缬沙坦对心肌梗死后大鼠钾通道Kv2.1变化的影响及其调控分子机制研究
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摘要
第一部分心肌梗死后大鼠钾通道Kv2.1基因表达的变化
目的研究大鼠心肌梗死(MI)后钾通道Kv2.1的动态变化。
方法通过结扎大鼠左前降支近端建立心肌梗死模型，手术后存活大鼠进入MI组(7，30天组)。同时，设立相应的假手术(SH)组。应用半定量RT-PCR方法和Western Blots方法检测左室心肌(MI者取梗死周边非梗死区左室心肌)钾通道Kv2.1mRNA及通道蛋白量。
结果与SH组比较，MI组(7天组、30天组)Kv2.1mRNA和蛋白量明显下降(P＜0.05或P＜0.01)。MI组内30天组与7天组比较，Kv2.1mRNA和蛋白量显著下降(P＜0.05)。
结论MI后钾通道Kv2.1基因表达呈时间依赖性下调，此可能是MI后易发心律失常的分子机制之一。
第二部分缬沙坦对心肌梗死后大鼠钾通道Kv2.1表达变化的影响
目的探讨缬沙坦对大鼠心肌梗死后梗死周边非梗死区左室心肌钾通道Kv2.1α-亚单位变化的影响。
方法通过结扎大鼠左前降支近端建立心肌梗死大鼠模型，手术后存活大鼠随机分入心肌梗死组(7天组，30天组)和缬沙坦组(7天组，30天组：缬沙坦30mg．kg~(-1)．day~(-1))，同时设立相应假手术组；心肌梗死组和假手术组对应给予等量盐水。应用半定量RT-PCR方法和Western Blots法检测非梗死左室心肌钾通道Kv2.1α-亚单位m RNA和通道蛋白量。
结果与假手术组比较，心肌梗死后钾通道Kv2.1m RNA和通道蛋白量均明显下降[分别为P＜0.05(7天)；P＜0.01(30天)]。与心肌梗死组比较，缬沙坦组钾通道Kv2.1m RNA和通道蛋白量均明显升高[分别为P＜0.05(7天)；P＜0.01(30天)]。缬沙坦组与假手术组比较钾通道Kv2.1m RNA和通道蛋白量差异无显著性(P＞0.05)。
结论缬沙坦可以明显逆转大鼠心肌梗死后钾通道Kv2.1的下调，这提示血管紧张素Ⅱ信号途径可能是心肌梗死后引起钾通道Kv2.1α-亚单位表达的下调的主要信号转导通路之一。
第三部分缬沙坦对心肌梗死后大鼠蛋白激酶C异构体、Giα-2和β肾上腺受体激酶-1基因表达变化的影响
目的研究缬沙坦对心肌梗死后梗死周边非梗死区左室心肌蛋白激酶C异构体(PKC—ε)、Giα—2和β肾上腺受体激酶—1基因表达变化的影响，初步探讨其调控心肌梗死后钾通道Kv2.1变化的分子机制。
方法通过结扎大鼠左前降支近端建立心肌梗死大鼠模型，手术后存活大鼠随机分入心肌梗死组(7天组，30天组)和缬沙坦组(7天组，30天组：缬沙坦30mg．kg~(-1)．day~(-1))，同时设立相应假手术组；心肌梗死组和假手术组对应给予等量盐水。应用半定量RT-PCR方法检测非梗死左室心肌蛋白激酶C异构体PKC—ε、Giα—2和β肾上腺受体激酶—1m RNA量。
结果与假手术组比较，心肌梗死组蛋白激酶C异构体PKC—ε、Giα—2和β肾上腺受体激酶—1m RNA量明显升高[分别为P＜0.05(7天)；P＜0.01(30天)]；与心肌梗死组比较，缬沙坦组蛋白激酶C异构体PKC—ε、Giα—2和β肾上腺受体激酶—1m RNA量明显减低[分别为P＜0.05(7天)；P＜0.01(30天)]。与假手术组比较，缬沙坦组蛋白激酶C异构体PKC—ε、Giα—2和β肾上腺受体激酶—1m RNA量差异无显著性(P＞0.05)。
结论缬沙坦可明显正常化蛋白激酶C异构体PKC—ε、Giα—2和β肾上腺受体激酶—1基因表达的上调，此可能是缬沙坦调控心肌梗死后钾通道Kv2.1变化的分子机制。
Part I
An experimental study of the dynamic changes of expression of
potassium channels Kv2.1 in post- myocardial infarction rat heart.
Objective To investigate the dynamic changes of the expression of potassium channel Kv2.1 in post-myocardial infarction (MI) rat heart.
Methods Using a rat model of MI, induced by the left anterior descending coronary artery (LAD) ligation in female Sprague-Dawley rats, the living rats were enrolled into post-MI group. Accordingly, the sham-operation group (sham-group) was established. According to the time of getting sample, the living rats in each group were divided into two subgroups (7 days group and 30 days group). Using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and western blots, we measured mRNA and channel protein of Kv2.1 in each group. Results Compared to the sham-group, Kv2.1 mRNA and channel protein in the post-MI group remarkably decreased regardless of 7 days or 30 days (P<0.05 or P<0.01). Compared to the 7 days post-MI group, Kv2.1 mRNA and protein in the 30 days post-MI group remarkably reduced (P<0.05).
Conclusion The expression of potassium channels Kv2.1 after myocardial infarction
exhibits the time-dependent downregulation, which may be one of the molecular
mechanisms that are able to cause the arrhythmia after myocardial infarction.
Part II
Effects of valsartan on the changes of expression of potassium channels Kv2.1 in post-myocardial infarction rat
Objective To study the effects of valsartan on the changes of the expression of potassium channels Kv2.1a-subunit of left ventricular non-infarcted myocardiums in post-myocardial infarction (post-MI) rats.
Methods Using a rat model of MI, induced by the left anterior descending coronary artery (LAD) ligation in female Sprague-Dawley rats, the living rats were randomly divided into post-MI group( 7 days group[n=10]; 30 days group[n=11]) or valsartan group(7 days group[n=10]; 30 days group[n=10]; valsartan 30mg.kg~(-1).day~(-1)). Accordingly, the sham-operation group (sham-group) was established. Using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and western blots, we measured the contents of Kv2.1 mRNA and protein in each group. Results Compared to sham-groups, the expression levels of Kv2.1 mRNA and protein in the post-MI group prominently reduced on 7 days (P<0.05) or 30 days (P＜0.01). Compared to Post-MI groups, the expression levels of Kv2.1 mRNA and protein in the valsartan groups increased remarkably on 7 days (P<0.05) or 30 days (P<0.01). There were no differences between the sham-groups and the valsartan groups (P>0.05).
Conclusion Valsartan may reverse the downregulation of expression of potassium channels Kv2.1 in post-myocardial infarction rat markedly, which suggests that angiotensin II signaling pathway can be one of major signaling-transduction pathway bringing potassium channel Kv2.1 α-subunit downregulation.
Part III
Effects of valsartan on the gene expression of protein kinase C
isoform, Giα-2, and β-adrenergic receptor kinase-1 in
post-myocardial infarction rat
Objective To study the effects of valsartan on the gene expression of protein kinase C isoforms (PKC-ε), Giα-2, and β-adrenergic receptor kinase-1 and to explore the molecular mechanism of valsartan modulating the changes of potassium channel Kv2.1 in post-myocardial infarction rat heart.
Methods Using a rat model of MI, induced by the left anterior descending coronary artery (LAD) ligation in female Sprague-Dawley rats, the living rats were randomly divided into post-MI group( 7 days group[n=10]; 30 days group[n=11]) or valsartan group(7 days group[n=10]; 30 days group[n=10]; valsartan 30mg.kg~(-1).day~(-1)). Accordingly, the sham-operation group (sham-group) was established. Using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), we measured the contents of protein kinase C isoforms (PKC-ε), Giα-2, and β-adrenergic receptor kinase-1 mRNA in each group.
Results Compared to sham-groups, the expression levels of protein kinase C isoforms (PKC-ε), Giα-2, and β-adrenergic receptor kinase-1 mRNA in the post-MI group prominently increased on 7 days (P＜0.05) or 30 days (P<0.01). Compared to Post-MI groups, the expression levels of protein kinase C isoforms (PKC-ε), Giα-2, and β-adrenergic receptor kinase-1 mRNA in the valsartan groups reduced remarkably on 7 days (P＜0.05) or 30 days (P<0.01). There were no differences between the sham-groups and the valsartan groups (P>0.05).
Conclusion The gene expressions of protein kinase C isoforms (PKC-ε), Giα-2, and β-adrenergic receptor kinase-1 are up-regulated remarkably in Post-MI rat heart; Valsartan may normalize these changes prominently, which can be the molecular mechanism of valsartan modulating the changes of potassium channel Kv2.1 in post-myocardial infarction rat.
目的研究大鼠心肌梗死(MI)后钾通道Kv2.1的动态变化。
方法通过结扎大鼠左前降支近端建立心肌梗死模型，手术后存活大鼠进入MI组(7，30天组)。同时，设立相应的假手术(SH)组。应用半定量RT-PCR方法和Western Blots方法检测左室心肌(MI者取梗死周边非梗死区左室心肌)钾通道Kv2.1mRNA及通道蛋白量。
结果与SH组比较，MI组(7天组、30天组)Kv2.1mRNA和蛋白量明显下降(P＜0.05或P＜0.01)。MI组内30天组与7天组比较，Kv2.1mRNA和蛋白量显著下降(P＜0.05)。
结论MI后钾通道Kv2.1基因表达呈时间依赖性下调，此可能是MI后易发心律失常的分子机制之一。
第二部分缬沙坦对心肌梗死后大鼠钾通道Kv2.1表达变化的影响
目的探讨缬沙坦对大鼠心肌梗死后梗死周边非梗死区左室心肌钾通道Kv2.1α-亚单位变化的影响。
方法通过结扎大鼠左前降支近端建立心肌梗死大鼠模型，手术后存活大鼠随机分入心肌梗死组(7天组，30天组)和缬沙坦组(7天组，30天组：缬沙坦30mg．kg~(-1)．day~(-1))，同时设立相应假手术组；心肌梗死组和假手术组对应给予等量盐水。应用半定量RT-PCR方法和Western Blots法检测非梗死左室心肌钾通道Kv2.1α-亚单位m RNA和通道蛋白量。
结果与假手术组比较，心肌梗死后钾通道Kv2.1m RNA和通道蛋白量均明显下降[分别为P＜0.05(7天)；P＜0.01(30天)]。与心肌梗死组比较，缬沙坦组钾通道Kv2.1m RNA和通道蛋白量均明显升高[分别为P＜0.05(7天)；P＜0.01(30天)]。缬沙坦组与假手术组比较钾通道Kv2.1m RNA和通道蛋白量差异无显著性(P＞0.05)。
结论缬沙坦可以明显逆转大鼠心肌梗死后钾通道Kv2.1的下调，这提示血管紧张素Ⅱ信号途径可能是心肌梗死后引起钾通道Kv2.1α-亚单位表达的下调的主要信号转导通路之一。
第三部分缬沙坦对心肌梗死后大鼠蛋白激酶C异构体、Giα-2和β肾上腺受体激酶-1基因表达变化的影响
目的研究缬沙坦对心肌梗死后梗死周边非梗死区左室心肌蛋白激酶C异构体(PKC—ε)、Giα—2和β肾上腺受体激酶—1基因表达变化的影响，初步探讨其调控心肌梗死后钾通道Kv2.1变化的分子机制。
方法通过结扎大鼠左前降支近端建立心肌梗死大鼠模型，手术后存活大鼠随机分入心肌梗死组(7天组，30天组)和缬沙坦组(7天组，30天组：缬沙坦30mg．kg~(-1)．day~(-1))，同时设立相应假手术组；心肌梗死组和假手术组对应给予等量盐水。应用半定量RT-PCR方法检测非梗死左室心肌蛋白激酶C异构体PKC—ε、Giα—2和β肾上腺受体激酶—1m RNA量。
结果与假手术组比较，心肌梗死组蛋白激酶C异构体PKC—ε、Giα—2和β肾上腺受体激酶—1m RNA量明显升高[分别为P＜0.05(7天)；P＜0.01(30天)]；与心肌梗死组比较，缬沙坦组蛋白激酶C异构体PKC—ε、Giα—2和β肾上腺受体激酶—1m RNA量明显减低[分别为P＜0.05(7天)；P＜0.01(30天)]。与假手术组比较，缬沙坦组蛋白激酶C异构体PKC—ε、Giα—2和β肾上腺受体激酶—1m RNA量差异无显著性(P＞0.05)。
结论缬沙坦可明显正常化蛋白激酶C异构体PKC—ε、Giα—2和β肾上腺受体激酶—1基因表达的上调，此可能是缬沙坦调控心肌梗死后钾通道Kv2.1变化的分子机制。
Part I
An experimental study of the dynamic changes of expression of
potassium channels Kv2.1 in post- myocardial infarction rat heart.
Objective To investigate the dynamic changes of the expression of potassium channel Kv2.1 in post-myocardial infarction (MI) rat heart.
Methods Using a rat model of MI, induced by the left anterior descending coronary artery (LAD) ligation in female Sprague-Dawley rats, the living rats were enrolled into post-MI group. Accordingly, the sham-operation group (sham-group) was established. According to the time of getting sample, the living rats in each group were divided into two subgroups (7 days group and 30 days group). Using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and western blots, we measured mRNA and channel protein of Kv2.1 in each group. Results Compared to the sham-group, Kv2.1 mRNA and channel protein in the post-MI group remarkably decreased regardless of 7 days or 30 days (P<0.05 or P<0.01). Compared to the 7 days post-MI group, Kv2.1 mRNA and protein in the 30 days post-MI group remarkably reduced (P<0.05).
Conclusion The expression of potassium channels Kv2.1 after myocardial infarction
exhibits the time-dependent downregulation, which may be one of the molecular
mechanisms that are able to cause the arrhythmia after myocardial infarction.
Part II
Effects of valsartan on the changes of expression of potassium channels Kv2.1 in post-myocardial infarction rat
Objective To study the effects of valsartan on the changes of the expression of potassium channels Kv2.1a-subunit of left ventricular non-infarcted myocardiums in post-myocardial infarction (post-MI) rats.
Methods Using a rat model of MI, induced by the left anterior descending coronary artery (LAD) ligation in female Sprague-Dawley rats, the living rats were randomly divided into post-MI group( 7 days group[n=10]; 30 days group[n=11]) or valsartan group(7 days group[n=10]; 30 days group[n=10]; valsartan 30mg.kg~(-1).day~(-1)). Accordingly, the sham-operation group (sham-group) was established. Using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and western blots, we measured the contents of Kv2.1 mRNA and protein in each group. Results Compared to sham-groups, the expression levels of Kv2.1 mRNA and protein in the post-MI group prominently reduced on 7 days (P<0.05) or 30 days (P＜0.01). Compared to Post-MI groups, the expression levels of Kv2.1 mRNA and protein in the valsartan groups increased remarkably on 7 days (P<0.05) or 30 days (P<0.01). There were no differences between the sham-groups and the valsartan groups (P>0.05).
Conclusion Valsartan may reverse the downregulation of expression of potassium channels Kv2.1 in post-myocardial infarction rat markedly, which suggests that angiotensin II signaling pathway can be one of major signaling-transduction pathway bringing potassium channel Kv2.1 α-subunit downregulation.
Part III
Effects of valsartan on the gene expression of protein kinase C
isoform, Giα-2, and β-adrenergic receptor kinase-1 in
post-myocardial infarction rat
Objective To study the effects of valsartan on the gene expression of protein kinase C isoforms (PKC-ε), Giα-2, and β-adrenergic receptor kinase-1 and to explore the molecular mechanism of valsartan modulating the changes of potassium channel Kv2.1 in post-myocardial infarction rat heart.
Methods Using a rat model of MI, induced by the left anterior descending coronary artery (LAD) ligation in female Sprague-Dawley rats, the living rats were randomly divided into post-MI group( 7 days group[n=10]; 30 days group[n=11]) or valsartan group(7 days group[n=10]; 30 days group[n=10]; valsartan 30mg.kg~(-1).day~(-1)). Accordingly, the sham-operation group (sham-group) was established. Using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), we measured the contents of protein kinase C isoforms (PKC-ε), Giα-2, and β-adrenergic receptor kinase-1 mRNA in each group.
Results Compared to sham-groups, the expression levels of protein kinase C isoforms (PKC-ε), Giα-2, and β-adrenergic receptor kinase-1 mRNA in the post-MI group prominently increased on 7 days (P＜0.05) or 30 days (P<0.01). Compared to Post-MI groups, the expression levels of protein kinase C isoforms (PKC-ε), Giα-2, and β-adrenergic receptor kinase-1 mRNA in the valsartan groups reduced remarkably on 7 days (P＜0.05) or 30 days (P<0.01). There were no differences between the sham-groups and the valsartan groups (P>0.05).
Conclusion The gene expressions of protein kinase C isoforms (PKC-ε), Giα-2, and β-adrenergic receptor kinase-1 are up-regulated remarkably in Post-MI rat heart; Valsartan may normalize these changes prominently, which can be the molecular mechanism of valsartan modulating the changes of potassium channel Kv2.1 in post-myocardial infarction rat.
引文
1. Rogers WJ, Canto JG, Lambrew CT, et al. Temporal trends in the treatment of over 1.5 million patients with myocardial infarction in the US from 1990 through 1999: the National Registry of Myocardial infarction 1, 2 and 3. J Am Coll Cardiol, 2000, 36: 2056-2063.
2. Roden DM, Balser JR, George Jr AL, et al. Cardiac ion channels. Annu Rev Physiol, 2002, 64: 431-475.
3. Surawicz B. Ventricular fibrillation and dispersion of repolarization. J Cardiovasc Electrophysiol, 1997, 8:1009-1012.
4. Carmeliet E. Cardiac ionic currents and acute ischemia: From channels to arrhythmias. Physiol Rev, 1999, 79: 917-1017.
5. Rudy B. Diversity and ubiquity of K channels. Neuroscience, 1988, 25(3):729-749.
6. Nerbonne JM. Molecular basis of functional voltage-gated K+ channel diversity in the mammalian myocardium. J Physiol, 2000, 525(2): 285-298.
7. Barry DM, Nerbonne JM. Myocardial potassium channels: electrophysiological and molecular diversity. Annu Rev Physiol, 1996, 58: 363-394.
8. Pongs O. Molecular biology of voltage-dependent potassium channels. Physiol Rev, 1992, 72: S69-88.
9. Dixon JE, McKinnon. Quantitative analysis of potassium channel mRNA expression in atrial and ventricular muscle of rats. Circ Res, 1994, 75: 252-260.
10. Xu HD, Barry DM, Li HL, et al. Attenuation of the slow component of delayed rectification, action potential prolongation, and triggered activity in mice expressing a dominant-negative Kv2 a subunit. Circ Res, 1999, 85: 623-633.
11.Wang W, Hino NK, Yamasaki H, et al. Kv2.1 K+ channels underlie major voltage-gated K~+ outward current in H9c2 myoblasts. Jpn J Physiol, 2002, 52:507-514.
12. Huang B, Qin D, E1-Sherif N. Spatial alterations of Kv channels expression and K~+ currents in post-MI remodeled rat heart. Cardiovasc Res, 2001, 52: 246-254.
13. Huang B, Qin D, E1-Sherif N. Early down-regulation of K+ channel genes and currents in the postinfarction heart. J Cardiovasc Electrophysiol, 2000, 11(11): 252-1261.
14. Gidh-Jain M, Huang B, Jain P, et al. Differential expression of voltage-gated K+ channel genes in left ventricular remodeled myocardium after experimental myocardial infarction. Circ Res, 1996, 79(4): 669-675.
15. Anversa P, Beghi C, Kikkawa Y, et al. Myocardial infarction in rats: infarct size, myocyte hypertrophy, and capillary growth. Circ Res, 1986, 58: 26-37.
16. Hart G. Cellular electrophysiology in cardiac hypertrophy and failure. Cardiovasc Res, 1994, 28: 933-946.
1 Dixon JE, Mckinnon D. Quantitative analysis of potassium channel mRNA expression in atrial and ventricular muscle of rats. Circ Res, 1994, 75: 252-260.
2 Kuno A, Yamada T, Masuda K, Et A1. Angiotensin converting enzyme inhibitor attenuates pancreatic in. ammation and fibrosis in male wistar bonn/kobori rats. Gastroenterology, 2003, 124: 1010—1019.
3 Roden DM, Balser JR, George Jr AL, et al. Cardiac ion channels. Annu Rev Physiol, 2002, 64: 431-475.
4 Xu H, Barry DM, Li H, et al. Attenuation of the slow component of delayed rectification, action potential prolongation, and triggered activity in mice expressing a dominant-negative Kv2 α subunit. Citc Res, 1999, 85: 623-633.
5 Cohen IS, Datyner NB, Gintant GA, et al. Time-dependent outward currents in the heart. In: Fozzard HA, Jennings RB, Haber E, Katz AM, Morgan HE, eds. The Heart and Cardiovascular System. New York, NY: Raven Press Publishers, 1986: 637-670.
6 Carmeliet E, Biermans G, Callewaert G, et al. Potassium currents in cardiac cells. Experientia, 1987, 43: 1175-1184.
7 Anumonwo JMB, Freeman LC, Kwok WM, et al. Potassium channels in the heart: electrophysiology and pharmacological regulation. Cardiovasc Drug Rev, 1991, 9: 299-316.
8 Boyle WA, Nerbonne JM. A novel type of depolarization-activated K~+ current in isolated adult rat atrial myocytes. Am J Physiol, 1991, 260: H1236-H1247.
9 Varro A, Lathrop DA, Hester SB, et al. Ionic currents and action potentials in rabbit, rat, and guinea pig ventricular myocytes. Basic Res Cardiol, 1993, 88: 93-102.
10 Rudy B. Diversity and ubiquity of K channels. Neuroscience, 1988, 25(3): 729-749.
11 Nerbonne JM. Molecular basis of functional voltage-gated K+ channel
---- diversity in the mammalian myocardium. J Physiol, 2000, 525(2): 285-298.
12 Barry DM, Nerbonne JM. Myocardial potassium channels: electrophysiological and molecular diversity. Annu Rev Physiol, 1996, 58:363-394.
13 Wang w, Hino NK, Yamasaki H, et al. Kv2.1 K~+ channels underlie major voltage-gated K~+ outward current in H9c2 myoblasts. Jpn J Physiol, 2002, 52:507-514.
14 Schultz JH, Volk T, Ehmke H. Heterogeneity of Kv2.1 mRNA expression and delayed rectifier current in single isolated myocytes from rat left ventricle.Circ Res, 2001, 88: 483-490.
15 Kramer JW, Post MA, Brown AM, et al. Modulation of potassium channel gating by coexpression of Kv2.1 with regulatory Kv5.1 or Kv6.1 α-subunits. Am J Physiol, 1998, 274:C1501-C1510.
16 Salinas M, Duprat F, Heurteaux C, et al. New modulatory a subunits for mammalian Shab K~+ channels. J Biol Chem, 1997, 272: 24371-24379.
17 Post MA, Kirsch GE, Brown AM. Kv2.1 and electrically silent Kv6.1 potassium channel subunits combine and express a novel current. FEBS Lett,1996, 399: 177-182.
18 Zhu XR, Netzer R, Bohlke K, et al. Structural and functional characterization of Kv6.2 a new y subunit of voltage-gated potassium channel. Receptors Channels. 1999, 6: 337-350.
19 Kerschensteiner D, Stacker M. Heteromeric assembly of Kv2.1 with Kv9.3: Effect on the state dependence of inactivation. Biophys J, 1999, 77: 248-257.
1. Barry DM, Nerbonne JM. Myocardial potassium channels: electrophysiological and molecular diversity. Annu Rev Physiol, 1996, 58: 363-394.
2. Nerbonne JM. Molecular basis of functional voltage-gated K+ channel diversity in the mammalian myocardium. J Physiol, 2000, 525(2): 285-298.
3. Rudy B. Diversity and ubiquity of K channels. Neuroscience, 1988, 25(3): 729-749.
4. Xu H, Barry DM, Li H, et al. Attenuation of the slow component of delayed rectification, action potential prolongation, and triggered activity in mice expressing a dominant-negative Kv2 α-subunit. Circ Res, 1999, 85: 623-33.
5. Wang W, Hino N, Yamasaki H, et al. Kv2.1 K~+ channels underlie major voltage-gated K~+ outward current in H9c2 myoblasts. Jpn J Physiol, 2001, 52: 507-14.
6. Zhou J, Kodirov S, Murata M, et al. Regional upregulation of Kv2.1-encoded current, Ik, slow2, in Kv1DN mice is abolished by crossbreeding wuth Kv2DN mice. Am J Physiol Heart Circ Physiol, 2003, 284: H491-H500.
7. Huang B, Qin D, E1-Sherif N. Spatial alterations of Kv channels expression and K~+ currents in post-MI remodeled rat heart. Cardiovasc Res, 2001, 52: 246-254.
8. Huang B, Qin D, E1-Sherif N. Early down-regulation of K+ channel genes and currents in the postinfarction heart. J Cardiovasc Electrophysiol, 2000, 11(11): 1252-1261.
9. Gidh-Jain M, Huang B, Jain P, et al. Differential expression of voltage-gated K+ channel genes in left ventricular remodeled myocardium after experimental myocardial infarction. Circ Res, 1996, 79(4): 669-675.
10. Cohen IS, Datyner NB, Gintant GA, et al. Time-dependent outward currents in the heart. In: Fozzard HA, Jennings RB, Haber E, Katz AM, Mortgan HE, eds. The Heart and Cardiovascular System. New York, NY: Raven Press Publishers, 1986: 637-670.
11. Carmeliet E, Beimans G, Callewaert G, et al. Potassium currents in cardiac cells.Experientia. 1987, 43: 1175-1184.
12. Anumonowo JMB, Freeman LC, Kwok WM, Kass RS. Potassium channels in the heart: electrophysiology and pharmacological regulation. Cardiovasc Drug Rev. 1991,9:299-316.
13. Antzelevitch C, Sicouri S, Litovsky SH, et al. Heterogeneity within the ventricular wall: electrophysiology and pharmacology of epicardial, endocardial, and M cells. Circ Res, 1991, 69: 1427-1449.
14. Dixon JE, Mckinnon D. Quantitative analysis of potassium channel mRNA expression in atrial and ventricular muscle of rats. Circ Res, 1994, 75: 252-60.
15. Schultz JH, Volk T, Ehmke H. Heterogeneity of Kv2.1 mRNA expression and delayed rectifier current in single isolated myocytes from rat left ventricle. Circ Res, 2001,88:483-90.
16. Kramer JW, Post MA, Brown AM, et al. Modulation of potassium channel gating by coexpression of Kv2.1 with regulatory Kv5.1 or Kv6.1 K-subunits. Am J Physiol, 1998,274:C1501-C1510.
17. Salinas M, Duprat F, Heurteaux C, et al. New modulatory a subunits for mammalian Shab K~+ channels. J Biol Chem, 1997, 272: 24371-24379.
18. Post MA, Kirsch GE, Brown AM. Kv2.1 and electrically silent Kv6.1 potassium channel subunits combine and express a novel current. FEBS Lett, 1996, 399:177-182.
19. Zhu XR, Netzer R, Bohlke K, et al. Structural and functional characterization of Kv6.2 a new y subunit of voltage-gated potassium channel. Receptors Channels.1999, 6: 337-350.
20. Kerschensteiner D, Stacker M. Heteromeric assembly of Kv2.1 with Kv9.3: Effect on the state dependence of inactivation. Biophys J, 1999, 77: 248-257.
21. Amberg GC, Rossow CF, Navedo MF, et al. NFATc3 regulates Kv2.1 expression in arterial smooth muscle. J Biol Chem, 2004, 279(45): 47 326-34.
22. Nishizuka, Y. Intracellular signaling by hydrolysis of phospholipids and activation of protein kinase C. Science , 1992, 258: 607-614.
23. Damron DS, Nadim HS, Sung JH, et al. Intracellular translocation of PKC isoforms in canine pulmonary artery smooth muscle cells by ANG II. Am J Physiol Lung Cell Mol Physiol, 1998,274: L278-L288.
24. Zhu MY, Gelband CH, Posner P, et al. Angiotensin II Decreases Neuronal Delayed Rectifier Potassium Current: Role of Calcium/Calmodulin-Dependent Protein Kinase II. J Neurophysiol, 1999, 82(3):1 560-68.
25. Anand-Srivastava, MB. Angiotensin II receptors negatively coupled to adenylate cyclase in rat aorta. Biochem Biophys Res Commun, 1983,117: 420-428.
26. Unger, T, Chung O, Csikos T,et al. Angiotensin receptors. J Hypertens Suppl,1996, 14: S95-S103.
27. Shaywitz AJ, Greenberg ME. CREB: a stimulus-induced transcription factor activated by a diverse array of extrecellular signals. Annu Rev Biochem, 1999, 68:821-861.
28. Lonze BE, Ginty DD, Function and regulation of CREB family transcription factors in the nervous system. Neuron, 2002, 35: 605-623.
29. Mayr B, Montminy M. Transcriptional regulation by the phosphorylation- dependent factor CREB. Nat Rev Mol Cell Biol, 2001, 2: 599-609.
30. Mori Y, Matsubara H, Folco E, et al. The transcription of a mammalian voltage-gated potassium channel is regulated by cAMP in a cell-specific manner. J Biol Chem, 1993, 268: 26482-26493.
31. Patberg KW, Plotnikov AN, Quamina A, et al. Cardiac memory is associated with decreased levels of the transcriptional factor CREB modulated by angiotensin Hand calcium. Circ Res, 2003, 93: 472-478.
32. Gah L, Perney TM, Kaczmarek LK. Cloning and characterization of the promoter for a potassium channel expressed in high frequency firing neurons. J Biol Chem,1996,271:5859-5865.
33. Beckh S, Pongs O. Members of the RCK potassium channel family are different expressed in the rat nervous system. EMBO J, 1990, 9: 777-782.
1 Suaen PH, Bogoyevitch MA. Intracellular signalling through protein kinase in the heart. Cardiovisc Res, 1995, 30: 478-491.
2 Bogoyevitch MA, Parker PJ, Sugden PH. Characterization of protein kinase C isotype expression in adult rat heart: Protein kinase C-ε is a major isotype present, and it is activated by phorbol esters, epinephrine, and endothelin. Circ Res, 1993, 72: 757-767.
3 Strasser RH, Simonis G, Schon SP, et al. Two distinct mechanisms mediate a differential regulation of protein kinase C isozymes in acute and prolonged myocardial ischemia. Circ Res, 1999, 85: 77-87.
4 Xiao RP. β-adrenergic signaling in the heart: dual coupling of the β_(2-) adrenergic receptor to G_s and G_i proteins. Sci. STKE. 104: RE15.
5 Dohlman HG, Thorner J, Caron MG, et al. Model systems for the study of seven-transmembrane-segment receptors. Annu Rev Biochem, 1991, 60: 653-688.
6 Anand-Srivastava, MB. Angiotensin Ⅱ receptors negatively coupled to adenylate cyclase in rat aorta. Biochem Biophys Res Commun, 1983, 117: 420-428.
7 Unger, T, Chung O, Csikos T, et al. Angiotensin receptors. J Hypertens Suppl, 1996, 14: S95-S103.
8 Kompa AR, Gu XH, Evans BA, et al. Desensitization of cardiac β-adrenoceptor signaling with heart failure produced by myocardial infarction in the rat. Evidence for the role of Gi but Gs or phosphorylating proteins. J Mol Cell Cardiol, 1999, 31: 1185-1201.
9 Ungerer M, Kessebohm K, Kronsbein K, et al. Activation of β-adrenergic receptor kinase during myocardial ischemia. Circ Res, 1996, 79: 455-460.
10 Vatner DE, Knight DR, Shen YT, et al. One hour of myocardial ischemia in conscious dogs increasesβ-adrenergic receptors, but decreases adenylate cyclase activity. J Mol Cell Cardiol, 1988, 20: 75-82.
11 Vatner DE, Young MA, Knight DR, et al. β-receptors and adenylate cyclase: comparison of nonischemic, ischemic, and postmortem tissue. Am J Physiol, 1990, 258: H140-H144.
12 Strasser RH, Krimmer J, Braun-Dullaeus R, et al. Dual sensitization of the adrenergic system in early myocardial ischemic: independent regulation of the P-adrenergic receptors and the adenylyl cyclase. J Mol Cell Cardiol, 1990, 22:1405-1423.
13 Lonse MJ. Molecular mechanisms of membrane receptor desensitization. Biochim BiophysActa, 1993, 1179: 171-188.
14 Inglese J, Freedman NJ, Koch WJ, et al. Structure and mechanism of the G protein-coupled receptor kinases. J Biol Chem, 1993, 268: 23735-23738.
15 Benovic JL, Mayor F, Staniszewski C, et al. Purification and characterization of the P-adrenergic receptors kinase. J Biol Chem, 1987, 262: 9026-9032.
16 Goldspink PH, Russell B. The cAMP response element binding protein is expressed and phosphorylated in cardiac myocytes. Circ Res, 1994, 74:1042-1049.
17 Kuno A, Yamada T, Masuda K, Et Al. Angiotensin converting enzyme inhibitor attenuates pancreatic in.ammation and fibrosis in male wistar bonn/kobori rats. Gastroenterology, 2003,124:1010-1019.
18 Naruse K, King GL. Protein kinase C and myocardfial biology and function. Circ Res, 2000, 86: 1104-1106.
19 Rybin VO, Steinberg SF. Protein kinase C isoform expression and regulation in the developing rat heart. Circ Res, 1994, 74: 299-309.
20 Schaap D, Parker PJ, Bristol A, et al. Unique substrate specificity and regulatory properties of PKC-e. A rationale for diversity. FEBS Lett, 1989, 243: 351-357.
21 Saurin AT, Pennington DJ, Raat NJH, et al. Targeted disruption of the protein kinase C epsilon geng abolishes the infarc size reduction that follows ischaemic preconditioning of isolated buffer-perfused mouse hearts. Cardiovasc Res, 2002,55: 672-680.
22 Ping P, Zhang J, Pierce WM Jr, et al. Functional proteomic analysis of protein kinase C epsilon signaling complexes in the normal heart and during cardioprotection. Circ Res, 2001, 88: 59-62.
23 Liu HP, Zhang HY, Zhu XD, et al. Preconditioning blocks cardiocyte apoptosis:role of Katp channels and PKC-8. Am J Physiol Heart Circ Physiol, 2002, 282:H1380-H1386.
24 D'Angelo DD, Sakata Y, Lorenz JN, et al. Transgenic G_(αq) overexpression induces cardiac contractile failure in mice. Proc Natl Acad Sci USA, 1997, 94: 8121-8126.
25 Paul K, Ball NA, Dorn GW II, et al. Left ventricular stretch stimulates angiotensin II -mediated phosphatidylinositol hydrolysis and protein kinase C epsilon isoform translocation in adult guinea pig hearts. Circ Res, 1997, 81: 643-650.
26 Jalili T, Takeishi Y, Song G, et al. PKC translocation without changes in G_(αq) and PLC-beta protein abundance in cardiac hypertrophy and failure. Am J Physiol,1999, 277: H2298-H2304.
27 Clement-Chomienne O, Walsh MP, Cole WC, et al. Angiotensin II activation of protein kinase C decreases delayed rectifier K~+ current in rabbit vascular myocytes. J Physiol, 1996, 425: 689-700.
28 Hayabuchi Y, Standen NB, Davies NW. Angiotensin II inhibits and alters kinetics of voltage-gated K~+ channels of rat arterial smooth muscle. Am J Physiol Heart Circ Physiol, 2001, 281: H2480-H2489.
29 Nerbonne JM. Molecular basis of functional voltage-gated K+ channel diversity in the mammalian myocardium. J Physiol, 2000, 525(2): 285-298.
30 Xu H, Barry DM, Li H, et al. Attenuation of the slow component of delayed rectification, action potential prolongation, and triggered activity in mice expressing a dominant-negative Kv2 a-subunit. Circ Res, 1999, 85: 623-33.
31 Wang W, Hino N, Yamasaki H, et al. Kv2.1 K~+ channels underlie major voltage-gated K~+ outward current in H9c2 myoblasts. Jpn J Physiol, 2001,52:507-14.
32 Shaywitz AJ, Greenberg ME. CREB: a stimulus-induced transcription factor activated by a diverse array of extrecellular signals. Annu Rev Biochem, 1999, 68:821-861.
33 Lonze BE, Ginty DD, Function and regulation of CREB family transcription factors in the nervous system. Neuron, 2002, 35: 605-623.
34 Mayr B, Montminy M. Transcriptional regulation by the phosphorylation- dependent factor CREB. Nat Rev Mol Cell Biol, 2001, 2: 599-609.
35 Mori Y, Matsubara H, Folco E, et al. The transcription of a mammalian voltage-gated potassium channel is regulated by cAMP in a cell-specific manner. J Biol Chem, 1993, 268: 26482-26493.
36 Patberg KW, Plotnikov AN, Quamina A, et al. Cardiac memory is associated with decreased levels of the transcriptional factor CREB modulated by angiotensin II and calcium. Circ Res, 2003, 93: 472-478.
37 Gah L, Perney TM, Kaczmarek LK. Cloning and characterization of the promoter for a potassium channel expressed in high frequency firing neurons. J Biol Chem,1996,271:5859-5865.
38 Barry DM, Nerbonne JM. Myocardial potassium channels: electrophysiological and molecular diversity. Annu Rev Physiol, 1996, 58: 363-394.
39 Beckh S, Pongs O. Members of the RCK potassium channel family are different expressed in the rat nervous system. EMBO J, 1990, 9: 777-782.
40 Maisel AS, Motulsky HJ, Insel PA. Externalization of beta-adrenergic receptors promoted by myocardial ischemia. Science, 1985, 230:183-186.
41 Ungerer M, Parruti G, Bohm M, et al. Expression of β-arrestins and B-adrenergic receptor kinases in the failing human heart. Circ Res, 1994, 74:206-213.
42 Perm RB, Benovic JL. Structure of the human gene encoding the beta-adrenergic receptor kinase. J Biol Chem, 1994, 269: 14924-14930.
43 Ramos-Ruiz R, Penela P, Penn RB, et al. Analysis of the human G protein-coupled receptor kinase 2 (GRK2) gene promoter: regulation by signal transduction systems in aortic smooth muscle cells. Circulation, 2000, 101: 2083-2089.
44 Winstel R, Freund S, Krasel C, et al. Protein kinase cross-talk: membrane targeting of the beta-adrenergic receptor kinase by protein kinase C. Proc Natl Acad Sci USA, 1996, 93: 2105-2109.
45 Neumann J, Schmitz W, Scholz H, et al. Increase in myocardial Gi-proteins in heart failure. Lancet, 1988, 2: 936-937.
46 Ping P, Hammond HK. Diverse G protein and B-adrenergic receptor mRNA expression in normal and failing procine hearts. Am J Physiol, 1994, 267: H2079-H2085.
47 Shi B, Heavner JE, McMahon KK, et al. Dynamic changes in Gαi-2 levels in rat hearts associated with impaired heart function after myocardial infarction. Am J Physiol, 1995, 269: H1073-H1079.
48 Steinberg SF, Zhang HL, Pak E, et al. Characteristics of the β-adrenergic receptor complex in the epicardial border zone of the 5-day infarced canine heart. Circulation, 1995, 91: 2824-2833.
49 Maurice JP, Shan AS, Kypson AP, et al. Molecular β-adrenergic signaling abnormalities in failing rabbit hearts after infarction. Am J Physiol Heart Circ Physiol, 1999, 276: H1853-H1860.
2003
1. Rudy B. Diversity and ubiquity of K channels. Neuroscience, 1988, 25(3):729-749.
2. Nerbonne JM. Molecular basis of functional voltage-gated K+ channel diversity in the mammalian myocardium. J Physiol, 2000, 525(2): 285-298.
3. Barry DM, Nerbonne JM. Myocardial potassium channels: electrophysiological and molecular diversity. Annu Rev Physiol, 1996, 58: 363-394.
4. Pongs O. Molecular biology of voltage-dependent potassium channels. Physiol Rev, 1992, 72: S69-88.
5. Kaplan WD, Trout WE. The behavior of four neurological mutations of Drosophila. Genetics, 1969, 61: 399-409.
6. Butler A, Wei A, Baker K, et al. A family of putative potassium channel genes in Drosophila. Science, 1989, 243: 943-947.
7. Roberds SL, Tamkun MM. Cloning and tissue-specific expression of five voltage-gated potassium channels cDNAs expressed in rat heart. Proc Natl Acad Sci USA, 1991,88: 1798-1802.
8. Mei A, Covarrubias M, Butler A, et al. K~+ current diversity is produced by an extended gene family conserved in Drosophila and mouse. Science, 1990, 248:599-603.
9. Tempel BL, Papazian DM, Schwarz TL, et al. Sequence of a probable potassium channel component encoded at the Shaker locus in Drosophila. Science, 1987, 237:770-774.
10. Jan LY, Jan YN. Structural elements involved in specific K~+ channel functions.Annu Rev Physiol. 1992, 54: 537-555.
11. Pongs O. Structure-function studies on the pore of potassium channels. J Membr Biol, 1993, 136: 1-8.
12. Andalib P, Wood MJ, Korn SJ. Control of outer vestibule dynamics and current magnitude in the Kv2.1 potassium channel. J Gen Physiol, 2002, 120: 739-755.
13. Doyle DA, Cabral JM, Pfuetzner RA, et al. The structure of the potassium channel: molecular basis of K~+ conduction and selectivity. Science, 1998, 280: 69-77.
14. Albrecht B, Lorra C, Stacker M, et al. Cloning and characterization of a human delayed rectifier potassium channel gene. Receptors Channels, 1993, 1(2): 99-110.
15. Frech GC, VanDongen AM, Schuster G, et al. A novel potassium channel with delayed rectifier properties isolated from rat brain by expression cloning. Nature,1989, 340(6235): 642-645.
16. VanDongen AM, Frech GC, Drewe JA, et al. Alteration and restoration of K~+ channel function by deletions at the N- and C-termini. Neuron, 1990, 5(4):433-443.
17. Pascual JM, Shieh CC, kirsch GE, et al. Contribution of the NH_2 terminus of Kv2.1 to channel activation. Am J Physiol Cell Physiol, 1997, 273: C1849-C1858.
18. Ju M, Stevens L, Leadbitter E, et al. The roles of N- and C-terminal determinants in the activation of the Kv2.1 potassium. J Biol Chem, 2003, 278(15):12769-12778.
19. Koopmann R, Scholle A, Ludwig J, et al. Role of the S2 and S3 segment in determining the activation kinetics in Kv2.1 channels. J Membr Biol, 2001,182(1):49-59.
20. Klemic KG, Shieh CC, Kirsch GE, et al. Inactivation of Kv2.1 potassium channels. Biophys J, 1998, 74:1779-1789.
21. Lopez-Barneo J, Hoshi T, Heinemann SH, et al. Effects of external cations and mutations in the pore region on C-type inactivation of Shaker potassium.Receptors Channels, 1: 61-71.
22. Baukrowitz T, Yellen G. Use-dependent blockers and exit rate of the last ion from the multi-ion pore of a K~+ channels. Science, 1996, 271:653-656.
23. Choi KL, Aldrich RW, Yellen G Tetraethylammonium blockade distinguishes two inactivation mechanisums in voltage-activated K~+ channels. Proc Natl Acad Sci USA, 1991, 88: 5092-5095.
24. Kramer JW, Post MA, Brown AM, et al. Modulation of potassium channel gating by coexpression of Kv2.1 with regulatory Kv5.1 or Kv6.1 α-subunits. Am J Physiol, 1998, 274:C1501-C1510.
25. Kerschensteiner D, Stacker M. Heteromeric assembly of Kv2.1 with Kv9.3: effect on the state dependence of inactivation. Biophys J, 1999, 77:248-257.
26. Klemic Kg, Kirsch GE, Jones SW. U-Type inactivation of Kv3.1 and Shaker potassium channels. Biophys J, 2001, 81:814-826.
27. Kurata HT, Soon GS, Eldstrom JR, et al. Amino-terminal determinants of U-type inactivation of voltage-gated K~+ chasnnels. J Biol Chem, 2002, 277(32):29045-29053.
28. Immke D, Korn SJ. Ion-ion interactions at the selectivity filter: evidence from K~+-dependent modulation of tetraethylammonium efficacy in Kv2.1 potassium channels. J Gen Physiol, 2000, 115:509-518.
29. Immke, D, Wood MJ, Kiss L, et al. Potassium-dependent changes in the conformation of the Kv2.1 potassium channel pore. J Gen Physiol., 1999,113:819-836.
30. Wood MJ, Korn SJ. Two mechanisms of K~+-dependent potentiation in Kv2.1 potassium channels. Biophys J, 2000, 79:2535-2546.
31. Hille B, Schwartz W. Potassium channels as multi-ion pores. J Gen Physiol, 1978,72:409-442.
32. Cohen IS, Datyner NB, Gintant GA, et al. Time-dependent outward currents in the heart. In: Fozzard HA, Jennings RB, Haber E, Katz AM, Morgan HE, eds. The Heart and Cardiovascular System. New York, NY: Raven Press Publishers,1986:637-670.
33. Carmeliet E, Biermans G, Callewaert G, et al. Potassium currents in cardiac cells. Experientia, 1987,43:1175-1184.
34. Anumonwo JMB, Freeman LC, Kwok WM, et al. Potassium channels in the heart: electrophysiology and pharmacological regulation. Cardiovasc Drug Rev, 1991,9:299-316.
35. Boyle WA, Nerbonne JM. A novel type of depolarization-activated K~+ current in isolated adult rat atrial myocytes. Am J Physiol, 1991, 260:H1236-H1247.
36. Varro A, Lathrop DA, Hester SB, et al. Ionic currents and action potentials in rabbit, rat, and guinea pig ventricular myocytes. Basic Res Cardiol, 1993,88:93-102.
37. Schram G, Pourrier M, Melnyk P, et al. Differential distribution of cardiac ion channel expression as a basis for regional specialization in electrical function. Circ Res, 2002, 90: 939-950.
38. Dixon JE, McKinnon. Quantitative analysis of potassium channel mRNA expression in atrial and ventricular muscle of rats. Circ Res, 1994, 75: 252-260.
39. Brahmajothi MV, Morales MJ, Liu SG, et al. In situ hybridization reveals extensive diversity of K~+ channel mRNA in isolated ferret cardiac myocytes. Circ Res, 1996, 78: 1083-1089.
40. Schultz JH, Volk T, Ehmke H. Heterogengity of Kv2.1 mRNA expression and delayed rectifier current in single isolated myocytes from rat left ventricle. Circ Res, 2001, 88: 483-490.
41. Barry DM, Trimmer JS, Merlie JP, et al. Differential expression of voltage-gated K~+ channel subunits in adult rat heart: Relation to function K~+ channel? Circ Res,1995,77:361-369.
42. Hwang PM, Glatt CE, Bredt DS, et al. A novel K~+ channel with unique localizations in mammalian brain: molecular cloning and characterization. Neuron,1992,8:473-481.
43. Tsunoda S, Salkoff L. The major delayed rectifier in both Drosophila neurons and muscle is encoded by Shab. J Neurosci, 1995, 15: 5209-5221.
44. Apkon M, Nerbonne JM. Characterization of two distinct depolarization-activated K~+ currents in isolated adult rat ventricular myocytes. J Gen Physiol, 1991, 97:973-1011.
45. Xu HD, Barry DM, Li HL, et al. Attenuation of the slow component of delayed rectification, action potential prolongation, and triggered activity in mice expressing a dominant-negative Kv2 a subunit. Circ Res, 1999, 85: 623-633.
46. Zhou J, Kodirov S, Murata M, et al. Regional upregulation of Kv2.1-encoded current, Ik, slow2, in Kv1DN mice is abolished by crossbreeding wuth Kv2DN mice. Am J Physiol Heart Circ Physiol, 2003, 284: H491-H500.
47. Bou-Abboud E, Nerbonne JM. Molecular correlates of the calcium-independent, depolarization-activated K+ currents in rat atrial myocytes. J Physiol, 1999, 517: 407-420.
48. Wang W, Hino N, Yamasaki H, et al. Kv2.1 K~+ channels underlie major voltage-gated K~+ outward current in H9c2 myoblasts. Jpn J Physiol, 2001, 52: 507-14.
49. Post MA, Kirsch GE, Brown AM. Kv2.1 and electrically silent Kv6.1 potassium channel subunits combine and express a novel current. FEBS Lett, 1996, 399: 177-182.
50. Zhu XR, Netzer R, Bohlke K, et al. Structural and functional characterization of Kv6.2 a new gamma-subunit of voltage-gated potassium channel. Receptors Channels, 1999, 6(5): 337-50.
51. Sano Y, Mochizuki S, Miyake A, et al. Molecular cloning and characterization of Kv6.3, a novel modulatory subunit for voltage-gated K(+) channel Kv2.1. FEBS Lett, 2002, 512: 230-234.
52. Salinas M, Duprat F, Heurteaux C, et al. New modulatory α subunits for mammalian Shab K+ channels. J Biol Chem, 1997, 272(39): 24371-24379.
53. Patel AJ, Lazdunski M, Honore E. Kv2.1/Kv9.3, a novel ATP-dependent delayed-rectifier K+ channel in oxygen-sensitive pulmonary artery myocytes. EMBO J, 1997, 16: 6615-6625.
54. Hulme JT, Coppock Ea, Felipe A, et al. Oxygen sensitivity of cloned voltaged-gated K~+ channels expressed in the pulmonary vasculature. Circ Res, 1999, 85: 489-497.
55. Kerschensteiner D, Soto F, Stocker M. Fluorescence measurements reveal stoichiometry of K+ channels formed by modulatory and delayed rectifier alpha-subunits. Proc Natl Acad Sci USA, 2005, 102: 6160-6165.
56. Ottschytsch N, Raes A, Hoorick V, et al. Obligatory heterotetramerization of three previously uncharacterized Kv channel α-subunits identified in the human genome. Proc Natl Acad Sci USA, 2002, 99(12): 7986-7991.
57. Huang B, Qin D, El-Sherif N. Spatial alterations of Kv channels expression and K~+ currents in post-MI remodeled rat heart. Cardiovasc Res, 2001, 52: 246-254.
58. Huang B, Qin D, El-Sherif N. Early down-regulation of K+ channel genes and currents in the postinfarction heart. J Cardiovasc Electrophysiol, 2000, 11(11): 1252-1261.
59. Gidh-Jain M, Huang B, Jain P, et al. Differential expression of voltage-gated K+ channel genes in left ventricular remodeled myocardium after experimental myocardial infarction. Circ Res, 1996, 79(4): 669-675.
60. Anversa P, Beghi C, Kikkawa Y, et al. Myocardial infarction in rats: infarct size, myocyte hypertrophy, and capillary growth. Circ Res, 1986, 58: 26-37.
61. Hart G. Cellular electrophysiology in cardiac hypertrophy and failure. Cardiovasc Res, 1994, 28: 933-946.
2. Roden DM, Balser JR, George Jr AL, et al. Cardiac ion channels. Annu Rev Physiol, 2002, 64: 431-475.
3. Surawicz B. Ventricular fibrillation and dispersion of repolarization. J Cardiovasc Electrophysiol, 1997, 8:1009-1012.
4. Carmeliet E. Cardiac ionic currents and acute ischemia: From channels to arrhythmias. Physiol Rev, 1999, 79: 917-1017.
5. Rudy B. Diversity and ubiquity of K channels. Neuroscience, 1988, 25(3):729-749.
6. Nerbonne JM. Molecular basis of functional voltage-gated K+ channel diversity in the mammalian myocardium. J Physiol, 2000, 525(2): 285-298.
7. Barry DM, Nerbonne JM. Myocardial potassium channels: electrophysiological and molecular diversity. Annu Rev Physiol, 1996, 58: 363-394.
8. Pongs O. Molecular biology of voltage-dependent potassium channels. Physiol Rev, 1992, 72: S69-88.
9. Dixon JE, McKinnon. Quantitative analysis of potassium channel mRNA expression in atrial and ventricular muscle of rats. Circ Res, 1994, 75: 252-260.
10. Xu HD, Barry DM, Li HL, et al. Attenuation of the slow component of delayed rectification, action potential prolongation, and triggered activity in mice expressing a dominant-negative Kv2 a subunit. Circ Res, 1999, 85: 623-633.
11.Wang W, Hino NK, Yamasaki H, et al. Kv2.1 K+ channels underlie major voltage-gated K~+ outward current in H9c2 myoblasts. Jpn J Physiol, 2002, 52:507-514.
12. Huang B, Qin D, E1-Sherif N. Spatial alterations of Kv channels expression and K~+ currents in post-MI remodeled rat heart. Cardiovasc Res, 2001, 52: 246-254.
13. Huang B, Qin D, E1-Sherif N. Early down-regulation of K+ channel genes and currents in the postinfarction heart. J Cardiovasc Electrophysiol, 2000, 11(11): 252-1261.
14. Gidh-Jain M, Huang B, Jain P, et al. Differential expression of voltage-gated K+ channel genes in left ventricular remodeled myocardium after experimental myocardial infarction. Circ Res, 1996, 79(4): 669-675.
15. Anversa P, Beghi C, Kikkawa Y, et al. Myocardial infarction in rats: infarct size, myocyte hypertrophy, and capillary growth. Circ Res, 1986, 58: 26-37.
16. Hart G. Cellular electrophysiology in cardiac hypertrophy and failure. Cardiovasc Res, 1994, 28: 933-946.
1 Dixon JE, Mckinnon D. Quantitative analysis of potassium channel mRNA expression in atrial and ventricular muscle of rats. Circ Res, 1994, 75: 252-260.
2 Kuno A, Yamada T, Masuda K, Et A1. Angiotensin converting enzyme inhibitor attenuates pancreatic in. ammation and fibrosis in male wistar bonn/kobori rats. Gastroenterology, 2003, 124: 1010—1019.
3 Roden DM, Balser JR, George Jr AL, et al. Cardiac ion channels. Annu Rev Physiol, 2002, 64: 431-475.
4 Xu H, Barry DM, Li H, et al. Attenuation of the slow component of delayed rectification, action potential prolongation, and triggered activity in mice expressing a dominant-negative Kv2 α subunit. Citc Res, 1999, 85: 623-633.
5 Cohen IS, Datyner NB, Gintant GA, et al. Time-dependent outward currents in the heart. In: Fozzard HA, Jennings RB, Haber E, Katz AM, Morgan HE, eds. The Heart and Cardiovascular System. New York, NY: Raven Press Publishers, 1986: 637-670.
6 Carmeliet E, Biermans G, Callewaert G, et al. Potassium currents in cardiac cells. Experientia, 1987, 43: 1175-1184.
7 Anumonwo JMB, Freeman LC, Kwok WM, et al. Potassium channels in the heart: electrophysiology and pharmacological regulation. Cardiovasc Drug Rev, 1991, 9: 299-316.
8 Boyle WA, Nerbonne JM. A novel type of depolarization-activated K~+ current in isolated adult rat atrial myocytes. Am J Physiol, 1991, 260: H1236-H1247.
9 Varro A, Lathrop DA, Hester SB, et al. Ionic currents and action potentials in rabbit, rat, and guinea pig ventricular myocytes. Basic Res Cardiol, 1993, 88: 93-102.
10 Rudy B. Diversity and ubiquity of K channels. Neuroscience, 1988, 25(3): 729-749.
11 Nerbonne JM. Molecular basis of functional voltage-gated K+ channel
---- diversity in the mammalian myocardium. J Physiol, 2000, 525(2): 285-298.
12 Barry DM, Nerbonne JM. Myocardial potassium channels: electrophysiological and molecular diversity. Annu Rev Physiol, 1996, 58:363-394.
13 Wang w, Hino NK, Yamasaki H, et al. Kv2.1 K~+ channels underlie major voltage-gated K~+ outward current in H9c2 myoblasts. Jpn J Physiol, 2002, 52:507-514.
14 Schultz JH, Volk T, Ehmke H. Heterogeneity of Kv2.1 mRNA expression and delayed rectifier current in single isolated myocytes from rat left ventricle.Circ Res, 2001, 88: 483-490.
15 Kramer JW, Post MA, Brown AM, et al. Modulation of potassium channel gating by coexpression of Kv2.1 with regulatory Kv5.1 or Kv6.1 α-subunits. Am J Physiol, 1998, 274:C1501-C1510.
16 Salinas M, Duprat F, Heurteaux C, et al. New modulatory a subunits for mammalian Shab K~+ channels. J Biol Chem, 1997, 272: 24371-24379.
17 Post MA, Kirsch GE, Brown AM. Kv2.1 and electrically silent Kv6.1 potassium channel subunits combine and express a novel current. FEBS Lett,1996, 399: 177-182.
18 Zhu XR, Netzer R, Bohlke K, et al. Structural and functional characterization of Kv6.2 a new y subunit of voltage-gated potassium channel. Receptors Channels. 1999, 6: 337-350.
19 Kerschensteiner D, Stacker M. Heteromeric assembly of Kv2.1 with Kv9.3: Effect on the state dependence of inactivation. Biophys J, 1999, 77: 248-257.
1. Barry DM, Nerbonne JM. Myocardial potassium channels: electrophysiological and molecular diversity. Annu Rev Physiol, 1996, 58: 363-394.
2. Nerbonne JM. Molecular basis of functional voltage-gated K+ channel diversity in the mammalian myocardium. J Physiol, 2000, 525(2): 285-298.
3. Rudy B. Diversity and ubiquity of K channels. Neuroscience, 1988, 25(3): 729-749.
4. Xu H, Barry DM, Li H, et al. Attenuation of the slow component of delayed rectification, action potential prolongation, and triggered activity in mice expressing a dominant-negative Kv2 α-subunit. Circ Res, 1999, 85: 623-33.
5. Wang W, Hino N, Yamasaki H, et al. Kv2.1 K~+ channels underlie major voltage-gated K~+ outward current in H9c2 myoblasts. Jpn J Physiol, 2001, 52: 507-14.
6. Zhou J, Kodirov S, Murata M, et al. Regional upregulation of Kv2.1-encoded current, Ik, slow2, in Kv1DN mice is abolished by crossbreeding wuth Kv2DN mice. Am J Physiol Heart Circ Physiol, 2003, 284: H491-H500.
7. Huang B, Qin D, E1-Sherif N. Spatial alterations of Kv channels expression and K~+ currents in post-MI remodeled rat heart. Cardiovasc Res, 2001, 52: 246-254.
8. Huang B, Qin D, E1-Sherif N. Early down-regulation of K+ channel genes and currents in the postinfarction heart. J Cardiovasc Electrophysiol, 2000, 11(11): 1252-1261.
9. Gidh-Jain M, Huang B, Jain P, et al. Differential expression of voltage-gated K+ channel genes in left ventricular remodeled myocardium after experimental myocardial infarction. Circ Res, 1996, 79(4): 669-675.
10. Cohen IS, Datyner NB, Gintant GA, et al. Time-dependent outward currents in the heart. In: Fozzard HA, Jennings RB, Haber E, Katz AM, Mortgan HE, eds. The Heart and Cardiovascular System. New York, NY: Raven Press Publishers, 1986: 637-670.
11. Carmeliet E, Beimans G, Callewaert G, et al. Potassium currents in cardiac cells.Experientia. 1987, 43: 1175-1184.
12. Anumonowo JMB, Freeman LC, Kwok WM, Kass RS. Potassium channels in the heart: electrophysiology and pharmacological regulation. Cardiovasc Drug Rev. 1991,9:299-316.
13. Antzelevitch C, Sicouri S, Litovsky SH, et al. Heterogeneity within the ventricular wall: electrophysiology and pharmacology of epicardial, endocardial, and M cells. Circ Res, 1991, 69: 1427-1449.
14. Dixon JE, Mckinnon D. Quantitative analysis of potassium channel mRNA expression in atrial and ventricular muscle of rats. Circ Res, 1994, 75: 252-60.
15. Schultz JH, Volk T, Ehmke H. Heterogeneity of Kv2.1 mRNA expression and delayed rectifier current in single isolated myocytes from rat left ventricle. Circ Res, 2001,88:483-90.
16. Kramer JW, Post MA, Brown AM, et al. Modulation of potassium channel gating by coexpression of Kv2.1 with regulatory Kv5.1 or Kv6.1 K-subunits. Am J Physiol, 1998,274:C1501-C1510.
17. Salinas M, Duprat F, Heurteaux C, et al. New modulatory a subunits for mammalian Shab K~+ channels. J Biol Chem, 1997, 272: 24371-24379.
18. Post MA, Kirsch GE, Brown AM. Kv2.1 and electrically silent Kv6.1 potassium channel subunits combine and express a novel current. FEBS Lett, 1996, 399:177-182.
19. Zhu XR, Netzer R, Bohlke K, et al. Structural and functional characterization of Kv6.2 a new y subunit of voltage-gated potassium channel. Receptors Channels.1999, 6: 337-350.
20. Kerschensteiner D, Stacker M. Heteromeric assembly of Kv2.1 with Kv9.3: Effect on the state dependence of inactivation. Biophys J, 1999, 77: 248-257.
21. Amberg GC, Rossow CF, Navedo MF, et al. NFATc3 regulates Kv2.1 expression in arterial smooth muscle. J Biol Chem, 2004, 279(45): 47 326-34.
22. Nishizuka, Y. Intracellular signaling by hydrolysis of phospholipids and activation of protein kinase C. Science , 1992, 258: 607-614.
23. Damron DS, Nadim HS, Sung JH, et al. Intracellular translocation of PKC isoforms in canine pulmonary artery smooth muscle cells by ANG II. Am J Physiol Lung Cell Mol Physiol, 1998,274: L278-L288.
24. Zhu MY, Gelband CH, Posner P, et al. Angiotensin II Decreases Neuronal Delayed Rectifier Potassium Current: Role of Calcium/Calmodulin-Dependent Protein Kinase II. J Neurophysiol, 1999, 82(3):1 560-68.
25. Anand-Srivastava, MB. Angiotensin II receptors negatively coupled to adenylate cyclase in rat aorta. Biochem Biophys Res Commun, 1983,117: 420-428.
26. Unger, T, Chung O, Csikos T,et al. Angiotensin receptors. J Hypertens Suppl,1996, 14: S95-S103.
27. Shaywitz AJ, Greenberg ME. CREB: a stimulus-induced transcription factor activated by a diverse array of extrecellular signals. Annu Rev Biochem, 1999, 68:821-861.
28. Lonze BE, Ginty DD, Function and regulation of CREB family transcription factors in the nervous system. Neuron, 2002, 35: 605-623.
29. Mayr B, Montminy M. Transcriptional regulation by the phosphorylation- dependent factor CREB. Nat Rev Mol Cell Biol, 2001, 2: 599-609.
30. Mori Y, Matsubara H, Folco E, et al. The transcription of a mammalian voltage-gated potassium channel is regulated by cAMP in a cell-specific manner. J Biol Chem, 1993, 268: 26482-26493.
31. Patberg KW, Plotnikov AN, Quamina A, et al. Cardiac memory is associated with decreased levels of the transcriptional factor CREB modulated by angiotensin Hand calcium. Circ Res, 2003, 93: 472-478.
32. Gah L, Perney TM, Kaczmarek LK. Cloning and characterization of the promoter for a potassium channel expressed in high frequency firing neurons. J Biol Chem,1996,271:5859-5865.
33. Beckh S, Pongs O. Members of the RCK potassium channel family are different expressed in the rat nervous system. EMBO J, 1990, 9: 777-782.
1 Suaen PH, Bogoyevitch MA. Intracellular signalling through protein kinase in the heart. Cardiovisc Res, 1995, 30: 478-491.
2 Bogoyevitch MA, Parker PJ, Sugden PH. Characterization of protein kinase C isotype expression in adult rat heart: Protein kinase C-ε is a major isotype present, and it is activated by phorbol esters, epinephrine, and endothelin. Circ Res, 1993, 72: 757-767.
3 Strasser RH, Simonis G, Schon SP, et al. Two distinct mechanisms mediate a differential regulation of protein kinase C isozymes in acute and prolonged myocardial ischemia. Circ Res, 1999, 85: 77-87.
4 Xiao RP. β-adrenergic signaling in the heart: dual coupling of the β_(2-) adrenergic receptor to G_s and G_i proteins. Sci. STKE. 104: RE15.
5 Dohlman HG, Thorner J, Caron MG, et al. Model systems for the study of seven-transmembrane-segment receptors. Annu Rev Biochem, 1991, 60: 653-688.
6 Anand-Srivastava, MB. Angiotensin Ⅱ receptors negatively coupled to adenylate cyclase in rat aorta. Biochem Biophys Res Commun, 1983, 117: 420-428.
7 Unger, T, Chung O, Csikos T, et al. Angiotensin receptors. J Hypertens Suppl, 1996, 14: S95-S103.
8 Kompa AR, Gu XH, Evans BA, et al. Desensitization of cardiac β-adrenoceptor signaling with heart failure produced by myocardial infarction in the rat. Evidence for the role of Gi but Gs or phosphorylating proteins. J Mol Cell Cardiol, 1999, 31: 1185-1201.
9 Ungerer M, Kessebohm K, Kronsbein K, et al. Activation of β-adrenergic receptor kinase during myocardial ischemia. Circ Res, 1996, 79: 455-460.
10 Vatner DE, Knight DR, Shen YT, et al. One hour of myocardial ischemia in conscious dogs increasesβ-adrenergic receptors, but decreases adenylate cyclase activity. J Mol Cell Cardiol, 1988, 20: 75-82.
11 Vatner DE, Young MA, Knight DR, et al. β-receptors and adenylate cyclase: comparison of nonischemic, ischemic, and postmortem tissue. Am J Physiol, 1990, 258: H140-H144.
12 Strasser RH, Krimmer J, Braun-Dullaeus R, et al. Dual sensitization of the adrenergic system in early myocardial ischemic: independent regulation of the P-adrenergic receptors and the adenylyl cyclase. J Mol Cell Cardiol, 1990, 22:1405-1423.
13 Lonse MJ. Molecular mechanisms of membrane receptor desensitization. Biochim BiophysActa, 1993, 1179: 171-188.
14 Inglese J, Freedman NJ, Koch WJ, et al. Structure and mechanism of the G protein-coupled receptor kinases. J Biol Chem, 1993, 268: 23735-23738.
15 Benovic JL, Mayor F, Staniszewski C, et al. Purification and characterization of the P-adrenergic receptors kinase. J Biol Chem, 1987, 262: 9026-9032.
16 Goldspink PH, Russell B. The cAMP response element binding protein is expressed and phosphorylated in cardiac myocytes. Circ Res, 1994, 74:1042-1049.
17 Kuno A, Yamada T, Masuda K, Et Al. Angiotensin converting enzyme inhibitor attenuates pancreatic in.ammation and fibrosis in male wistar bonn/kobori rats. Gastroenterology, 2003,124:1010-1019.
18 Naruse K, King GL. Protein kinase C and myocardfial biology and function. Circ Res, 2000, 86: 1104-1106.
19 Rybin VO, Steinberg SF. Protein kinase C isoform expression and regulation in the developing rat heart. Circ Res, 1994, 74: 299-309.
20 Schaap D, Parker PJ, Bristol A, et al. Unique substrate specificity and regulatory properties of PKC-e. A rationale for diversity. FEBS Lett, 1989, 243: 351-357.
21 Saurin AT, Pennington DJ, Raat NJH, et al. Targeted disruption of the protein kinase C epsilon geng abolishes the infarc size reduction that follows ischaemic preconditioning of isolated buffer-perfused mouse hearts. Cardiovasc Res, 2002,55: 672-680.
22 Ping P, Zhang J, Pierce WM Jr, et al. Functional proteomic analysis of protein kinase C epsilon signaling complexes in the normal heart and during cardioprotection. Circ Res, 2001, 88: 59-62.
23 Liu HP, Zhang HY, Zhu XD, et al. Preconditioning blocks cardiocyte apoptosis:role of Katp channels and PKC-8. Am J Physiol Heart Circ Physiol, 2002, 282:H1380-H1386.
24 D'Angelo DD, Sakata Y, Lorenz JN, et al. Transgenic G_(αq) overexpression induces cardiac contractile failure in mice. Proc Natl Acad Sci USA, 1997, 94: 8121-8126.
25 Paul K, Ball NA, Dorn GW II, et al. Left ventricular stretch stimulates angiotensin II -mediated phosphatidylinositol hydrolysis and protein kinase C epsilon isoform translocation in adult guinea pig hearts. Circ Res, 1997, 81: 643-650.
26 Jalili T, Takeishi Y, Song G, et al. PKC translocation without changes in G_(αq) and PLC-beta protein abundance in cardiac hypertrophy and failure. Am J Physiol,1999, 277: H2298-H2304.
27 Clement-Chomienne O, Walsh MP, Cole WC, et al. Angiotensin II activation of protein kinase C decreases delayed rectifier K~+ current in rabbit vascular myocytes. J Physiol, 1996, 425: 689-700.
28 Hayabuchi Y, Standen NB, Davies NW. Angiotensin II inhibits and alters kinetics of voltage-gated K~+ channels of rat arterial smooth muscle. Am J Physiol Heart Circ Physiol, 2001, 281: H2480-H2489.
29 Nerbonne JM. Molecular basis of functional voltage-gated K+ channel diversity in the mammalian myocardium. J Physiol, 2000, 525(2): 285-298.
30 Xu H, Barry DM, Li H, et al. Attenuation of the slow component of delayed rectification, action potential prolongation, and triggered activity in mice expressing a dominant-negative Kv2 a-subunit. Circ Res, 1999, 85: 623-33.
31 Wang W, Hino N, Yamasaki H, et al. Kv2.1 K~+ channels underlie major voltage-gated K~+ outward current in H9c2 myoblasts. Jpn J Physiol, 2001,52:507-14.
32 Shaywitz AJ, Greenberg ME. CREB: a stimulus-induced transcription factor activated by a diverse array of extrecellular signals. Annu Rev Biochem, 1999, 68:821-861.
33 Lonze BE, Ginty DD, Function and regulation of CREB family transcription factors in the nervous system. Neuron, 2002, 35: 605-623.
34 Mayr B, Montminy M. Transcriptional regulation by the phosphorylation- dependent factor CREB. Nat Rev Mol Cell Biol, 2001, 2: 599-609.
35 Mori Y, Matsubara H, Folco E, et al. The transcription of a mammalian voltage-gated potassium channel is regulated by cAMP in a cell-specific manner. J Biol Chem, 1993, 268: 26482-26493.
36 Patberg KW, Plotnikov AN, Quamina A, et al. Cardiac memory is associated with decreased levels of the transcriptional factor CREB modulated by angiotensin II and calcium. Circ Res, 2003, 93: 472-478.
37 Gah L, Perney TM, Kaczmarek LK. Cloning and characterization of the promoter for a potassium channel expressed in high frequency firing neurons. J Biol Chem,1996,271:5859-5865.
38 Barry DM, Nerbonne JM. Myocardial potassium channels: electrophysiological and molecular diversity. Annu Rev Physiol, 1996, 58: 363-394.
39 Beckh S, Pongs O. Members of the RCK potassium channel family are different expressed in the rat nervous system. EMBO J, 1990, 9: 777-782.
40 Maisel AS, Motulsky HJ, Insel PA. Externalization of beta-adrenergic receptors promoted by myocardial ischemia. Science, 1985, 230:183-186.
41 Ungerer M, Parruti G, Bohm M, et al. Expression of β-arrestins and B-adrenergic receptor kinases in the failing human heart. Circ Res, 1994, 74:206-213.
42 Perm RB, Benovic JL. Structure of the human gene encoding the beta-adrenergic receptor kinase. J Biol Chem, 1994, 269: 14924-14930.
43 Ramos-Ruiz R, Penela P, Penn RB, et al. Analysis of the human G protein-coupled receptor kinase 2 (GRK2) gene promoter: regulation by signal transduction systems in aortic smooth muscle cells. Circulation, 2000, 101: 2083-2089.
44 Winstel R, Freund S, Krasel C, et al. Protein kinase cross-talk: membrane targeting of the beta-adrenergic receptor kinase by protein kinase C. Proc Natl Acad Sci USA, 1996, 93: 2105-2109.
45 Neumann J, Schmitz W, Scholz H, et al. Increase in myocardial Gi-proteins in heart failure. Lancet, 1988, 2: 936-937.
46 Ping P, Hammond HK. Diverse G protein and B-adrenergic receptor mRNA expression in normal and failing procine hearts. Am J Physiol, 1994, 267: H2079-H2085.
47 Shi B, Heavner JE, McMahon KK, et al. Dynamic changes in Gαi-2 levels in rat hearts associated with impaired heart function after myocardial infarction. Am J Physiol, 1995, 269: H1073-H1079.
48 Steinberg SF, Zhang HL, Pak E, et al. Characteristics of the β-adrenergic receptor complex in the epicardial border zone of the 5-day infarced canine heart. Circulation, 1995, 91: 2824-2833.
49 Maurice JP, Shan AS, Kypson AP, et al. Molecular β-adrenergic signaling abnormalities in failing rabbit hearts after infarction. Am J Physiol Heart Circ Physiol, 1999, 276: H1853-H1860.
2003
1. Rudy B. Diversity and ubiquity of K channels. Neuroscience, 1988, 25(3):729-749.
2. Nerbonne JM. Molecular basis of functional voltage-gated K+ channel diversity in the mammalian myocardium. J Physiol, 2000, 525(2): 285-298.
3. Barry DM, Nerbonne JM. Myocardial potassium channels: electrophysiological and molecular diversity. Annu Rev Physiol, 1996, 58: 363-394.
4. Pongs O. Molecular biology of voltage-dependent potassium channels. Physiol Rev, 1992, 72: S69-88.
5. Kaplan WD, Trout WE. The behavior of four neurological mutations of Drosophila. Genetics, 1969, 61: 399-409.
6. Butler A, Wei A, Baker K, et al. A family of putative potassium channel genes in Drosophila. Science, 1989, 243: 943-947.
7. Roberds SL, Tamkun MM. Cloning and tissue-specific expression of five voltage-gated potassium channels cDNAs expressed in rat heart. Proc Natl Acad Sci USA, 1991,88: 1798-1802.
8. Mei A, Covarrubias M, Butler A, et al. K~+ current diversity is produced by an extended gene family conserved in Drosophila and mouse. Science, 1990, 248:599-603.
9. Tempel BL, Papazian DM, Schwarz TL, et al. Sequence of a probable potassium channel component encoded at the Shaker locus in Drosophila. Science, 1987, 237:770-774.
10. Jan LY, Jan YN. Structural elements involved in specific K~+ channel functions.Annu Rev Physiol. 1992, 54: 537-555.
11. Pongs O. Structure-function studies on the pore of potassium channels. J Membr Biol, 1993, 136: 1-8.
12. Andalib P, Wood MJ, Korn SJ. Control of outer vestibule dynamics and current magnitude in the Kv2.1 potassium channel. J Gen Physiol, 2002, 120: 739-755.
13. Doyle DA, Cabral JM, Pfuetzner RA, et al. The structure of the potassium channel: molecular basis of K~+ conduction and selectivity. Science, 1998, 280: 69-77.
14. Albrecht B, Lorra C, Stacker M, et al. Cloning and characterization of a human delayed rectifier potassium channel gene. Receptors Channels, 1993, 1(2): 99-110.
15. Frech GC, VanDongen AM, Schuster G, et al. A novel potassium channel with delayed rectifier properties isolated from rat brain by expression cloning. Nature,1989, 340(6235): 642-645.
16. VanDongen AM, Frech GC, Drewe JA, et al. Alteration and restoration of K~+ channel function by deletions at the N- and C-termini. Neuron, 1990, 5(4):433-443.
17. Pascual JM, Shieh CC, kirsch GE, et al. Contribution of the NH_2 terminus of Kv2.1 to channel activation. Am J Physiol Cell Physiol, 1997, 273: C1849-C1858.
18. Ju M, Stevens L, Leadbitter E, et al. The roles of N- and C-terminal determinants in the activation of the Kv2.1 potassium. J Biol Chem, 2003, 278(15):12769-12778.
19. Koopmann R, Scholle A, Ludwig J, et al. Role of the S2 and S3 segment in determining the activation kinetics in Kv2.1 channels. J Membr Biol, 2001,182(1):49-59.
20. Klemic KG, Shieh CC, Kirsch GE, et al. Inactivation of Kv2.1 potassium channels. Biophys J, 1998, 74:1779-1789.
21. Lopez-Barneo J, Hoshi T, Heinemann SH, et al. Effects of external cations and mutations in the pore region on C-type inactivation of Shaker potassium.Receptors Channels, 1: 61-71.
22. Baukrowitz T, Yellen G. Use-dependent blockers and exit rate of the last ion from the multi-ion pore of a K~+ channels. Science, 1996, 271:653-656.
23. Choi KL, Aldrich RW, Yellen G Tetraethylammonium blockade distinguishes two inactivation mechanisums in voltage-activated K~+ channels. Proc Natl Acad Sci USA, 1991, 88: 5092-5095.
24. Kramer JW, Post MA, Brown AM, et al. Modulation of potassium channel gating by coexpression of Kv2.1 with regulatory Kv5.1 or Kv6.1 α-subunits. Am J Physiol, 1998, 274:C1501-C1510.
25. Kerschensteiner D, Stacker M. Heteromeric assembly of Kv2.1 with Kv9.3: effect on the state dependence of inactivation. Biophys J, 1999, 77:248-257.
26. Klemic Kg, Kirsch GE, Jones SW. U-Type inactivation of Kv3.1 and Shaker potassium channels. Biophys J, 2001, 81:814-826.
27. Kurata HT, Soon GS, Eldstrom JR, et al. Amino-terminal determinants of U-type inactivation of voltage-gated K~+ chasnnels. J Biol Chem, 2002, 277(32):29045-29053.
28. Immke D, Korn SJ. Ion-ion interactions at the selectivity filter: evidence from K~+-dependent modulation of tetraethylammonium efficacy in Kv2.1 potassium channels. J Gen Physiol, 2000, 115:509-518.
29. Immke, D, Wood MJ, Kiss L, et al. Potassium-dependent changes in the conformation of the Kv2.1 potassium channel pore. J Gen Physiol., 1999,113:819-836.
30. Wood MJ, Korn SJ. Two mechanisms of K~+-dependent potentiation in Kv2.1 potassium channels. Biophys J, 2000, 79:2535-2546.
31. Hille B, Schwartz W. Potassium channels as multi-ion pores. J Gen Physiol, 1978,72:409-442.
32. Cohen IS, Datyner NB, Gintant GA, et al. Time-dependent outward currents in the heart. In: Fozzard HA, Jennings RB, Haber E, Katz AM, Morgan HE, eds. The Heart and Cardiovascular System. New York, NY: Raven Press Publishers,1986:637-670.
33. Carmeliet E, Biermans G, Callewaert G, et al. Potassium currents in cardiac cells. Experientia, 1987,43:1175-1184.
34. Anumonwo JMB, Freeman LC, Kwok WM, et al. Potassium channels in the heart: electrophysiology and pharmacological regulation. Cardiovasc Drug Rev, 1991,9:299-316.
35. Boyle WA, Nerbonne JM. A novel type of depolarization-activated K~+ current in isolated adult rat atrial myocytes. Am J Physiol, 1991, 260:H1236-H1247.
36. Varro A, Lathrop DA, Hester SB, et al. Ionic currents and action potentials in rabbit, rat, and guinea pig ventricular myocytes. Basic Res Cardiol, 1993,88:93-102.
37. Schram G, Pourrier M, Melnyk P, et al. Differential distribution of cardiac ion channel expression as a basis for regional specialization in electrical function. Circ Res, 2002, 90: 939-950.
38. Dixon JE, McKinnon. Quantitative analysis of potassium channel mRNA expression in atrial and ventricular muscle of rats. Circ Res, 1994, 75: 252-260.
39. Brahmajothi MV, Morales MJ, Liu SG, et al. In situ hybridization reveals extensive diversity of K~+ channel mRNA in isolated ferret cardiac myocytes. Circ Res, 1996, 78: 1083-1089.
40. Schultz JH, Volk T, Ehmke H. Heterogengity of Kv2.1 mRNA expression and delayed rectifier current in single isolated myocytes from rat left ventricle. Circ Res, 2001, 88: 483-490.
41. Barry DM, Trimmer JS, Merlie JP, et al. Differential expression of voltage-gated K~+ channel subunits in adult rat heart: Relation to function K~+ channel? Circ Res,1995,77:361-369.
42. Hwang PM, Glatt CE, Bredt DS, et al. A novel K~+ channel with unique localizations in mammalian brain: molecular cloning and characterization. Neuron,1992,8:473-481.
43. Tsunoda S, Salkoff L. The major delayed rectifier in both Drosophila neurons and muscle is encoded by Shab. J Neurosci, 1995, 15: 5209-5221.
44. Apkon M, Nerbonne JM. Characterization of two distinct depolarization-activated K~+ currents in isolated adult rat ventricular myocytes. J Gen Physiol, 1991, 97:973-1011.
45. Xu HD, Barry DM, Li HL, et al. Attenuation of the slow component of delayed rectification, action potential prolongation, and triggered activity in mice expressing a dominant-negative Kv2 a subunit. Circ Res, 1999, 85: 623-633.
46. Zhou J, Kodirov S, Murata M, et al. Regional upregulation of Kv2.1-encoded current, Ik, slow2, in Kv1DN mice is abolished by crossbreeding wuth Kv2DN mice. Am J Physiol Heart Circ Physiol, 2003, 284: H491-H500.
47. Bou-Abboud E, Nerbonne JM. Molecular correlates of the calcium-independent, depolarization-activated K+ currents in rat atrial myocytes. J Physiol, 1999, 517: 407-420.
48. Wang W, Hino N, Yamasaki H, et al. Kv2.1 K~+ channels underlie major voltage-gated K~+ outward current in H9c2 myoblasts. Jpn J Physiol, 2001, 52: 507-14.
49. Post MA, Kirsch GE, Brown AM. Kv2.1 and electrically silent Kv6.1 potassium channel subunits combine and express a novel current. FEBS Lett, 1996, 399: 177-182.
50. Zhu XR, Netzer R, Bohlke K, et al. Structural and functional characterization of Kv6.2 a new gamma-subunit of voltage-gated potassium channel. Receptors Channels, 1999, 6(5): 337-50.
51. Sano Y, Mochizuki S, Miyake A, et al. Molecular cloning and characterization of Kv6.3, a novel modulatory subunit for voltage-gated K(+) channel Kv2.1. FEBS Lett, 2002, 512: 230-234.
52. Salinas M, Duprat F, Heurteaux C, et al. New modulatory α subunits for mammalian Shab K+ channels. J Biol Chem, 1997, 272(39): 24371-24379.
53. Patel AJ, Lazdunski M, Honore E. Kv2.1/Kv9.3, a novel ATP-dependent delayed-rectifier K+ channel in oxygen-sensitive pulmonary artery myocytes. EMBO J, 1997, 16: 6615-6625.
54. Hulme JT, Coppock Ea, Felipe A, et al. Oxygen sensitivity of cloned voltaged-gated K~+ channels expressed in the pulmonary vasculature. Circ Res, 1999, 85: 489-497.
55. Kerschensteiner D, Soto F, Stocker M. Fluorescence measurements reveal stoichiometry of K+ channels formed by modulatory and delayed rectifier alpha-subunits. Proc Natl Acad Sci USA, 2005, 102: 6160-6165.
56. Ottschytsch N, Raes A, Hoorick V, et al. Obligatory heterotetramerization of three previously uncharacterized Kv channel α-subunits identified in the human genome. Proc Natl Acad Sci USA, 2002, 99(12): 7986-7991.
57. Huang B, Qin D, El-Sherif N. Spatial alterations of Kv channels expression and K~+ currents in post-MI remodeled rat heart. Cardiovasc Res, 2001, 52: 246-254.
58. Huang B, Qin D, El-Sherif N. Early down-regulation of K+ channel genes and currents in the postinfarction heart. J Cardiovasc Electrophysiol, 2000, 11(11): 1252-1261.
59. Gidh-Jain M, Huang B, Jain P, et al. Differential expression of voltage-gated K+ channel genes in left ventricular remodeled myocardium after experimental myocardial infarction. Circ Res, 1996, 79(4): 669-675.
60. Anversa P, Beghi C, Kikkawa Y, et al. Myocardial infarction in rats: infarct size, myocyte hypertrophy, and capillary growth. Circ Res, 1986, 58: 26-37.
61. Hart G. Cellular electrophysiology in cardiac hypertrophy and failure. Cardiovasc Res, 1994, 28: 933-946.
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