Inactivation of Smad5 in Endothelial Cells and Smooth Muscle Cells Demonstrates that Smad5 Is Required for Cardiac Homeostasis
- 1 May 2007
- journal article
- Published by Elsevier in The American Journal of Pathology
- Vol. 170 (5) , 1460-1472
- https://doi.org/10.2353/ajpath.2007.060839
Abstract
No abstract availableKeywords
This publication has 47 references indexed in Scilit:
- A critical developmental role for tgfbr2 in myogenic cell lineages is revealed in mice expressing SM22-Cre, not SMMHC-CreJournal of Molecular and Cellular Cardiology, 2006
- Identification of BMP9 and BMP10 as functional activators of the orphan activin receptor-like kinase 1 (ALK1) in endothelial cellsBlood, 2006
- Smad5 determines murine amnion fate through the control of bone morphogenetic protein expression and signalling levelsDevelopment, 2006
- Dose-dependent Smad1, Smad5 and Smad8 signaling in the early mouse embryoDevelopmental Biology, 2006
- Crystal Structure of BMP-9 and Functional Interactions with Pro-region and ReceptorsJournal of Biological Chemistry, 2005
- Smad1 and Smad8 Function Similarly in Mammalian Central Nervous System DevelopmentMolecular and Cellular Biology, 2005
- Defective paracrine signalling by TGFβ in yolk sac vasculature of endoglin mutant mice: a paradigm for hereditary haemorrhagic telangiectasiaDevelopment, 2004
- Generation of a floxed allele of Smad5 for cre‐mediated conditional knockout in the mouseGenesis, 2003
- Tie2-Cre Transgenic Mice: A New Model for Endothelial Cell-Lineage Analysis in VivoDevelopmental Biology, 2001
- Remarkable versatility of Smad proteins in the nucleus of transforming growth factor-β activated cellsCytokine & Growth Factor Reviews, 1999