作者: Yuka Okada , Yuko Ueshin , Ayako Isotani , Tomoko Saito-Fujita , Hisako Nakashima
DOI: 10.1038/NBT1280
关键词:
摘要: Placental dysfunction underlies many complications during pregnancy, and better understanding of gene function placentation could have considerable clinical relevance. However, the lack a facile method for placenta-specific manipulation has hampered investigation placental organogenesis treatment dysfunction. We showed previously that transduction fertilized mouse eggs with lentiviral vectors leads to transgene expression in both fetus placenta. Here we report incorporation by blastocysts after removal zona pellucida. All placentas analyzed, but none fetuses, were transgenic. Application this substantially rescued mice deficient Ets2, Mapk14 (also known as p38alpha) Mapk1 Erk2) from embryonic lethality caused defects. Ectopic Mapk11 also complemented deficiency placentation.