces of animals analyzed in B. (B) SWD characteristics of HCN2EA (light blue, n = 5) and global HCN2-KO (dark blue, n = 6) animals compared with WT traces (gray, n = 6) regarding the time between 2 SDWs (left), mean SWD duration (middle), and the time per day in SWDs (right). NS, not significant (1-way ANOVA, Bonferroni’s post hoc test). (C) Time spent in different vigilance states (wake, NREM and REM sleep) during light and dark conditions (HCN2EA, blue; WT, gray; n = 7). (D) Power spectra of NREM sleep in HCN2EA (blue, n = 7) and WT animals (gray, n = 7). **P < 0.01 by 2-way ANOVA. (E) Mean sigma power in HCN2EA (blue, n = 7) and WT animals (gray, n = 7). *P = 0.0175 by Mann-Whitney test.

    Article Snippet: Co-IPs were performed with anti-HCN2 antibody (Alomone, APC-030), anti-HCN4 (Alomone, APC-052), or anti-Trip8b (N212/7, Neuromab) using Novex Protein G magnetic beads (Thermo Fisher Scientific) according to the manufacturer’s protocol. qRT-PCR.

    Techniques: Activity Assay, MANN-WHITNEY

    (A) Strategy for specific deletion of HCN channels in the VB. Left panel: Scheme of the AAV2/8-hSyn-Cre-EGFP vector that was injected stereotactically into the VB of HCNfl/fl mice. The schematic brain shows the injected region in the thalamus. Only cells in the VB show the green EGFP signal due to viral transfection. (B) Staining with anti-HCN2 antibody (red) in the VB region shows that Cre/EGFP–positive neurons (green) lack HCN2, while nontransduced (EGFP-negative) cells express HCN2 in the plasma membrane (marked by white arrows). Scale bar: 5 μm. VM, ventromedial region. (C) VB-specific HCN2-KO mice show SWDs (marked with an asterisk) in EEG traces (representative trace, n = 3). The inset shows a magnification of the SWD. (D) Representative EEG (green) and EMG (black) traces of an HCN2fl/fl mouse that was injected with a control AAV vector that expresses only EGFP (n = 3). (D) Representative EEG (green) and EMG (black) traces of a VB-specific HCN4-KO animal that was generated by injecting the same vector as displayed in Figure 7A into the VB of an HCN4fl/fl mouse (n = 3).

    Journal: JCI Insight

    Article Title: Abolishing cAMP sensitivity in HCN2 pacemaker channels induces generalized seizures

    doi: 10.1172/jci.insight.126418

    Figure Lengend Snippet: (A) Strategy for specific deletion of HCN channels in the VB. Left panel: Scheme of the AAV2/8-hSyn-Cre-EGFP vector that was injected stereotactically into the VB of HCNfl/fl mice. The schematic brain shows the injected region in the thalamus. Only cells in the VB show the green EGFP signal due to viral transfection. (B) Staining with anti-HCN2 antibody (red) in the VB region shows that Cre/EGFP–positive neurons (green) lack HCN2, while nontransduced (EGFP-negative) cells express HCN2 in the plasma membrane (marked by white arrows). Scale bar: 5 μm. VM, ventromedial region. (C) VB-specific HCN2-KO mice show SWDs (marked with an asterisk) in EEG traces (representative trace, n = 3). The inset shows a magnification of the SWD. (D) Representative EEG (green) and EMG (black) traces of an HCN2fl/fl mouse that was injected with a control AAV vector that expresses only EGFP (n = 3). (D) Representative EEG (green) and EMG (black) traces of a VB-specific HCN4-KO animal that was generated by injecting the same vector as displayed in Figure 7A into the VB of an HCN4fl/fl mouse (n = 3).

    Article Snippet: Co-IPs were performed with anti-HCN2 antibody (Alomone, APC-030), anti-HCN4 (Alomone, APC-052), or anti-Trip8b (N212/7, Neuromab) using Novex Protein G magnetic beads (Thermo Fisher Scientific) according to the manufacturer’s protocol. qRT-PCR.

    Techniques: Plasmid Preparation, Injection, Transfection, Staining, Generated