Erratum: Endothelial Notch signaling is upregulated in human brain arteriovenous malformations and a mouse model of the disease

Abstract

Correction to: Laboratory Investigation (2009), 89, 971–982; doi:10.1038/labinvest.2009.62 In this article, the authors have identified errors in the figures and figure legends. P values in the figures and figure legends state the significance of a two-tailed Student's t test, assuming equal variation. Correction to: Laboratory Investigation (2009), 89, 971–982; doi:10.1038/labinvest.2009.62 In this article, the authors have identified errors in the figures and figure legends. P values in the figures and figure legends state the significance of a two-tailed Student's t test, assuming equal variation. Correction to:Laboratory Investigation (2009), 89, 971–982; doi:10.1038/labinvest.2009.62 In this article, the authors have identified errors in the figures and figure legends. P values in the figures and figure legends state the significance of a two-tailed Student's t test, assuming equal variation. However, these values should state the P values of a two-tailed Wilcoxon's rank sum non-parametric test. In Figure 2, ‘BAVM vs autopsy controls P=0.001; BAVM vs biopsy controls P=0.039' In Figure 3, ‘BAVM vs autopsy controls P=0.0006; BAVM vs biopsy controls P=0.015' In Figure 4, ‘P=0.0253' In Figure 5, ‘P=0.0253' Endothelial Notch signaling is upregulated in human brain arteriovenous malformations and a mouse model of the diseaseLaboratory InvestigationVol. 89Issue 9PreviewBrain arteriovenous malformations (BAVMs) can cause lethal hemorrhagic stroke and have no effective treatment. The cellular and molecular basis for this disease is largely unknown. We have previously shown that expression of constitutively-active Notch4 receptor in the endothelium elicits and maintains the hallmarks of BAVM in mice, thus establishing a mouse model of the disease. Our work suggested that Notch pathway could be a critical molecular mediator of BAVM pathogenesis. Here, we investigated the hypothesis that upregulated Notch activation contributes to the pathogenesis of human BAVM. Full-Text PDF Open Access