Subject Areas on Research
- ALK5 phosphorylation of the endoglin cytoplasmic domain regulates Smad1/5/8 signaling and endothelial cell migration.
- Axonally translated SMADs link up BDNF and retrograde BMP signaling.
- Bone morphogenetic proteins induce pancreatic cancer cell invasiveness through a Smad1-dependent mechanism that involves matrix metalloproteinase-2.
- Bone morphogenetic proteins signal through the transforming growth factor-beta type III receptor.
- Ecsit is required for Bmp signaling and mesoderm formation during mouse embryogenesis.
- Endoglin mediates fibronectin/α5β1 integrin and TGF-β pathway crosstalk in endothelial cells.
- Endoglin promotes transforming growth factor beta-mediated Smad 1/5/8 signaling and inhibits endothelial cell migration through its association with GIPC.
- Endometrial receptivity and implantation require uterine BMP signaling through an ACVR2A-SMAD1/SMAD5 axis.
- Evidence that Mothers-against-dpp-related 1 (Madr1) plays a role in the initiation and maintenance of spermatogenesis in the mouse.
- Identification of mZnf8, a mouse Krüppel-like transcriptional repressor, as a novel nuclear interaction partner of Smad1.
- Parathyroid hormone-related peptide represses chondrocyte hypertrophy through a protein phosphatase 2A/histone deacetylase 4/MEF2 pathway.
- Reciprocal SOX2 regulation by SMAD1-SMAD3 is critical for anoikis resistance and metastasis in cancer.
- TGFbeta-stimulated Smad1/5 phosphorylation requires the ALK5 L45 loop and mediates the pro-migratory TGFbeta switch.
Keywords of People
- Hogan, Brigid L. M., Research Professor of Cell Biology, Cell Biology