Physiological role of the α1- and α2-isoforms of the Na+-K+-ATPase and biological significance of their cardiac glycoside binding site
暂无分享,去创建一个
[1] J. Lingrel,et al. The highly conserved cardiac glycoside binding site of Na,K-ATPase plays a role in blood pressure regulation. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[2] M. Blaustein,et al. Sodium pump α2 subunits control myogenic tone and blood pressure in mice , 2005 .
[3] K. Sweadner. Phospholemman: a new force in cardiac contractility. , 2005, Circulation research.
[4] P. Rizzon,et al. High circulating levels of endogenous ouabain in the offspring of hypertensive and normotensive individuals , 2005, Journal of hypertension.
[5] K. Geering,et al. FXYD3 (Mat-8), a new regulator of Na,K-ATPase. , 2005, Molecular biology of the cell.
[6] R. Schwinger,et al. Ouabain-Like Compound Changes Rapidly on Physical Exercise in Humans and Dogs: Effects of &bgr;-Blockade and Angiotensin-Converting Enzyme Inhibition , 2005, Hypertension.
[7] J. Lingrel,et al. The alpha2-isoform of Na-K-ATPase mediates ouabain-induced hypertension in mice and increased vascular contractility in vitro. , 2005, American journal of physiology. Heart and circulatory physiology.
[8] B. Aronow,et al. Genetic Profiling Reveals Global Changes in Multiple Biological Pathways in the Hearts of Na, K-ATPase Alpha 1 Isoform Haploinsufficient Mice , 2005, Cellular Physiology and Biochemistry.
[9] J. Lingrel,et al. The α1 Isoform of Na,K-ATPase Regulates Cardiac Contractility and Functionally Interacts and Co-localizes with the Na/Ca Exchanger in Heart* , 2004, Journal of Biological Chemistry.
[10] J. Yamada,et al. Malfunction of Respiratory-Related Neuronal Activity in Na+, K+-ATPase α2 Subunit-Deficient Mice Is Attributable to Abnormal Cl- Homeostasis in Brainstem Neurons , 2004, The Journal of Neuroscience.
[11] I. Grupp,et al. Attenuation of cardiac contractility in Na,K-ATPase alpha1 isoform-deficient hearts under reduced calcium conditions. , 2004, Journal of molecular and cellular cardiology.
[12] J. Huysse,et al. Pressor response to CSF sodium in mice: mediation by a ouabain-like substance and renin–angiotensin system in the brain , 2004, Brain Research.
[13] J. Lingrel,et al. Deletion of the Na/K-ATPase α1-subunit gene (Atp1a1) does not prevent cavitation of the preimplantation mouse embryo , 2004, Mechanisms of Development.
[14] I. Grupp,et al. The α2 Isoform of Na,K-ATPase Mediates Ouabain-induced Cardiac Inotropy in Mice* , 2003, Journal of Biological Chemistry.
[15] C. Deber,et al. Modulation of Na,K-ATPase by the gamma subunit: studies with transfected cells and transmembrane mimetic peptides. , 2003, The Journal of biological chemistry.
[16] K. Sweadner,et al. FXYD Proteins as Regulators of the Na,K‐ATPase in the Kidney , 2003, Annals of the New York Academy of Sciences.
[17] L. Jones,et al. Phospholemman, a Single-Span Membrane Protein, Is an Accessory Protein of Na,K-ATPase in Cerebellum and Choroid Plexus , 2003, The Journal of Neuroscience.
[18] J. Ramirez,et al. The Na,K-ATPase α2 Isoform Is Expressed in Neurons, and Its Absence Disrupts Neuronal Activity in Newborn Mice* , 2003, The Journal of Biological Chemistry.
[19] K. Geering,et al. Phospholemman (FXYD1) associates with Na,K-ATPase and regulates its transport properties , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[20] M. N. Margolies,et al. Ouabain-Binding Protein(s) From Human Plasma , 2002, Hypertension.
[21] W. Schoner. Endogenous cardiac glycosides, a new class of steroid hormones. , 2002, European journal of biochemistry.
[22] J. Lingrel,et al. The α1- and α2-isoforms of Na-K-ATPase play different roles in skeletal muscle contractility , 2001 .
[23] K. Geering,et al. CHIF, a member of the FXYD protein family, is a regulator of Na,K‐ATPase distinct from the γ‐subunit , 2001, The EMBO journal.
[24] D. Cusi,et al. Plasma Ouabain-Like Factor During Acute and Chronic Changes in Sodium Balance in Essential Hypertension , 2001, Hypertension.
[25] C. Terracciano. Rapid inhibition of the Na+‐K+ pump affects Na+‐Ca2+ exchanger‐mediated relaxation in rabbit ventricular myocytes , 2001, The Journal of physiology.
[26] W. Tourtellotte,et al. The α4 Isoform of the Na,K-ATPase Is Expressed in the Germ Cells of the Testes , 2000 .
[27] J. Lingrel,et al. Sperm Motility Is Dependent on a Unique Isoform of the Na,K-ATPase* , 2000, The Journal of Biological Chemistry.
[28] F. Leenen,et al. Chronic blockade of brain "ouabain" prevents sympathetic hyper-reactivity and impairment of acute baroreflex resetting in rats with congestive heart failure. , 1999, Canadian journal of physiology and pharmacology.
[29] K. Sweadner,et al. The γ Subunit Modulates Na+ and K+Affinity of the Renal Na,K-ATPase* , 1999, The Journal of Biological Chemistry.
[30] D. Cusi,et al. Left ventricular mass, stroke volume, and ouabain-like factor in essential hypertension. , 1999, Hypertension.
[31] R. Walsh,et al. Identification of a specific role for the Na,K-ATPase alpha 2 isoform as a regulator of calcium in the heart. , 1999, Molecular cell.
[32] M. Blaustein,et al. The cellular mechanism of action of cardiotonic steroids: a new hypothesis. , 1998, Clinical and experimental hypertension.
[33] O. Fedorova,et al. Plasma marinobufagenin-like and ouabain-like immunoreactivity in adrenocorticotropin-treated rats. , 1998, American journal of hypertension.
[34] A. Therien,et al. Tissue-specific Distribution and Modulatory Role of the γ Subunit of the Na,K-ATPase , 1997, The Journal of Biological Chemistry.
[35] J. Hoffman,et al. Na,K-ATPase subunit isoforms in human reticulocytes: Evidence from reverse transcription–PCR for the presence of α1, α3, β2, β3, and γ , 1997 .
[36] M. Omata,et al. Adrenocorticotropin-induced hypertension in rats: role of ouabain-like compound. , 1997, American journal of hypertension.
[37] M. Blaustein,et al. Na+ pump low and high ouabain affinity alpha subunit isoforms are differently distributed in cells. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[38] J. Whitworth,et al. Hemodynamic effects of the Fab fragment of digoxin antibody (digibind) in corticotropin (ACTH)-induced hypertension. , 1997, American journal of hypertension.
[39] M. Tóth,et al. Production of ouabain by rat adrenocortical cells. , 1996, Endocrine research.
[40] M. Omata,et al. Ouabainlike compound in hypertension associated with ectopic corticotropin syndrome. , 1996, Hypertension.
[41] M. Blaustein,et al. Localization of the Na+‐Ca2+ Exchanger in Vascular Smooth Muscle, and in Neurons and Astrocytesa , 1996, Annals of the New York Academy of Sciences.
[42] O. Shamraj,et al. A putative fourth Na+,K(+)-ATPase alpha-subunit gene is expressed in testis. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[43] J. Lingrel,et al. Na+,K(+)-ATPase. , 1994, The Journal of biological chemistry.
[44] J. Hamlyn,et al. Ouabain is secreted by bovine adrenocortical cells. , 1994, Endocrinology.
[45] F. Leenen,et al. Brain "ouabain" mediates the sympathoexcitatory and hypertensive effects of high sodium intake in Dahl salt-sensitive rats. , 1994, Circulation research.
[46] P. Doris. Regulation of Na,K-ATPase by Endogenous Ouabain-like Materials , 1994, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.
[47] M. Blaustein,et al. Physiological effects of endogenous ouabain: control of intracellular Ca2+ stores and cell responsiveness. , 1993, The American journal of physiology.
[48] V. Canfield,et al. Molecular cloning and characterization of Na,K-ATPase from Hydra vulgaris: implications for enzyme evolution and ouabain sensitivity. , 1992, The New biologist.
[49] O. Shamraj,et al. Expression of Na,K-ATPase isoforms in human heart. , 1991, Biochemical and biophysical research communications.
[50] M. Blaustein,et al. Identification and characterization of a ouabain-like compound from human plasma. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[51] O. Fedorova,et al. Endogenous plasma Na,K-ATPase inhibitory activity and digoxin like immunoreactivity after acute myocardial infarction. , 1991, Cardiovascular research.
[52] A. Lechi,et al. High plasma levels of a ouabain‐like factor in normal pregnancy and in pre‐eclampsia* , 1989, European journal of clinical investigation.
[53] A. Lechi,et al. High plasma levels of a ouabain‐like factor in normal pregnancy and in pre‐eclampsia * , 1989 .
[54] J. Lingrel,et al. Structure-function relationships in the sodium-potassium ATPase .alpha. subunit: site-directed mutagenesis of glutamine-111 to arginine and asparagine-122 to aspartic acid generates a ouabain-resistant enzyme , 1988 .
[55] M. Blaustein,et al. A circulating inhibitor of (Na+ + K+) ATPase associated with essential hypertension , 1982, Nature.
[56] M. Blaustein,et al. Sodium pump alpha2 subunits control myogenic tone and blood pressure in mice. , 2005, The Journal of physiology.
[57] J. Kaplan,et al. Biochemistry of Na,K-ATPase. , 2002, Annual review of biochemistry.
[58] W. Tourtellotte,et al. The alpha4 isoform of the Na,K-ATPase is expressed in the germ cells of the testes. , 2000, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.
[59] J. Hoffman,et al. Na,K-ATPase subunit isoforms in human reticulocytes: evidence from reverse transcription-PCR for the presence of alpha1, alpha3, beta2, beta3, and gamma. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[60] Laxmaiah Manchikanti,et al. An Invited Review , 1995 .
[61] J. Whitworth,et al. Adrenocorticotrophin-induced hypertension in rats. Role of progesterone and digoxin-like substances. , 1994, American journal of hypertension.
[62] J. Lingrel,et al. Structure-function relationships in the Na,K-ATPase alpha subunit: site-directed mutagenesis of glutamine-111 to arginine and asparagine-122 to aspartic acid generates a ouabain-resistant enzyme. , 1988, Biochemistry.
[63] J. Zicha,et al. The importance of endogenous digoxin-like factors in rats with various forms of experimental hypertension. , 1985, Clinical and experimental hypertension. Part A, Theory and practice.