Gab1 is a key downstream effector of PDGF signaling and essential to oligodendrocyte differentiation by linking PDGF signaling with GSK3β/β-catenin module.

Studies in zebrafish and mouse implicate the PDGF signaling pathway in the communication between the endoderm and the myocardium that drives medial myocardial movement and thereby initiates cardiac morphogenesis.

A muscle-derived signaling molecule suppresses excessive accumulation of lipids in the Drosophila adipose tissue by activating the Pi3K/Akt/mTOR signaling cascade in the Drosophila hepatocyte-like cells.

Lineage tracing using a knockin Pdgfra-rtTA tool indicates distinct contributions of this cell lineage to myofibroblasts in normal development, fibrosis and bronchopulmonary dysplasia models.

Combined fate mapping and genetic deletion studies reveal that PDGFRα+ cells and PDGFRα gene itself are required for adipose tissue development but not for adult tissue homeostasis.

Deletion of the ATM cofactor ATMIN reduces PDGFRA expression and strongly suppresses tumorigenesis in a TP53-deficient mouse model of glioblastoma.

PDGF and FGF signal via distinct intracellular pathways to confer different cellular outcomes during craniofacial development.

The skeletal muscle of fruit flies communicates with other organs to prevent the accumulation of too much fat and to protect adults against obesity.

PDGFRα+ Sca-1+ bone marrow stromal/stem cells in whole bone marrow grafts can trigger the onset of autoimmune-related fibrosis in a mouse model of scleroderma.