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Molecular and Cellular Biology, June 2009, p. 3451, Vol. 29, No. 12
0270-7306/09/$08.00+0 doi:10.1128/MCB.00466-09
| AUTHOR'S CORRECTION |
Division of Molecular and Vascular Medicine, Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215
Volume 29, no. 8, p. 2011-2022, 2009. After publication, we identified an article describing Ang-2 as a weaker activator of Tie-2 than Ang-1 (E. Bogdanovic, V. P. Nguyen, and D. J. Dumont, J. Cell Sci. 119:3551-3560, 2006), leading those authors to propose that Ang-2 may be a partial agonist of the receptor. Our paper confirms this weak agonist activity of exogenous Ang-2 and extends their findings by demonstrating that endogenous Ang-2 is critical for basal Tie-2 activity in cultured ECs and that exogenous Ang-2 inhibits Ang-1-induced Tie-2 activation, thus acting as a partial antagonist as well.
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