N. Pece-Barbara

Regulation of Smurf2 ubiquitin ligase activity by anchoring the E2 to the HECT domain.

J. Wrana, C. Le Roy, F. Sicheri, 2005, Molecular cell.

Analysis of ALK-1 and endoglin in newborns from families with hereditary hemorrhagic telangiectasia type 2.

N. Pece-Barbara, M. Letarte, C. Bernabéu, 2000, Human molecular genetics.

Expression analysis of four endoglin missense mutations suggests that haploinsufficiency is the predominant mechanism for hereditary hemorrhagic telangiectasia type 1.

D. Marchuk, N. Pece-Barbara, M. Letarte, 1999, Human molecular genetics.

Identification of Hereditary Hemorrhagic Telangiectasia Type 1 in Newborns by Protein Expression and Mutation Analysis of Endoglin

Robert I. White, N. Pece-Barbara, M. Letarte, 2000, Pediatric Research.

Reduced endothelial secretion and plasma levels of transforming growth factor-beta1 in patients with hereditary hemorrhagic telangiectasia type 1.

N. Pece-Barbara, Shant Kumar, M. Letarte, 2005, Cardiovascular research.

Analysis of several endoglin mutants reveals no endogenous mature or secreted protein capable of interfering with normal endoglin function.

N. Pece-Barbara, M. Letarte, U. Cymerman, 2001, Human molecular genetics.

Endoglin Null Endothelial Cells Proliferate Faster and Are More Responsive to Transforming Growth Factor β1 with Higher Affinity Receptors and an Activated Alk1 Pathway*

J. Wrana, E. Dejana, S. Liebner, 2005, Journal of Biological Chemistry.