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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2003.1
- 수록면
- 125 - 135 (11page)
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The nul mutation of cardiac Na+-Ca2+ exchanger (NCX1) gene in mice caused death of embryo in utero at embryonic day (ED) 9.0-9.5 and this em-bryonic lethality appears resulted from abnormal heart development. In the present study, we in-vestigated whether transgenic re-expression of these lethal defects. Transgenic mice expresing the canine NCX1 in a cardiac specific maner were bred into the NCX1 knock-out background but did not prevent the fetal lethality asociated with the NCX1 nul alele. However, the NCX1 knock-out embryos with an NCX1 transgene sur-vived with heart beatings until ED 10.5 which was one day longer than the survival of the NCX1 knock-out embryos (ED 9.5). At ED 10.5, however, the partialy rescued NCX1 embryos might have succumbed to the lack of an organized vascula-ture in the yolk sacs. The placental labyrinth la-The transgenic re-expression of NCX1 rescued heart beatings and survived longer, but was stil insuficient for the mice to be completely rescued. Importantly, NCX1 was observed to expres in the yolk sac and the placenta of wild type mice. The results sugest that defects in extra-embryo-nic compartments are causal to the lethality, and that NCX1 may play an important role in es-tablishing vascularization in extra-embryonic tis-sues.
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