M. Meyer

发表

Altered cardiac phenotype in transgenic mice carrying the delta337 threonine thyroid hormone receptor beta mutant derived from the S family.

B. Gloss, M. R. Sayen, W. Bluhm, 1999, Endocrinology.

Alterations in intracellular calcium handling associated with the inverse force-frequency relation in human dilated cardiomyopathy.

G. Hasenfuss, B. Pieske, K. Minami, 1995, Circulation.

Influence of endothelin 1 on human atrial myocardium—myocardial function and subcellular pathways

S. Lehnart, G. Hasenfuss, B. Pieske, 1996, Basic Research in Cardiology.

Relationship Between Myocardial Function and Expression of Calcium Cycling Proteins in Nonfailing and Failing Human Myocardium

H. Drexler, G. Hasenfuss, B. Pieske, 1995 .

A recombinant antibody increases cardiac contractility by mimicking phospholamban phosphorylation

T. Dieterle, G. Silverman, D. Belke, 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

Effects of mutant and antisense RNA of phospholamban on SR Ca(2+)-ATPase activity and cardiac myocyte contractility.

W. Lew, J. Martín, W. Dillmann, 1999, Circulation.

Basic Science and Experimental Studies The Na/Ca 2 Exchanger/SR Ca 2 ATPase Transport Capacity Regulates the Contractility of Normal and Hypertrophied Feline Ventricular Myocytes

S. Houser, J. Gaughan, B. McGowan, 2005 .

Phospholamban-to-SERCA2 ratio controls the force-frequency relationship.

W. Lew, S. Post, W. Bluhm, 1999, American journal of physiology. Heart and circulatory physiology.

Phospholamban-to-SERCA2 ratio controls the force-frequency relationship.

W. Lew, S. Post, W. Bluhm, 1999, The American journal of physiology.

Overexpression of the rat sarcoplasmic reticulum Ca2+ ATPase gene in the heart of transgenic mice accelerates calcium transients and cardiac relaxation.

H. Rockman, D. Choi, M. R. Sayen, 1997, The Journal of clinical investigation.

Phospholamban: a major determinant of the cardiac force-frequency relationship.

E. Kranias, W F Bluhm, M Meyer, 2000, American journal of physiology. Heart and circulatory physiology.

The Na+/Ca2+ exchanger/SR Ca2+ ATPase transport capacity regulates the contractility of normal and hypertrophied feline ventricular myocytes.

S. Houser, J. Gaughan, B. McGowan, 2005, Journal of cardiac failure.

Relation between myocardial function and expression of sarcoplasmic reticulum Ca(2+)-ATPase in failing and nonfailing human myocardium.

H. Drexler, G. Hasenfuss, B. Pieske, 1994, Circulation research.

Protection against myocardial dysfunction after a brief ischemic period in transgenic mice expressing inducible heat shock protein 70.

J. Omens, J. Covell, R. Mestril, 1998, The Journal of clinical investigation.

Overexpression of the sarcoplasmic reticulum Ca(2+)-ATPase improves myocardial contractility in diabetic cardiomyopathy.

D. Belke, W. Bluhm, W. Dillmann, 2002, Diabetes.

Diminished post-rest potentiation of contractile force in human dilated cardiomyopathy. Functional evidence for alterations in intracellular Ca2+ handling.

M. Olschewski, G. Hasenfuss, B. Pieske, 1996, The Journal of clinical investigation.

Alterations of sarcoplasmic reticulum proteins in failing human dilated cardiomyopathy.

K. Mikoshiba, G. Kuwajima, G. Hasenfuss, 1995, Circulation.

Calcium handling proteins in the failing human heart

G. Hasenfuss, W. Schillinger, M. Preuss, 2004, Basic Research in Cardiology.

Overexpression of sarcoplasmic reticulum Ca(2+)-ATPase improves cardiac contractile function in hypothyroid mice.

W F Bluhm, M Meyer, M R Sayen, 1999, Cardiovascular research.

Unaltered ryanodine receptor protein levels in ischemic cardiomvopathy

K. Mikoshiba, G. Kuwajima, G. Hasenfuss, 1996, Molecular and Cellular Biochemistry.

Thermodynamic limitation for Ca2+ handling contributes to decreased contractile reserve in rat hearts.

J. Halow, V. Figueredo, S. A. Camacho, 1998, American journal of physiology. Heart and circulatory physiology.

Calcium cycling proteins and forcefrequency relationship in heart failure

H. Drexler, G. Hasenfuss, B. Pieske, 2004, Basic Research in Cardiology.

Impaired sarcoplasmic reticulum function leads to contractile dysfunction and cardiac hypertrophy.

H. Knot, W. Bluhm, W. Dillmann, 2001, American journal of physiology. Heart and circulatory physiology.

Influence of SR Ca2+-ATPase and Na+-Ca2+-exchanger on the force frequency relation

G. Hasenfuss, W. Schillinger, M. Preuss, 1998, Basic Research in Cardiology.

Altered Cardiac Phenotype in Transgenic Mice Carrying the Δ337 Threonine Thyroid Hormone Receptor β Mutant Derived from the S Family.

B. Gloss, M. R. Sayen, W. Bluhm, 1999, Endocrinology.

Adenovirus-mediated gene transfer reconstitutes depressed sarcoplasmic reticulum Ca2+-ATPase levels and shortens prolonged cardiac myocyte Ca2+ transients.

M. R. Sayen, F. Giordano, W. Dillmann, 1997, Circulation.

Gene transfer of a phospholamban-targeted antibody improves calcium handling and cardiac function in heart failure.

J. Ross, Yusu Gu, K. Peterson, 2005, Cardiovascular research.

Frequency-dependence of myocardial energetics in failing human myocardium as quantified by a new method for the measurement of oxygen consumption in muscle strip preparations.

J. Holmes, S. Lehnart, G. Hasenfuss, 1998, Journal of molecular and cellular cardiology.

Thermodynamic limitation for Ca2+ handling contributes to decreased contractile reserve in rat hearts.

R. Tian, W. Dillmann, M. Meyer, 1998, American journal of physiology. Heart and circulatory physiology.

Intravenous administration of the natriuretic peptide urodilatin at low doses during coronary reperfusion limits infarct size in anesthetized pigs.

L. Agulló, M. Mirabet, J. Soler‐Soler, 2001, Cardiovascular research.

Sarcoplasmic reticulum Ca2+-ATPase overexpression by adenovirus mediated gene transfer and in transgenic mice

W. Dillmann, M. Meyer, 1998 .

Sarcoplasmic reticulum Ca(2+)-ATPase overexpression by adenovirus mediated gene transfer and in transgenic mice.

W. Dillmann, M. Meyer, 1998, Cardiovascular research.