Merck, 265005-100MG, Dexamethasone

General description
Most active and highly stable glucocorticoid. Causes a reduction in cyclin A and Cdk2 activity, and inhibition of G₁/S transition in osteoblasts. Inhibits the phosphorylation of retinoblastoma (Rb) protein. Inhibits the expression of inducible but not constitutive nitric oxide synthase in vascular endothelial cells (IC₅₀ = 5 nM). Enhances active cation transport in aortic smooth muscle cells by stimulating the Na⁺ - K⁺ pump. Induces apoptosis in human thymocytes.
Biochem/physiol Actions
Cell permeable: no
Primary Target
Phosphorylation of rb protein
Product does not compete with ATP.
Reversible: no
Target IC₅₀: 5 nM Inhibiting the expression of inducible but not constitutive nitric oxide synthase in vascular endothelial cells
Preparation Note
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 2 months at -20°C.
Other Notes
Reil, T.D., et al. 2000. J. Surg. Res.92, 108.
Smith, E., et al. 2000. J.Biol. Chem. 275, 1992.
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Donis, J.A., et al. 1993. Biotechniques15, 786.
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Vandewalle, A., et al. 1993. J. Cell Physiol.156, 383.
Nieto, M.A., et al. 1992. Clin. Exp. Immunol.88, 341.
Walsh, D., and Avashia, J. 1992. Cleveland Clin. J. Med. 59, 505.
Warters, R.L. 1992. Cancer Res.52, 883.
Sperber, K., et al. 1991. J. Allergy Clin. Immunol.87, 490.
Radomski, M.W., et al. 1990. Proc. Natl. Acad. Sci. USA 87, 10043.
Bettger, W.J., et al. 1981. Proc. Natl. Acad. Sci. USA78, 5588.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Toxicity: Carcinogenic / Teratogenic (D)