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Research
2022.04.28
Inefficient development of syncytiotrophoblasts in the Atp11a-deficient mouse placenta (Nagata G, in PNAS)
PRESS RELEASE
Yuki Ochiai, Katsumori Segawa (present: Tokyo Medical and Dental University), Shigekazu Nagata (Biochemistry & Immunology, IFReC), and the research group showed that a flippase Atp11a at the plasma membrane plays an important role in the formation of syncytiotrophoblasts in placental development.
Figure 1.
Embryonic lethality of Atp11a-/- mice. Atp11a-/- mouse embryos died at E14.5 with thin-walled heart ventricles.
However, the cardiomyocyte- or epiblast-specific Atp11a deletion did not affect mouse development,
suggesting the inability of Atp11a-/- placentas to support the embryos.
Commentary (PDF)
Article (External Link)
Contact:
Shigekazu Nagata (Biochemistry & Immunology)
+81-6-6879-4953
snagataifrec.osaka-u.ac.jp