Y. Zhao

发表

Pulmonary endothelial cell barrier enhancement by FTY720 does not require the S1P1 receptor.

S. Dudek, Yutong Zhao, V. Natarajan, 2007, Cellular signalling.

Assembly and activation of HK-PK complex on endothelial cells results in bradykinin liberation and NO formation.

A. Schmaier, Z. Shariat-Madar, F. Mahdi, 2001, American journal of physiology. Heart and circulatory physiology.

Vasorelaxing action of vasonatrin peptide is associated with activation of large-conductance Ca(2+)-activated potassium channels in vascular smooth muscle cells.

Miaozhang Zhu, Jun Yu, Y. Zhao, 2010, Physiological research.

Roles of K+ and Cl- channels in cAMP-induced pulmonary vasodilation.

L. Rubin, Y. Zhao, X. J. Yuan, 1998, Experimental lung research.

Direct and endothelial cell-mediated effect of cyclosporin A on the proliferation of rat smooth muscle cells in vitro.

D. Leszczyński, Y. Zhao, M. Foegh, 1993, The American journal of pathology.

Pulmonary vasoconstrictor effects of prostacyclin in rats: potential role of thromboxane receptors.

L. Rubin, Y. Zhao, X. J. Yuan, 1996, Journal of applied physiology.

Apoptosis of vascular smooth muscle cells. Protein kinase C and oncoprotein Bcl-2 are involved in regulation of apoptosis in non-transformed rat vascular smooth muscle cells.

Dariusz Leszczyński, Y. Zhao, M. Foegh, 1994, The American journal of pathology.

MAPK and PKC activity are not required for H(2)O(2)-induced arterial muscle contraction.

C. Packer, H. Davis, A. Mak, 2000, American journal of physiology. Heart and circulatory physiology.

Pulmonary vein contracts in response to hypoxia.

C. Packer, Y. Zhao, R. Rhoades, 1993, The American journal of physiology.

Heterogeneity in the response of vascular smooth muscle to heparin: altered signaling in heparin-resistant cells.

D. Templeton, Y. Zhao, M. Fan, 2000, Cardiovascular research.

Role of MARCKS in regulating endothelial cell proliferation.

H. Davis, Y. Zhao, B. Neltner, 2000, American journal of physiology. Cell physiology.

Thrombin‐induced phosphorylation of the myristoylated alanine‐rich C kinase substrate (MARCKS) protein in bovine pulmonary artery endothelial cells

H. Davis, Y. Zhao, Ying Zhao, 1996, Journal of cellular physiology.

Inhibition of K(V) and K(Ca) channels antagonizes NO-induced relaxation in pulmonary artery.

L. Rubin, J. Wang, Y. Zhao, 1997, The American journal of physiology.

Chronic hypoxia impairs pulmonary venous smooth muscle contraction.

C. Packer, Y. Zhao, R. Rhoades, 1995, Respiration physiology.

beta-hexosaminidase-induced activation of p44/42 mitogen-activated protein kinase is dependent on p21Ras and protein kinase C and mediates bovine airway smooth-muscle proliferation.

K. Malik, Y. Zhao, M. Muthalif, 1999, American journal of respiratory cell and molecular biology.

Rat heart smooth muscle cells express high and low affinity receptors for somatostatin-14, which are involved in regulation of cell proliferation.

D. Leszczyński, J. Nilsson, S. Cathapermal, 1993, Life sciences.

Thrombin-induced phosphorylation of MARCKS does not alter its interactions with calmodulin or actin.

D. Sacks, H. Davis, Y. Zhao, 2000, Cellular signalling.

Signaling pathways in thrombin-induced actin reorganization in pulmonary artery endothelial cells.

H. Davis, Y. Zhao, 1999, Experimental lung research.

The vein utilizes different sources of energy than the artery during pulmonary hypoxic vasoconstriction.

C. Packer, Y. Zhao, R. Rhoades, 1996, Experimental lung research.