机译:肥大细胞和巨噬细胞的耗尽损害过型骨化骨化在ACVR1 R206H ACVR1 R206H R206H鼠标模型中的纤维型普拉西亚骨骼进展
Department of Orthopaedic SurgeryUniversity of PennsylvaniaPhiladelphia PA USA;
Department of Orthopaedic SurgeryUniversity of PennsylvaniaPhiladelphia PA USA;
Department of Pathology and Laboratory MedicineUniversity of PennsylvaniaPhiladelphia PA USA;
Department of Orthopaedic SurgeryUniversity of PennsylvaniaPhiladelphia PA USA;
Department of Orthopaedic SurgeryUniversity of PennsylvaniaPhiladelphia PA USA;
Department of Pathology and Laboratory MedicineUniversity of PennsylvaniaPhiladelphia PA USA;
Department of Orthopaedic SurgeryUniversity of PennsylvaniaPhiladelphia PA USA;
Department of Orthopaedic SurgeryUniversity of PennsylvaniaPhiladelphia PA USA;
FIBRODYSPLASIA OSSIFICANS PROGRESSIVA; FOP; HETEROTOPIC OSSIFICATION; TISSUE INJURY; CHRONIC INFLAMMATION; BONE MORPHOGENETIC PROTEIN SIGNALING; BMP; ACVR1;
机译:肥大细胞和巨噬细胞的耗尽损害过型骨化骨化在ACVR1 R206H ACVR1 R206H R206H鼠标模型中的纤维型普拉西亚骨骼进展
机译:一只Acvr1 R206H敲入小鼠患有骨化性纤维增生
机译:在骨增生性纤维增生中发现ACVR1 R206H突变可通过BMP介导的SMAD1 / 5/8信号增加人诱导的多能干细胞衍生的内皮细胞形成和胶原蛋白的产生
机译:生成诱导多能干细胞衍生的纤维型胰腺类骨质人进化患者的内皮细胞 - Activina和BMP诱导的Alk2受体激活=普通钨患者的疾病模型= Induzierten ploripotenten
机译:Acvr1 R206H敲入小鼠患有骨化性纤维增生
机译:在骨增生性纤维增生中发现ACVR1 R206H突变可通过BMP介导的SMAD1 / 5/8信号增加人诱导的多能干细胞衍生的内皮细胞形成和胶原蛋白的产生