Inverted Formin 2 Regulates Intracellular Trafficking, Placentation
RESEARCH ARTICLE Inverted formin 2 regulates intracellular trafficking, placentation, and pregnancy outcome Katherine Young Bezold Lamm1,2,3,4*, Maddison L Johnson5, Julie Baker Phillips5, Michael B Muntifering4, Jeanne M James6, Helen N Jones3, Raymond W Redline7, Antonis Rokas5, Louis J Muglia1,2,8* 1Center for the Prevention of Preterm Birth, Perinatal Institute, Cincinnati Children’s Hospital Medical Center, Cincinnati, United States; 2Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, United States; 3Molecular and Developmental Biology Graduate Program, University of Cincinnati College of Medicine, Cincinnati Children’s Hospital Medical Center, Cincinnati, United States; 4Division of Developmental Biology, Cincinnati Children’s Hospital Medical Center, Cincinnati, United States; 5Department of Biological Sciences, Vanderbilt University, Nashville, United States; 6The Heart Institute, Cincinnati Children’s Hospital Medical Center, Cincinnati, United States; 7Department of Pathology, University Hospitals Cleveland Medical Center, Cleveland, United States; 8Division of Human Genetics, Cincinnati Children’s Hospital Medical Center, Cincinnati, United States Abstract Healthy pregnancy depends on proper placentation—including proliferation, differentiation, and invasion of trophoblast cells—which, if impaired, causes placental ischemia resulting in intrauterine growth restriction and preeclampsia. Mechanisms regulating trophoblast invasion, however, are unknown. We report that reduction of Inverted formin
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