Zobrazeno 1 - 10
of 40
pro vyhledávání: '"Amy L. Tucker"'
Autor:
Steven R. Houser, Xue-Qian Zhang, Amy L. Tucker, JuFang Wang, Blaise Z. Peterson, Joseph E. Rabinowitz, Xiongwen Chen, Joseph Y. Cheung, Jianliang Song, Arthur M. Feldman
Publikováno v:
Journal of Molecular and Cellular Cardiology. 84:104-111
We evaluated whether phospholemman (PLM) regulates L-type Ca2 + current (ICa) in mouse ventricular myocytes. Expression of α1-subunit of L-type Ca2 + channels between wild-type (WT) and PLM knockout (KO) hearts was similar. Compared to WT myocytes,
Autor:
Bryan T. Lawlor, Amy L. Tucker, Jeffrey P. Chidester, Aaron K. Blakeney, Michael Salerno, Michael A. Millard, Fahad H. Alhajri, Idil Aktan, Ellen C. Keeley, Nancy M. Fauber, Michael J. Loguidice, Vertilio M. Cornielle-Caamano, Kathryn K. Ward, Ishan T. Shah
Publikováno v:
Circulation. Cardiovascular quality and outcomes. 10(9)
Approximately 20% of Medicare beneficiaries are readmitted to the hospital after an index myocardial infarction (MI). Since July 2009, the Centers for Medicare and Medicaid Services began publically reporting hospital data on 30-day readmission rates
Publikováno v:
Menopause. 20:244-247
Autor:
Jianliang Song, M. Ayoub Mirza, Amy L. Tucker, Kwame Akosah, JuFang Wang, Themis Karaoli, John A. Hossack, Zequan Yang, Susan Lane, Xue-Qian Zhang, Joseph Y. Cheung, Marcia McDuffie
Publikováno v:
Clinical and Translational Science. 5:235-242
Phospholemman (PLM) regulates [Na+]i, [Ca2+]i and contractility through its interactions with Na+‐K+‐ATPase (NKA) and Na+/Ca2+ exchanger (NCX1) in the heart. Both expression and phosphorylation of PLM are altered after myocardial infarction (MI)
Regulation of cardiac myocyte contractility by phospholemman: Na+/Ca2+ exchange versus Na+-K+-ATPase
Autor:
Joseph Y. Cheung, JuFang Wang, Amy L. Tucker, Xue-Qian Zhang, Tung O. Chan, Ellina Cheskis, Jianliang Song, Arthur M. Feldman
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 295:H1615-H1625
Phospholemman (PLM) regulates cardiac Na+/Ca2+ exchanger (NCX1) and Na+-K+-ATPase in cardiac myocytes. PLM, when phosphorylated at Ser68, disinhibits Na+-K+-ATPase but inhibits NCX1. PLM regulates cardiac contractility by modulating Na+-K+-ATPase and
Publikováno v:
Circulation. 117:1849-1855
Background— Cardiac Na/K-ATPase (NKA) regulates intracellular Na ([Na] i ), which in turn affects intracellular Ca and thus contractility via Na/Ca exchange. Recent evidence shows that phosphorylation of the NKA-associated small transmembrane prote
Autor:
Pamela Donoghue, K Dighe, J. Randall Moorman, Erika J. Kennington, Michael J. Shattock, William Fuller, Michael J. Dunn, James Clark, Philip Eaton, Li-Guo Jia, Jimmy D. Bell, Michael S. Marber, Amy L. Tucker
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 294:H613-H621
Phospholemman (PLM, FXYD1), abundantly expressed in the heart, is the primary cardiac sarcolemmal substrate for PKA and PKC. Evidence supports the hypothesis that PLM is part of the cardiac Na-K pump complex and provides the link between kinase activ
Publikováno v:
Journal of the American College of Cardiology. 51(3):389-393
Publikováno v:
Physiological Research. :669-676
Phosphorylation of phospholemman (PLM) on ser68 has been proposed to at least partially mediate cyclic AMP (cAMP) mediated relaxation of arterial smooth muscle. We evaluated the time course of the phosphorylation of phospholemman (PLM) on ser68, myos
Autor:
Qing Yu, Mani S. Mahadevan, Richard P. Harvey, Amy L. Tucker, Jack Puymirat, Carla D Frenzel-McCardell, Owen W.J. Prall, Charles A. Thornton, Ramesh S. Yadava, Varadamurthy Srinivasan
Publikováno v:
Nature Genetics. 40:61-68
Myotonic muscular dystrophy (DM1) is the most common inherited neuromuscular disorder in adults and is considered the first example of a disease caused by RNA toxicity. Using a reversible transgenic mouse model of RNA toxicity in DM1, we provide evid