gene knock-outs of inositol 1,4,5-trisphosphate receptors types 1 and 2 result in perturbation of cardiogenesis基因淘汰赛的肌醇1 4 5-trisphosphate受体类型1和2 cardiogenesis导致扰动.pdfVIP

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2017-09-01 发布于上海
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gene knock-outs of inositol 1,4,5-trisphosphate receptors types 1 and 2 result in perturbation of cardiogenesis基因淘汰赛的肌醇1 4 5-trisphosphate受体类型1和2 cardiogenesis导致扰动.pdf

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gene knock-outs of inositol 1,4,5-trisphosphate receptors types 1 and 2 result in perturbation of cardiogenesis基因淘汰赛的肌醇1 4 5-trisphosphate受体类型1和2 cardiogenesis导致扰动

Gene Knock-Outs of Inositol 1,4,5-Trisphosphate Receptors Types 1 and 2 Result in Perturbation of Cardiogenesis 1. 1. 1 1 2 Keiko Uchida , Megumi Aramaki , Maki Nakazawa , Chihiro Yamagishi , Shinji Makino , Keiichi 2 3{ 1 3,4 1 Fukuda , Takeshi Nakamura , Takao Takahashi , Katsuhiko Mikoshiba *, Hiroyuki Yamagishi * 1 Department of Pediatrics, Keio University School of Medicine, Tokyo, Japan, 2 Department of Regenerative Medicine and Advanced Cardiac Therapeutics, Keio University School of Medicine, Tokyo, Japan, 3 Calcium Oscillation Project, ICORP-SORST, Japan Science and Technology Agency, Saitama, Japan, 4 Laboratory for Developmental Neurobiology, Brain Science Institute (BSI), RIKEN, Saitama, Japan Abstract Background: Inositol 1,4,5-trisphosphate receptors (IP R1, 2, and 3) are intracellular Ca2+ release channels that regulate 3 various vital processes. Although the ryanodine receptor type 2, another type of intracellular Ca2+ release channel, has been shown to play a role in embryonic cardiomyocytes, the functions of the IP3Rs in cardiogenesis remain unclear. Methodology/Principal Findings: We found that IP R12/ 2-IP R22/ 2 double-mutant mice died in utero with developmental 3 3 defects of the ventricular myocardium and atrioventricular (AV) canal of the heart by embryonic day (E) 11.5, even though no cardiac defect was detectable in IP R12/ 2 or IP R22/ 2 single-mutant m