voltage gated potassium channel 1 1  (Alomone Labs)

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Article Title: Candesartan Cilexetil Attenuates Arrhythmogenicity Following Pressure Overload in Rats via the Modulation of Cardiac Electrical and Structural Remodeling and Calcium Handling Dysfunction

doi: 10.1161/JAHA.121.024285

Figure Lengend Snippet: Top in each: Representative immunoblot images of ion channel proteins. β‐actin was used as the loading control. Arrow indicates the band used for densitometric quantification. Bottom in each: Mean normalized densitometry of ion channel proteins. Bars represent mean±SD of 8, 13, 8, 12, 9, 12, 14, and 10 hearts in each group for the study of voltage‐gated potassium 4.2 channel subunit (Kv4.2), voltage‐gated potassium 4.3 channel subunit (Kv4.3), voltage‐gated potassium 1.4 channel subunit (Kv1.4), Kv‐channel interacting protein 2 (KChIP2), voltage‐gated potassium 2.1 channel subunit (Kv2.1), inwardly rectifying potassium 2.1 channel subunit (Kir2.1), voltage‐gated L‐type calcium 1.2a channel subunit (Ca V 1.2a), and voltage‐gated sodium 1.5 channel subunit (Na V 1.5), respectively. All measurements were normalized to the protein levels of β‐actin. ** P <0.01 and # P <0.001 vs Sham+Veh group; ‡ P <0.01 vs AB+Veh group by 1‐way ANOVA with a Tukey post hoc test. AB indicates aortic banding; Can, candesartan cilexetil; S, sham; and Veh, vehicle.

Article Snippet: Membranes were blocked and then incubated overnight at 4 °C with primary antibody against ryanodine receptor Ca 2+ release channel 2 (RyR2) (1:1000; ThermoFisher Scientific, Waltham, MA), Ser 2808 ‐phosphorylated RyR2 (pSer 2808 ‐RyR2) (1:5000; Badrilla, Leeds, United Kingdom), pSer 2814 ‐RyR2 (1:500; Badrilla), SERCA2a (sarco[endo]plasmic reticulum Ca 2+ ‐ATPase) (1:5000; Badrilla), phospholamban (1:2000; Badrilla), pSer 16 ‐phospholamban (1:2000; Millipore, Temecula, CA), pThr 17 ‐phospholamban (1:2000; Badrilla), Na + ‐Ca 2+ exchanger 1 (NCX1) (1:500; Santa Cruz Biotechnology, Santa Cruz, CA), voltage‐gated L‐type calcium 1.2a channel subunit (Ca V 1.2a) (1:400; Millipore), voltage‐gated sodium 1.5 channel subunit (Na V 1.5) (1:500; Alomone, Jerusalem, Israel), voltage‐gated potassium 4.2 channel subunit (Kv4.2) (1:200; Millipore), voltage‐gated potassium 4.3 channel subunit (Kv4.3) (1:200; Alomone), voltage‐gated potassium 1.4 channel subunit (Kv1.4) (1:200; Alomone), Kv‐channel interacting protein 2 (KChIP2) (1:500; ThermoFisher Scientific), voltage‐gated potassium 2.1 channel subunit (Kv2.1) (1:500; Alomone), and inwardly rectifying potassium 2.1 channel subunit (Kir2.1) (1:600; Alomone).

Techniques: Western Blot

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Article Title: Candesartan Cilexetil Attenuates Arrhythmogenicity Following Pressure Overload in Rats via the Modulation of Cardiac Electrical and Structural Remodeling and Calcium Handling Dysfunction

doi: 10.1161/JAHA.121.024285

Figure Lengend Snippet: Top in each: Representative immunoblot images of ion channel proteins. β‐actin was used as the loading control. Arrow indicates the band used for densitometric quantification. Bottom in each: Mean normalized densitometry of ion channel proteins. Bars represent mean±SD of 8, 13, 8, 12, 9, 12, 14, and 10 hearts in each group for the study of voltage‐gated potassium 4.2 channel subunit (Kv4.2), voltage‐gated potassium 4.3 channel subunit (Kv4.3), voltage‐gated potassium 1.4 channel subunit (Kv1.4), Kv‐channel interacting protein 2 (KChIP2), voltage‐gated potassium 2.1 channel subunit (Kv2.1), inwardly rectifying potassium 2.1 channel subunit (Kir2.1), voltage‐gated L‐type calcium 1.2a channel subunit (Ca V 1.2a), and voltage‐gated sodium 1.5 channel subunit (Na V 1.5), respectively. All measurements were normalized to the protein levels of β‐actin. ** P <0.01 and # P <0.001 vs Sham+Veh group; ‡ P <0.01 vs AB+Veh group by 1‐way ANOVA with a Tukey post hoc test. AB indicates aortic banding; Can, candesartan cilexetil; S, sham; and Veh, vehicle.

Article Snippet: Membranes were blocked and then incubated overnight at 4 °C with primary antibody against ryanodine receptor Ca 2+ release channel 2 (RyR2) (1:1000; ThermoFisher Scientific, Waltham, MA), Ser 2808 ‐phosphorylated RyR2 (pSer 2808 ‐RyR2) (1:5000; Badrilla, Leeds, United Kingdom), pSer 2814 ‐RyR2 (1:500; Badrilla), SERCA2a (sarco[endo]plasmic reticulum Ca 2+ ‐ATPase) (1:5000; Badrilla), phospholamban (1:2000; Badrilla), pSer 16 ‐phospholamban (1:2000; Millipore, Temecula, CA), pThr 17 ‐phospholamban (1:2000; Badrilla), Na + ‐Ca 2+ exchanger 1 (NCX1) (1:500; Santa Cruz Biotechnology, Santa Cruz, CA), voltage‐gated L‐type calcium 1.2a channel subunit (Ca V 1.2a) (1:400; Millipore), voltage‐gated sodium 1.5 channel subunit (Na V 1.5) (1:500; Alomone, Jerusalem, Israel), voltage‐gated potassium 4.2 channel subunit (Kv4.2) (1:200; Millipore), voltage‐gated potassium 4.3 channel subunit (Kv4.3) (1:200; Alomone), voltage‐gated potassium 1.4 channel subunit (Kv1.4) (1:200; Alomone), Kv‐channel interacting protein 2 (KChIP2) (1:500; ThermoFisher Scientific), voltage‐gated potassium 2.1 channel subunit (Kv2.1) (1:500; Alomone), and inwardly rectifying potassium 2.1 channel subunit (Kir2.1) (1:600; Alomone).

Techniques: Western Blot