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Inefficient development of syncytiotrophoblasts in the Atp11a-deficient mouse placenta (Nagata G, in PNAS)

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 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.



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Contact:
Shigekazu Nagata

Shigekazu Nagata (Biochemistry & Immunology)


Tel+81-6-6879-4953
Mail snagataifrec.osaka-u.ac.jp

Immunology Frontier Research Center, Osaka University (WPI-IFReC)

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