V. Kaartinen

Publications158
h-index50
Citations7,592
Highly Influential Citations371
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Abnormal lung development and cleft palate in mice lacking TGF–β3 indicates defects of epithelial–mesenchymal interaction
TLDR
This study demonstrates an essential function for TGF–β3 in the normal morphogenesis of palate and lung, and directly implicates this cytokine in mechanisms of epithelial–mesenchymal interaction.
TGF-β3-induced Palatogenesis Requires Matrix Metalloproteinases
TLDR
Observations indicate for the first time that the proteolytic degradation of the ECM by MMPs is a necessary step for palatal fusion.
TGF-beta3-induced palatogenesis requires matrix metalloproteinases.
TLDR
Observations indicate for the first time that the proteolytic degradation of the ECM by MMPs is a necessary step for palatal fusion.
A Poised Chromatin Platform for TGF-β Access to Master Regulators
Craniofacial defects in mice lacking BMP type I receptor Alk2 in neural crest cells
Abr and Bcr are multifunctional regulators of the Rho GTP-binding protein family.
TLDR
The data suggest the multifunctional Bcr and Abr proteins might interact simultaneously and/or sequentially with members of the Rho family to regulate and coordinate cellular signaling.
Atrioventricular cushion transformation is mediated by ALK2 in the developing mouse heart.
ALK5- and TGFBR2-independent role of ALK1 in the pathogenesis of hereditary hemorrhagic telangiectasia type 2.
TLDR
Comparing phenotypes of mice in which the Alk1, Alk5, or Tgfbr2 gene was conditionally deleted in restricted vascular endothelia using a novel endothelial Cre transgenic line indicates that neither ALK5 nor TGFBR2 is required for ALK1 signaling pertinent to the pathogenesis of HHT and suggests that HHT might not be a TGF-beta subfamily disease.
Modulation of morphogenesis by noncanonical Wnt signaling requires ATF/CREB family–mediated transcriptional activation of TGFβ2
TLDR
It is proposed that transcriptional readout mediated at least in part by a Wnt11 → ATF/CREB → TGFβ2 pathway is critical in regulating morphogenesis in response to noncanonical Wnt signaling.
Signaling via the Tgf-beta type I receptor Alk5 in heart development.
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