Aviv Hassid

Affiliations: 
University of Tennessee Health Science Center, Memphis, TN, United States 
Area:
Cell Biology
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"Aviv Hassid"
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Publications

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Zhuang D, Balani P, Pu Q, et al. (2011) Suppression of PKG by PDGF or nitric oxide in differentiated aortic smooth muscle cells: obligatory role of protein tyrosine phosphatase 1B. American Journal of Physiology. Heart and Circulatory Physiology. 300: H57-63
Pu Q, Zhuang D, Thakran S, et al. (2011) Mechanisms related to NO-induced motility in differentiated rat aortic smooth muscle cells. American Journal of Physiology. Heart and Circulatory Physiology. 300: H101-8
Pu Q, Chang Y, Zhang C, et al. (2009) Chronic insulin treatment suppresses PTP1B function, induces increased PDGF signaling, and amplifies neointima formation in the balloon-injured rat artery. American Journal of Physiology. Heart and Circulatory Physiology. 296: H132-9
Zhuang D, Pu Q, Ceacareanu B, et al. (2008) Chronic insulin treatment amplifies PDGF-induced motility in differentiated aortic smooth muscle cells by suppressing the expression and function of PTP1B. American Journal of Physiology. Heart and Circulatory Physiology. 295: H163-73
Xi Q, Adebiyi A, Zhao G, et al. (2008) IP3 constricts cerebral arteries via IP3 receptor-mediated TRPC3 channel activation and independently of sarcoplasmic reticulum Ca2+ release. Circulation Research. 102: 1118-26
Rafiq K, Kolpakov MA, Abdelfettah M, et al. (2006) Role of protein-tyrosine phosphatase SHP2 in focal adhesion kinase down-regulation during neutrophil cathepsin G-induced cardiomyocytes anoikis. The Journal of Biological Chemistry. 281: 19781-92
Chang Y, Ceacareanu B, Zhuang D, et al. (2006) Counter-regulatory function of protein tyrosine phosphatase 1B in platelet-derived growth factor- or fibroblast growth factor-induced motility and proliferation of cultured smooth muscle cells and in neointima formation. Arteriosclerosis, Thrombosis, and Vascular Biology. 26: 501-7
Ceacareanu AC, Ceacareanu B, Zhuang D, et al. (2006) Nitric oxide attenuates IGF-I-induced aortic smooth muscle cell motility by decreasing Rac1 activity: essential role of PTP-PEST and p130cas. American Journal of Physiology. Cell Physiology. 290: C1263-70
Dixit M, Loot AE, Mohamed A, et al. (2005) Gab1, SHP2, and protein kinase A are crucial for the activation of the endothelial NO synthase by fluid shear stress. Circulation Research. 97: 1236-44
Zhuang D, Ceacareanu AC, Ceacareanu B, et al. (2005) Essential role of protein kinase G and decreased cytoplasmic Ca2+ levels in NO-induced inhibition of rat aortic smooth muscle cell motility. American Journal of Physiology. Heart and Circulatory Physiology. 288: H1859-66
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