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.

Upon PDGFRα signaling in mouse embryonic palatal mesenchyme cells, Srsf3 exhibits differential transcript binding, resulting in retention of the receptor in early endosomes and increased downstream PI3K-mediated Akt signaling.

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

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

In a mouse model of menstruation stromal cells respond to breakdown of the tissue by changing their identity to become epithelial cells that are incorporated into the luminal epithelium which is rapidly 'healed' without scarring.

The inclusive, exclusive, and hierarchical atlas of NFATc1⁺/PDGFR-α⁺ cells in dental and periodontal mesenchyme is described.

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.

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

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.

Fibro-inflammatory progenitors represent a subpopulation of perivascular cells in visceral adipose tissues of mice that promote inflammation and fibrosis.