Qinghang Liu

Antiadrenergic effects of adenosine A(1) receptor-mediated protein phosphatase 2a activation in the heart.

Modulation of protein phosphatase 2a by adenosine A1 receptors in cardiomyocytes: role for p38 MAPK.

Acute p38 MAPK activation decreases force development in ventricular myocytes.

Protein phosphatase 2A-mediated cross-talk between p38 MAPK and ERK in apoptosis of cardiac myocytes.

Direct interaction and reciprocal regulation between ASK1 and calcineurin-NFAT control cardiomyocyte death and growth.

Interaction between TAK1-TAB1-TAB2 and RCAN1-calcineurin defines a signalling nodal control point.

Protein kinase C{alpha}, but not PKC{beta} or PKC{gamma}, regulates contractility and heart failure susceptibility: implications for ruboxistaurin as a novel therapeutic approach.

CaMKII negatively regulates calcineurin-NFAT signaling in cardiac myocytes.

ASK1 regulates cardiomyocyte death but not hypertrophy in transgenic mice.

Functional divergence of platelet protein kinase C (PKC) isoforms in thrombus formation on collagen.

Protein kinase Cα as a heart failure therapeutic target.

Interaction between NFκB and NFAT coordinates cardiac hypertrophy and pathological remodeling.

Mechanism of the selective catalytic oxidation of slip ammonia over Ru-modified Ce-Zr complexes determined by in situ diffuse reflectance infrared Fourier transform spectroscopy.

Transforming growth factor β-activated kinase 1 signaling pathway critically regulates myocardial survival and remodeling.

TAK1 Regulates Myocardial Response to Pathological Stress via NFAT, NFκB, and Bnip3 Pathways.

Oxidative stress decreases microtubule growth and stability in ventricular myocytes.

Which factors are associated with extremely short-term survival after surgery in patients with esophageal squamous cell carcinoma?