Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Koji Nobe

Department of Pharmacology

School of Pharmaceutical Sciences

Showa University

Tokyo

Japan

[email]@*.showa-u.ac.jp

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Affiliation

Department of Pharmacology, School of Pharmaceutical Sciences, Showa University, Tokyo, Japan. 1998 - 2010

References

Rho A and the Rho kinase pathway regulate fibroblast contraction: Enhanced contraction in constitutively active Rho A fibroblast cells. Nobe, K., Nobe, H., Yoshida, H., Kolodney, M.S., Paul, R.J., Honda, K. Biochem. Biophys. Res. Commun. (2010) [Pubmed]
Glucose-dependent enhancement of diabetic bladder contraction is associated with a rho kinase-regulated protein kinase C pathway. Nobe, K., Yamazaki, T., Tsumita, N., Hashimoto, T., Honda, K. J. Pharmacol. Exp. Ther. (2009) [Pubmed]
Intra- and extrarenal arteries exhibit different profiles of contractile responses in high glucose conditions. Nobe, K., Nezu, Y., Tsumita, N., Hashimoto, T., Honda, K. Br. J. Pharmacol. (2008) [Pubmed]
Alterations of glucose-dependent and -independent bladder smooth muscle contraction in spontaneously hypertensive and hyperlipidemic rat. Nobe, K., Yamazaki, T., Kumai, T., Okazaki, M., Iwai, S., Hashimoto, T., Kobayashi, S., Oguchi, K., Honda, K. J. Pharmacol. Exp. Ther. (2008) [Pubmed]
Distinct agonist responsibilities of the first and second branches of mouse mesenteric artery. Nobe, K., Hagiwara, C., Nezu, Y., Honda, K. J. Cardiovasc. Pharmacol. (2006) [Pubmed]
High-glucose-altered endothelial cell function involves both disruption of cell-to-cell connection and enhancement of force development. Nobe, K., Miyatake, M., Sone, T., Honda, K. J. Pharmacol. Exp. Ther. (2006) [Pubmed]
Thrombin-induced force development in vascular endothelial cells: contribution to alteration of permeability mediated by calcium-dependent and -independent pathways. Nobe, K., Sone, T., Paul, R.J., Honda, K. J. Pharmacol. Sci. (2005) [Pubmed]
Glucose-dependent enhancement of spontaneous phasic contraction is suppressed in diabetic mouse portal vein: association with diacylglycerol-protein kinase C pathway. Nobe, K., Suzuki, H., Sakai, Y., Nobe, H., Paul, R.J., Momose, K. J. Pharmacol. Exp. Ther. (2004) [Pubmed]
Novel diacylglycerol kinase inhibitor selectively suppressed an U46619-induced enhancement of mouse portal vein contraction under high glucose conditions. Nobe, K., Miyatake, M., Nobe, H., Sakai, Y., Takashima, J., Momose, K. Br. J. Pharmacol. (2004) [Pubmed]
Enhancement effect under high-glucose conditions on U46619-induced spontaneous phasic contraction in mouse portal vein. Nobe, K., Sakai, Y., Nobe, H., Takashima, J., Paul, R.J., Momose, K. J. Pharmacol. Exp. Ther. (2003) [Pubmed]
Dysfunction of aorta involves different patterns of intracellular signaling pathways in diabetic rats. Nobe, K., Sakai, Y., Nobe, H., Momose, K. Eur. J. Pharmacol. (2003) [Pubmed]
High-glucose enhances a thromboxane A2-induced aortic contraction mediated by an alteration of phosphatidylinositol turnover. Nobe, K., Suzuki, H., Nobe, H., Sakai, Y., Momose, K. J. Pharmacol. Sci. (2003) [Pubmed]
Hyper-reactivity of diacylglycerol kinase is involved in the dysfunction of aortic smooth muscle contractility in streptozotocin-induced diabetic rats. Nobe, K., Sakai, Y., Maruyama, Y., Momose, K. Br. J. Pharmacol. (2002) [Pubmed]
Alternations of diacylglycerol kinase in streptozotocin-induced diabetic rats. Nobe, K., Sakai, Y., Momose, K. Cell. Signal. (1998) [Pubmed]

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