inward rectifying k channel 2 1  (Alomone Labs)


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    Alomone Labs inward rectifying k channel 2 1
    Inward rectifier K + current I K1 expression and function in transgenic atrial myocytes. Experimental animals involved wild‐type mice (WT) and transgenic mice (TG) expressing the repressor isoform of cyclic adenosine monophosphate response element modulator, CREM‐IbΔC‐X, and were distributed according to age in 6‐week‐old (WT 6w and TG 6w ) and 12‐week‐old (WT 12w and TG 12w ) groups. A , Representative traces of inward rectifiers K + channel (I K1 ) recorded in WT 12w and TG 12w myocytes before and after application of 10 μmol/L BaCl 2 using a ramp protocol (inset, scale bar 0.2 seconds). The traces show current densitiy (expressed in picoamperes/picofarads [pA/pF]) over time. ( Aa ). Current–voltage plots of I K1 averaged from traces of all cells. For WT 6w , n/N are 8/5, for TG 6w n/N are 10/6, for WT 12w n/N are 13/7, and for TG 12w n/N are 9/6 ( Ab ). B , Data show mean±SE of relative mRNA levels of atrial K + voltage‐gated channel subfamily J member 2 ( Kcnj2 ) and 4 ( Kcnj4 ) normalized to WT 6w vs Hprt1 (hypoxanthine phosphoribosyltransferase 1) as the housekeeping gene; N=8 per group. Y‐axes scale is Log2. Ca through c , Representative immunoblots ( Ca ) and quantification of K + inwardly rectifying channel subunits <t>Kir2.1</t> ( Cb ) and Kir2.3 ( Cc ) protein levels normalized to calsequestrin (CSQ). Data show mean±SE of 7 mice per group. Da through b , Representative action potentials recorded before (normal Tyrode [NT] as control) and after application of 10 μmol/L BaCl 2 in 1 atrial myocyte of each group ( Da ). Quantification of the percentages of action potential duration (APD) change in BaCl 2 vs NT at 50% (APD 50 ) and 90% (APD 90 ) repolarization. Data show mean±SE of n/N for WT 6w (7/5), TG 6w (5/5), WT 12w (11/6), and TG 12w (5/4) ( Db ). * P
    Inward Rectifying K Channel 2 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/inward rectifying k channel 2 1/product/Alomone Labs
    Average 93 stars, based on 5 article reviews
    Price from $9.99 to $1999.99
    inward rectifying k channel 2 1 - by Bioz Stars, 2022-12
    93/100 stars

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    1) Product Images from "Inward Rectifier K+ Currents Contribute to the Proarrhythmic Electrical Phenotype of Atria Overexpressing Cyclic Adenosine Monophosphate Response Element Modulator Isoform CREM‐IbΔC‐X"

    Article Title: Inward Rectifier K+ Currents Contribute to the Proarrhythmic Electrical Phenotype of Atria Overexpressing Cyclic Adenosine Monophosphate Response Element Modulator Isoform CREM‐IbΔC‐X

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

    doi: 10.1161/JAHA.119.016144

    Inward rectifier K + current I K1 expression and function in transgenic atrial myocytes. Experimental animals involved wild‐type mice (WT) and transgenic mice (TG) expressing the repressor isoform of cyclic adenosine monophosphate response element modulator, CREM‐IbΔC‐X, and were distributed according to age in 6‐week‐old (WT 6w and TG 6w ) and 12‐week‐old (WT 12w and TG 12w ) groups. A , Representative traces of inward rectifiers K + channel (I K1 ) recorded in WT 12w and TG 12w myocytes before and after application of 10 μmol/L BaCl 2 using a ramp protocol (inset, scale bar 0.2 seconds). The traces show current densitiy (expressed in picoamperes/picofarads [pA/pF]) over time. ( Aa ). Current–voltage plots of I K1 averaged from traces of all cells. For WT 6w , n/N are 8/5, for TG 6w n/N are 10/6, for WT 12w n/N are 13/7, and for TG 12w n/N are 9/6 ( Ab ). B , Data show mean±SE of relative mRNA levels of atrial K + voltage‐gated channel subfamily J member 2 ( Kcnj2 ) and 4 ( Kcnj4 ) normalized to WT 6w vs Hprt1 (hypoxanthine phosphoribosyltransferase 1) as the housekeeping gene; N=8 per group. Y‐axes scale is Log2. Ca through c , Representative immunoblots ( Ca ) and quantification of K + inwardly rectifying channel subunits Kir2.1 ( Cb ) and Kir2.3 ( Cc ) protein levels normalized to calsequestrin (CSQ). Data show mean±SE of 7 mice per group. Da through b , Representative action potentials recorded before (normal Tyrode [NT] as control) and after application of 10 μmol/L BaCl 2 in 1 atrial myocyte of each group ( Da ). Quantification of the percentages of action potential duration (APD) change in BaCl 2 vs NT at 50% (APD 50 ) and 90% (APD 90 ) repolarization. Data show mean±SE of n/N for WT 6w (7/5), TG 6w (5/5), WT 12w (11/6), and TG 12w (5/4) ( Db ). * P
    Figure Legend Snippet: Inward rectifier K + current I K1 expression and function in transgenic atrial myocytes. Experimental animals involved wild‐type mice (WT) and transgenic mice (TG) expressing the repressor isoform of cyclic adenosine monophosphate response element modulator, CREM‐IbΔC‐X, and were distributed according to age in 6‐week‐old (WT 6w and TG 6w ) and 12‐week‐old (WT 12w and TG 12w ) groups. A , Representative traces of inward rectifiers K + channel (I K1 ) recorded in WT 12w and TG 12w myocytes before and after application of 10 μmol/L BaCl 2 using a ramp protocol (inset, scale bar 0.2 seconds). The traces show current densitiy (expressed in picoamperes/picofarads [pA/pF]) over time. ( Aa ). Current–voltage plots of I K1 averaged from traces of all cells. For WT 6w , n/N are 8/5, for TG 6w n/N are 10/6, for WT 12w n/N are 13/7, and for TG 12w n/N are 9/6 ( Ab ). B , Data show mean±SE of relative mRNA levels of atrial K + voltage‐gated channel subfamily J member 2 ( Kcnj2 ) and 4 ( Kcnj4 ) normalized to WT 6w vs Hprt1 (hypoxanthine phosphoribosyltransferase 1) as the housekeeping gene; N=8 per group. Y‐axes scale is Log2. Ca through c , Representative immunoblots ( Ca ) and quantification of K + inwardly rectifying channel subunits Kir2.1 ( Cb ) and Kir2.3 ( Cc ) protein levels normalized to calsequestrin (CSQ). Data show mean±SE of 7 mice per group. Da through b , Representative action potentials recorded before (normal Tyrode [NT] as control) and after application of 10 μmol/L BaCl 2 in 1 atrial myocyte of each group ( Da ). Quantification of the percentages of action potential duration (APD) change in BaCl 2 vs NT at 50% (APD 50 ) and 90% (APD 90 ) repolarization. Data show mean±SE of n/N for WT 6w (7/5), TG 6w (5/5), WT 12w (11/6), and TG 12w (5/4) ( Db ). * P

    Techniques Used: Expressing, Transgenic Assay, Mouse Assay, Western Blot

    2) Product Images from "Fluid flow facilitates inward rectifier K+ current by convectively restoring [K+] at the cell membrane surface"

    Article Title: Fluid flow facilitates inward rectifier K+ current by convectively restoring [K+] at the cell membrane surface

    Journal: Scientific Reports

    doi: 10.1038/srep39585

    ( A ) Kir2.1 channel conductance-[K + ] relationship. The conductance-[K + ] relationship was obtained under the fluid-flow condition. Note the right-shifted conductance-[K + ] relationship at −50 mV compared to the corresponding relationship at −100 mV. ( B ) Summary of the facilitating effect of fluid flow on the IKir2.1 at 150 and 200 mM extracellular [K + ] at a voltage of −100 mV; **p
    Figure Legend Snippet: ( A ) Kir2.1 channel conductance-[K + ] relationship. The conductance-[K + ] relationship was obtained under the fluid-flow condition. Note the right-shifted conductance-[K + ] relationship at −50 mV compared to the corresponding relationship at −100 mV. ( B ) Summary of the facilitating effect of fluid flow on the IKir2.1 at 150 and 200 mM extracellular [K + ] at a voltage of −100 mV; **p

    Techniques Used: Flow Cytometry

    IKir2.1 in RBL-2H3 cells is increased by fluid flow. ( A ) Representative Kir2.1 currents elicited by voltage steps starting from a holding potential of 0 mV, under control (static) and fluid-flow conditions in a high-extracellular-K + solution. ( B ) Representative tracing of IKir2.1 at −100 mV before and after fluid-flow application. ( C ) Average current-voltage (I–V) relationships in the absence and presence of fluid flow (n = 8); *p
    Figure Legend Snippet: IKir2.1 in RBL-2H3 cells is increased by fluid flow. ( A ) Representative Kir2.1 currents elicited by voltage steps starting from a holding potential of 0 mV, under control (static) and fluid-flow conditions in a high-extracellular-K + solution. ( B ) Representative tracing of IKir2.1 at −100 mV before and after fluid-flow application. ( C ) Average current-voltage (I–V) relationships in the absence and presence of fluid flow (n = 8); *p

    Techniques Used: Flow Cytometry

    Kir2.1 activity is increased by fluid-flow in HEK293T cells in which Kir2.1 was ectopically over-expressed. ( A , D ) Representative tracing of currents at −140 mV in HEK293T cells expressing Kir2.1 ( A ) and non-transfected cells ( D ) before and after fluid-flow application. ( B , E ) Representative current recordings of HEK293T cells expressing Kir2.1 ( B ) and non-transfected cells ( E ) under control (static) and fluid-flow conditions. Currents were elicited by voltage steps from −160 mV to 0 mV at a holding potential of −80 mV. ( C , F ) Average current-voltage (I–V) relationships in the absence (black) and presence (red) of fluid flow in HEK293T cells expressing Kir2.1 ( C ) and non-transfected cells ( F ); **p
    Figure Legend Snippet: Kir2.1 activity is increased by fluid-flow in HEK293T cells in which Kir2.1 was ectopically over-expressed. ( A , D ) Representative tracing of currents at −140 mV in HEK293T cells expressing Kir2.1 ( A ) and non-transfected cells ( D ) before and after fluid-flow application. ( B , E ) Representative current recordings of HEK293T cells expressing Kir2.1 ( B ) and non-transfected cells ( E ) under control (static) and fluid-flow conditions. Currents were elicited by voltage steps from −160 mV to 0 mV at a holding potential of −80 mV. ( C , F ) Average current-voltage (I–V) relationships in the absence (black) and presence (red) of fluid flow in HEK293T cells expressing Kir2.1 ( C ) and non-transfected cells ( F ); **p

    Techniques Used: Activity Assay, Flow Cytometry, Expressing, Transfection

    3) Product Images from "Fluid flow facilitates inward rectifier K+ current by convectively restoring [K+] at the cell membrane surface"

    Article Title: Fluid flow facilitates inward rectifier K+ current by convectively restoring [K+] at the cell membrane surface

    Journal: Scientific Reports

    doi: 10.1038/srep39585

    ( A ) Kir2.1 channel conductance-[K + ] relationship. The conductance-[K + ] relationship was obtained under the fluid-flow condition. Note the right-shifted conductance-[K + ] relationship at −50 mV compared to the corresponding relationship at −100 mV. ( B ) Summary of the facilitating effect of fluid flow on the IKir2.1 at 150 and 200 mM extracellular [K + ] at a voltage of −100 mV; **p
    Figure Legend Snippet: ( A ) Kir2.1 channel conductance-[K + ] relationship. The conductance-[K + ] relationship was obtained under the fluid-flow condition. Note the right-shifted conductance-[K + ] relationship at −50 mV compared to the corresponding relationship at −100 mV. ( B ) Summary of the facilitating effect of fluid flow on the IKir2.1 at 150 and 200 mM extracellular [K + ] at a voltage of −100 mV; **p

    Techniques Used: Flow Cytometry

    IKir2.1 in RBL-2H3 cells is increased by fluid flow. ( A ) Representative Kir2.1 currents elicited by voltage steps starting from a holding potential of 0 mV, under control (static) and fluid-flow conditions in a high-extracellular-K + solution. ( B ) Representative tracing of IKir2.1 at −100 mV before and after fluid-flow application. ( C ) Average current-voltage (I–V) relationships in the absence and presence of fluid flow (n = 8); *p
    Figure Legend Snippet: IKir2.1 in RBL-2H3 cells is increased by fluid flow. ( A ) Representative Kir2.1 currents elicited by voltage steps starting from a holding potential of 0 mV, under control (static) and fluid-flow conditions in a high-extracellular-K + solution. ( B ) Representative tracing of IKir2.1 at −100 mV before and after fluid-flow application. ( C ) Average current-voltage (I–V) relationships in the absence and presence of fluid flow (n = 8); *p

    Techniques Used: Flow Cytometry

    Kir2.1 activity is increased by fluid-flow in HEK293T cells in which Kir2.1 was ectopically over-expressed. ( A , D ) Representative tracing of currents at −140 mV in HEK293T cells expressing Kir2.1 ( A ) and non-transfected cells ( D ) before and after fluid-flow application. ( B , E ) Representative current recordings of HEK293T cells expressing Kir2.1 ( B ) and non-transfected cells ( E ) under control (static) and fluid-flow conditions. Currents were elicited by voltage steps from −160 mV to 0 mV at a holding potential of −80 mV. ( C , F ) Average current-voltage (I–V) relationships in the absence (black) and presence (red) of fluid flow in HEK293T cells expressing Kir2.1 ( C ) and non-transfected cells ( F ); **p
    Figure Legend Snippet: Kir2.1 activity is increased by fluid-flow in HEK293T cells in which Kir2.1 was ectopically over-expressed. ( A , D ) Representative tracing of currents at −140 mV in HEK293T cells expressing Kir2.1 ( A ) and non-transfected cells ( D ) before and after fluid-flow application. ( B , E ) Representative current recordings of HEK293T cells expressing Kir2.1 ( B ) and non-transfected cells ( E ) under control (static) and fluid-flow conditions. Currents were elicited by voltage steps from −160 mV to 0 mV at a holding potential of −80 mV. ( C , F ) Average current-voltage (I–V) relationships in the absence (black) and presence (red) of fluid flow in HEK293T cells expressing Kir2.1 ( C ) and non-transfected cells ( F ); **p

    Techniques Used: Activity Assay, Flow Cytometry, Expressing, Transfection

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    Alomone Labs inward rectifying k channel 2 1
    Inward rectifier K + current I K1 expression and function in transgenic atrial myocytes. Experimental animals involved wild‐type mice (WT) and transgenic mice (TG) expressing the repressor isoform of cyclic adenosine monophosphate response element modulator, CREM‐IbΔC‐X, and were distributed according to age in 6‐week‐old (WT 6w and TG 6w ) and 12‐week‐old (WT 12w and TG 12w ) groups. A , Representative traces of inward rectifiers K + channel (I K1 ) recorded in WT 12w and TG 12w myocytes before and after application of 10 μmol/L BaCl 2 using a ramp protocol (inset, scale bar 0.2 seconds). The traces show current densitiy (expressed in picoamperes/picofarads [pA/pF]) over time. ( Aa ). Current–voltage plots of I K1 averaged from traces of all cells. For WT 6w , n/N are 8/5, for TG 6w n/N are 10/6, for WT 12w n/N are 13/7, and for TG 12w n/N are 9/6 ( Ab ). B , Data show mean±SE of relative mRNA levels of atrial K + voltage‐gated channel subfamily J member 2 ( Kcnj2 ) and 4 ( Kcnj4 ) normalized to WT 6w vs Hprt1 (hypoxanthine phosphoribosyltransferase 1) as the housekeeping gene; N=8 per group. Y‐axes scale is Log2. Ca through c , Representative immunoblots ( Ca ) and quantification of K + inwardly rectifying channel subunits <t>Kir2.1</t> ( Cb ) and Kir2.3 ( Cc ) protein levels normalized to calsequestrin (CSQ). Data show mean±SE of 7 mice per group. Da through b , Representative action potentials recorded before (normal Tyrode [NT] as control) and after application of 10 μmol/L BaCl 2 in 1 atrial myocyte of each group ( Da ). Quantification of the percentages of action potential duration (APD) change in BaCl 2 vs NT at 50% (APD 50 ) and 90% (APD 90 ) repolarization. Data show mean±SE of n/N for WT 6w (7/5), TG 6w (5/5), WT 12w (11/6), and TG 12w (5/4) ( Db ). * P
    Inward Rectifying K Channel 2 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/inward rectifying k channel 2 1/product/Alomone Labs
    Average 93 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    inward rectifying k channel 2 1 - by Bioz Stars, 2022-12
    93/100 stars
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    Inward rectifier K + current I K1 expression and function in transgenic atrial myocytes. Experimental animals involved wild‐type mice (WT) and transgenic mice (TG) expressing the repressor isoform of cyclic adenosine monophosphate response element modulator, CREM‐IbΔC‐X, and were distributed according to age in 6‐week‐old (WT 6w and TG 6w ) and 12‐week‐old (WT 12w and TG 12w ) groups. A , Representative traces of inward rectifiers K + channel (I K1 ) recorded in WT 12w and TG 12w myocytes before and after application of 10 μmol/L BaCl 2 using a ramp protocol (inset, scale bar 0.2 seconds). The traces show current densitiy (expressed in picoamperes/picofarads [pA/pF]) over time. ( Aa ). Current–voltage plots of I K1 averaged from traces of all cells. For WT 6w , n/N are 8/5, for TG 6w n/N are 10/6, for WT 12w n/N are 13/7, and for TG 12w n/N are 9/6 ( Ab ). B , Data show mean±SE of relative mRNA levels of atrial K + voltage‐gated channel subfamily J member 2 ( Kcnj2 ) and 4 ( Kcnj4 ) normalized to WT 6w vs Hprt1 (hypoxanthine phosphoribosyltransferase 1) as the housekeeping gene; N=8 per group. Y‐axes scale is Log2. Ca through c , Representative immunoblots ( Ca ) and quantification of K + inwardly rectifying channel subunits Kir2.1 ( Cb ) and Kir2.3 ( Cc ) protein levels normalized to calsequestrin (CSQ). Data show mean±SE of 7 mice per group. Da through b , Representative action potentials recorded before (normal Tyrode [NT] as control) and after application of 10 μmol/L BaCl 2 in 1 atrial myocyte of each group ( Da ). Quantification of the percentages of action potential duration (APD) change in BaCl 2 vs NT at 50% (APD 50 ) and 90% (APD 90 ) repolarization. Data show mean±SE of n/N for WT 6w (7/5), TG 6w (5/5), WT 12w (11/6), and TG 12w (5/4) ( Db ). * P

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

    Article Title: Inward Rectifier K+ Currents Contribute to the Proarrhythmic Electrical Phenotype of Atria Overexpressing Cyclic Adenosine Monophosphate Response Element Modulator Isoform CREM‐IbΔC‐X

    doi: 10.1161/JAHA.119.016144

    Figure Lengend Snippet: Inward rectifier K + current I K1 expression and function in transgenic atrial myocytes. Experimental animals involved wild‐type mice (WT) and transgenic mice (TG) expressing the repressor isoform of cyclic adenosine monophosphate response element modulator, CREM‐IbΔC‐X, and were distributed according to age in 6‐week‐old (WT 6w and TG 6w ) and 12‐week‐old (WT 12w and TG 12w ) groups. A , Representative traces of inward rectifiers K + channel (I K1 ) recorded in WT 12w and TG 12w myocytes before and after application of 10 μmol/L BaCl 2 using a ramp protocol (inset, scale bar 0.2 seconds). The traces show current densitiy (expressed in picoamperes/picofarads [pA/pF]) over time. ( Aa ). Current–voltage plots of I K1 averaged from traces of all cells. For WT 6w , n/N are 8/5, for TG 6w n/N are 10/6, for WT 12w n/N are 13/7, and for TG 12w n/N are 9/6 ( Ab ). B , Data show mean±SE of relative mRNA levels of atrial K + voltage‐gated channel subfamily J member 2 ( Kcnj2 ) and 4 ( Kcnj4 ) normalized to WT 6w vs Hprt1 (hypoxanthine phosphoribosyltransferase 1) as the housekeeping gene; N=8 per group. Y‐axes scale is Log2. Ca through c , Representative immunoblots ( Ca ) and quantification of K + inwardly rectifying channel subunits Kir2.1 ( Cb ) and Kir2.3 ( Cc ) protein levels normalized to calsequestrin (CSQ). Data show mean±SE of 7 mice per group. Da through b , Representative action potentials recorded before (normal Tyrode [NT] as control) and after application of 10 μmol/L BaCl 2 in 1 atrial myocyte of each group ( Da ). Quantification of the percentages of action potential duration (APD) change in BaCl 2 vs NT at 50% (APD 50 ) and 90% (APD 90 ) repolarization. Data show mean±SE of n/N for WT 6w (7/5), TG 6w (5/5), WT 12w (11/6), and TG 12w (5/4) ( Db ). * P

    Article Snippet: The following rabbit polyclonal primary antibodies were used against K + voltage‐gated channels (Kv) subunits Kv4.2 (1:200, APC 023, Alomone Labs, Jerusalem, Israel), Kv4.3 (1:200, APC 017, Alomone Labs), K + channel interacting protein 2 (KChIP2) (1:200, sc‐25685, Santa Cruz Biotechnology Inc, Santa Cruz, CA), and K + inwardly rectifying channel (Kir) subunits Kir2.1 (1:200, APC 159, Alomone Labs), Kir2.3 (1:1000, APC 032, Alomone Labs), Kir3.1 (1:200, APC 005, Alomone Labs), Kir3.4 (1:200, APC 027, Alomone Labs), and as loading control calsequestrin (1:2500, PA1‐913, Thermo Fisher Scientific).

    Techniques: Expressing, Transgenic Assay, Mouse Assay, Western Blot

    ( A ) Kir2.1 channel conductance-[K + ] relationship. The conductance-[K + ] relationship was obtained under the fluid-flow condition. Note the right-shifted conductance-[K + ] relationship at −50 mV compared to the corresponding relationship at −100 mV. ( B ) Summary of the facilitating effect of fluid flow on the IKir2.1 at 150 and 200 mM extracellular [K + ] at a voltage of −100 mV; **p

    Journal: Scientific Reports

    Article Title: Fluid flow facilitates inward rectifier K+ current by convectively restoring [K+] at the cell membrane surface

    doi: 10.1038/srep39585

    Figure Lengend Snippet: ( A ) Kir2.1 channel conductance-[K + ] relationship. The conductance-[K + ] relationship was obtained under the fluid-flow condition. Note the right-shifted conductance-[K + ] relationship at −50 mV compared to the corresponding relationship at −100 mV. ( B ) Summary of the facilitating effect of fluid flow on the IKir2.1 at 150 and 200 mM extracellular [K + ] at a voltage of −100 mV; **p

    Article Snippet: Samples were run on a 10% SDS-polyacrylamide non-reducing gel and then transferred to a polyvinylidene fluoride membrane (Millipore, Bedford, MA, USA), and the membrane was blocked with 5% BSA for 1 h. Western blotting was performed using rabbit primary antibodies against Kir2.1 channel (1:500; Alomone Lab, Jerusalem, Israel) and secondary antibodies conjugated with horseradish peroxidase (1:1,000; Cell Signaling Technology, Danvers, MA, USA).

    Techniques: Flow Cytometry

    IKir2.1 in RBL-2H3 cells is increased by fluid flow. ( A ) Representative Kir2.1 currents elicited by voltage steps starting from a holding potential of 0 mV, under control (static) and fluid-flow conditions in a high-extracellular-K + solution. ( B ) Representative tracing of IKir2.1 at −100 mV before and after fluid-flow application. ( C ) Average current-voltage (I–V) relationships in the absence and presence of fluid flow (n = 8); *p

    Journal: Scientific Reports

    Article Title: Fluid flow facilitates inward rectifier K+ current by convectively restoring [K+] at the cell membrane surface

    doi: 10.1038/srep39585

    Figure Lengend Snippet: IKir2.1 in RBL-2H3 cells is increased by fluid flow. ( A ) Representative Kir2.1 currents elicited by voltage steps starting from a holding potential of 0 mV, under control (static) and fluid-flow conditions in a high-extracellular-K + solution. ( B ) Representative tracing of IKir2.1 at −100 mV before and after fluid-flow application. ( C ) Average current-voltage (I–V) relationships in the absence and presence of fluid flow (n = 8); *p

    Article Snippet: Samples were run on a 10% SDS-polyacrylamide non-reducing gel and then transferred to a polyvinylidene fluoride membrane (Millipore, Bedford, MA, USA), and the membrane was blocked with 5% BSA for 1 h. Western blotting was performed using rabbit primary antibodies against Kir2.1 channel (1:500; Alomone Lab, Jerusalem, Israel) and secondary antibodies conjugated with horseradish peroxidase (1:1,000; Cell Signaling Technology, Danvers, MA, USA).

    Techniques: Flow Cytometry

    Kir2.1 activity is increased by fluid-flow in HEK293T cells in which Kir2.1 was ectopically over-expressed. ( A , D ) Representative tracing of currents at −140 mV in HEK293T cells expressing Kir2.1 ( A ) and non-transfected cells ( D ) before and after fluid-flow application. ( B , E ) Representative current recordings of HEK293T cells expressing Kir2.1 ( B ) and non-transfected cells ( E ) under control (static) and fluid-flow conditions. Currents were elicited by voltage steps from −160 mV to 0 mV at a holding potential of −80 mV. ( C , F ) Average current-voltage (I–V) relationships in the absence (black) and presence (red) of fluid flow in HEK293T cells expressing Kir2.1 ( C ) and non-transfected cells ( F ); **p

    Journal: Scientific Reports

    Article Title: Fluid flow facilitates inward rectifier K+ current by convectively restoring [K+] at the cell membrane surface

    doi: 10.1038/srep39585

    Figure Lengend Snippet: Kir2.1 activity is increased by fluid-flow in HEK293T cells in which Kir2.1 was ectopically over-expressed. ( A , D ) Representative tracing of currents at −140 mV in HEK293T cells expressing Kir2.1 ( A ) and non-transfected cells ( D ) before and after fluid-flow application. ( B , E ) Representative current recordings of HEK293T cells expressing Kir2.1 ( B ) and non-transfected cells ( E ) under control (static) and fluid-flow conditions. Currents were elicited by voltage steps from −160 mV to 0 mV at a holding potential of −80 mV. ( C , F ) Average current-voltage (I–V) relationships in the absence (black) and presence (red) of fluid flow in HEK293T cells expressing Kir2.1 ( C ) and non-transfected cells ( F ); **p

    Article Snippet: Samples were run on a 10% SDS-polyacrylamide non-reducing gel and then transferred to a polyvinylidene fluoride membrane (Millipore, Bedford, MA, USA), and the membrane was blocked with 5% BSA for 1 h. Western blotting was performed using rabbit primary antibodies against Kir2.1 channel (1:500; Alomone Lab, Jerusalem, Israel) and secondary antibodies conjugated with horseradish peroxidase (1:1,000; Cell Signaling Technology, Danvers, MA, USA).

    Techniques: Activity Assay, Flow Cytometry, Expressing, Transfection