Placenta

This unpublished dataset is based on three genes that cause placentation defects: (1) Atp11a: Predicted to enable phosphatidylethanolamine flippase activity and phosphatidylserine flippase activity. Involved in positive regulation of myotube differentiation. Acts upstream of or within in utero embryonic development. Predicted to be located in intracellular membrane-bounded organelle. Predicted to be integral component of plasma membrane. Predicted to be part of phospholipid-translocating ATPase complex. Predicted to be active in several cellular components, including endoplasmic reticulum; recycling endosome; and trans-Golgi network. Is expressed in several structures, including alimentary system; central nervous system; genitourinary system; lung; and sensory organ. Orthologous to human ATP11A. (2) Smg9: Predicted to enable identical protein binding activity. Involved in brain development; eye development; and heart development. Acts upstream of or within in utero embryonic development. Orthologous to human SMG9. (3) Ssr2: Acts upstream of or within in utero embryonic development. Predicted to be located in membrane. Predicted to be integral component of membrane. Predicted to be active in endoplasmic reticulum. Is expressed in cranium; genitourinary system; and pancreas epithelium. Orthologous to human SSR2.