%0 Journal Article %1 Ande_2004_152 %A Anderson, Mark E %D 2004 %J Trends Cardiovasc. Med. %K 80 AMP-Dependent Action Adenoma, Adjuvant, Adolescent, Adrenergic Adul, Adult, Aged, Aldehydes, Alveolar Analysis Animals, Antineoplastic Arrhythmia, Atrial Atrioventricular Biological, C57BL, Calcium Calcium, Calmodulin, Capillaries, Cardiac Cardiomegaly, Cardiomyopathies, Cell Channels, Chemotherapy Chemotherapy, Choristoma, Cohort Combined Computer-Assisted, Congestive, Cyclic Cyclophosphamide, Dacarbazine, Dependent Diagnosis, Differential, Disease Disease, Diseases, Doxorubicin, Enzymologic, Expression Extramural, Failure, Female, Fibrillation, Flecainide, Gastrointestinal Gene Genetic Genetic, Heart Heart, Hematoma, Hemorrhage, Homeostasis, Humans, Ifosfamide, Image Inbred Isoprostanes, Isoproterenol, Kinase, Kinases, Knockout, L-Type, Line, Lipid Long Low, Male, Mediastinal Node, Output, Part, Peroxidation, Potentials, Predisposition Processing, Protein Protocols, QT Regulation, Screening, Soft Studies, Susceptibility, Syndrome, Variance, and beta-Antagonists, of over, to {C}a$^{2+}$-Calmodulin %N 4 %P 152--161 %R 10.1016/j.tcm.2004.02.005 %T Calmodulin kinase and L-type calcium channels; a recipe for arrhythmias? %U http://dx.doi.org/10.1016/j.tcm.2004.02.005 %V 14 %X L-type Ca$^2+$ channels (LTCCs) are the main portal for Ca$^2+$ entry into cardiac myocytes. These ion channel proteins open in response to cell membrane depolarizations elicited by action potentials, and LTCC current (I(Ca)) flows during the action potential plateau, to increase cellular Ca$^2+$ (Ca$^2+$(i)) and trigger myocardial contraction. I(Ca) is also implicated in the genesis of cardiac arrhythmias under conditions such as heart failure and cardiac hypertrophy, in which the action potential plateau and QT interval are prolonged. This article reviews recent findings about the molecular regulation of LTCCs by the Ca$^2+$-dependent signaling molecule, calmodulin kinase II (CaMKII), and compares this form of regulation with regulation by calmodulin-binding domains and beta-adrenergic receptor agonists. LTCC dysregulation is discussed in the context of new results showing that CaMKII can be a proarrhythmic signal in disease conditions in which Ca$^2+$(i) is disordered and cardiac repolarization is excessively prolonged.

@article{Ande_2004_152, abstract = {L-type {C}a$^{2+}$ channels (LTCCs) are the main portal for {C}a$^{2+}$ entry into cardiac myocytes. These ion channel proteins open in response to cell membrane depolarizations elicited by action potentials, and LTCC current (I(Ca)) flows during the action potential plateau, to increase cellular {C}a$^{2+}$ ({C}a$^{2+}$(i)) and trigger myocardial contraction. I(Ca) is also implicated in the genesis of cardiac arrhythmias under conditions such as heart failure and cardiac hypertrophy, in which the action potential plateau and QT interval are prolonged. This article reviews recent findings about the molecular regulation of LTCCs by the {C}a$^{2+}$-dependent signaling molecule, calmodulin kinase II (CaMKII), and compares this form of regulation with regulation by calmodulin-binding domains and beta-adrenergic receptor agonists. LTCC dysregulation is discussed in the context of new results showing that CaMKII can be a proarrhythmic signal in disease conditions in which {C}a$^{2+}$(i) is disordered and cardiac repolarization is excessively prolonged.}, added-at = {2009-06-03T11:20:58.000+0200}, author = {Anderson, Mark E}, biburl = {https://www.bibsonomy.org/bibtex/20ecbf04d5c2eb18f019a26175360e594/hake}, description = {The whole bibliography file I use.}, doi = {10.1016/j.tcm.2004.02.005}, file = {Ande_2004_152.pdf:Ande_2004_152.pdf:PDF}, interhash = {aa00cf8510550f4486eafa096a2317d6}, intrahash = {0ecbf04d5c2eb18f019a26175360e594}, journal = {Trends Cardiovasc. Med.}, key = 283, keywords = {80 AMP-Dependent Action Adenoma, Adjuvant, Adolescent, Adrenergic Adul, Adult, Aged, Aldehydes, Alveolar Analysis Animals, Antineoplastic Arrhythmia, Atrial Atrioventricular Biological, C57BL, Calcium Calcium, Calmodulin, Capillaries, Cardiac Cardiomegaly, Cardiomyopathies, Cell Channels, Chemotherapy Chemotherapy, Choristoma, Cohort Combined Computer-Assisted, Congestive, Cyclic Cyclophosphamide, Dacarbazine, Dependent Diagnosis, Differential, Disease Disease, Diseases, Doxorubicin, Enzymologic, Expression Extramural, Failure, Female, Fibrillation, Flecainide, Gastrointestinal Gene Genetic Genetic, Heart Heart, Hematoma, Hemorrhage, Homeostasis, Humans, Ifosfamide, Image Inbred Isoprostanes, Isoproterenol, Kinase, Kinases, Knockout, L-Type, Line, Lipid Long Low, Male, Mediastinal Node, Output, Part, Peroxidation, Potentials, Predisposition Processing, Protein Protocols, QT Regulation, Screening, Soft Studies, Susceptibility, Syndrome, Variance, and beta-Antagonists, of over, to {C}a$^{2+}$-Calmodulin}, month = May, number = 4, pages = {152--161}, pii = {S1050173804000283}, pmid = {15177266}, timestamp = {2009-06-03T11:21:00.000+0200}, title = {Calmodulin kinase and L-type calcium channels; a recipe for arrhythmias?}, url = {http://dx.doi.org/10.1016/j.tcm.2004.02.005}, volume = 14, year = 2004 }