V. Lasko

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hypertension using a modified two-kidney , one-clip approach in mice is not dependent on the 1 or 2 NaK-ATPase ouabain-binding site

J. Lingrel, J. Lorenz, V. Prasad, 2011 .

Renovascular hypertension using a modified two-kidney, one-clip approach in mice is not dependent on the α1 or α2 Na-K-ATPase ouabain-binding site.

J. Lingrel, J. Lorenz, V. Prasad, 2011, American journal of physiology. Renal physiology.

Mice expressing ouabain‐sensitive α1 Na,K‐ATPase have increased susceptibility to pressure overload‐induced cardiac hypertrophy

J. Lingrel, J. Lorenz, A. Wansapura, 2009, American journal of physiology. Heart and circulatory physiology.

Probenecid: novel use as a non-injurious positive inotrope acting via cardiac TRPV2 stimulation.

Sheryl E. Koch, Nathan Robbins, Jack Rubinstein, 2012, Journal of molecular and cellular cardiology.

Loss of the AE3 anion exchanger in a hypertrophic cardiomyopathy model causes rapid decompensation and heart failure.

S. Alper, J. Lorenz, V. Prasad, 2011, Journal of molecular and cellular cardiology.

Knockout of the Na,K-ATPase α2-isoform in cardiac myocytes delays pressure overload-induced cardiac dysfunction.

J. Lingrel, J. Lorenz, M. Nieman, 2013, American journal of physiology. Heart and circulatory physiology.

ACTH-induced hypertension is dependent on the ouabain-binding site of the alpha2-Na+-K+-ATPase subunit.

J. Lingrel, J. Lorenz, J. Schnetzer, 2008, American journal of physiology. Heart and circulatory physiology.

Knockout of the Na,K-ATPase α₂-isoform in the cardiovascular system does not alter basal blood pressure but prevents ACTH-induced hypertension.

J. Lingrel, J. Lorenz, J. Neumann, 2011, American journal of physiology. Heart and circulatory physiology.

SERCA2 Haploinsufficiency in a Mouse Model of Darier Disease Causes a Selective Predisposition to Heart Failure

Wei Huang, Yigang Wang, J. Lorenz, 2015, BioMed research international.

Ablation of plasma membrane Ca(2+)-ATPase isoform 4 prevents development of hypertrophy in a model of hypertrophic cardiomyopathy.

Jack Rubinstein, J. Lorenz, V. Prasad, 2014, Journal of molecular and cellular cardiology.

Marinobufagenin enhances cardiac contractility in mice with ouabain-sensitive alpha1 Na+-K+-ATPase.

J. Lingrel, J. Lorenz, Zijian Xie, 2008, American journal of physiology. Heart and circulatory physiology.

Marinobufagenin enhances cardiac contractility in mice with ouabain-sensitive (cid:1) Na -ATPase

J. Lingrel, J. Lorenz, Zijian Xie, 2009 .

Novel role of transient receptor potential vanilloid 2 in the regulation of cardiac performance.

Nathan Robbins, Jack Rubinstein, J. Lorenz, 2014, American journal of physiology. Heart and circulatory physiology.

Loss of the AE3 Cl−/HCO−3 exchanger in mice affects rate-dependent inotropy and stress-related AKT signaling in heart

J. Lorenz, V. Prasad, G. Shull, 2013, Front. Physiol..

A Critical Function for Ser-282 in Cardiac Myosin Binding Protein-C Phosphorylation and Cardiac Function

D. Bers, J. Molkentin, J. Lorenz, 2011, Circulation research.

Marinobufagenin enhances cardiac contractility in mice with ouabain‐sensitive α1 Na,K‐ATPase (NKA)

J. Lingrel, J. Lorenz, O. Fedorova, 2008 .

A Critical Function for Ser-282 in Cardiac Myosin Binding Protein-C Phosphorylation and Cardiac Function

D. Bers, J. Molkentin, J. Lorenz, 2011, Circulation research.

Novel role of transient receptor potential vanilloid 2 in the regulation of cardiac performance.

Sheryl E. Koch, Nathan Robbins, Jack Rubinstein, 2014, American journal of physiology. Heart and circulatory physiology.