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The targeted disruption of the MYPT1 gene results in embryonic lethality |
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| Authors: | Ryuji Okamoto Masaaki Ito Noboru Suzuki Mariko Kongo Nobuyuki Moriki Hiromitsu Saito Hideki Tsumura Kyoko Imanaka-Yoshida Kazushi Kimura Akira Mizoguchi David J Hartshorne Takeshi Nakano |
| Institution: | (1) The First Department of Internal Medicine, Mie University School of Medicine, 2-174 Edobashi, 514-8507 Mie, Tsu, Japan;(2) Functional Genomics Institutes, Life Science Research Center, Mie University, 2-174 Edobashi, 514-8507 Mie, Tsu, Japan;(3) Department of Pathology, Mie University School of Medicine, 2-174 Edobashi, 514-8507 Mie, Tsu, Japan;(4) Department of Anatomy, Mie University School of Medicine, 2-174 Edobashi, 514-8507 Mie, Tsu, Japan;(5) Muscle Biology Group, University of Arizona, 85721 Tucson, AZ, USA |
| Abstract: | Myosin phosphatase (MP) is a major phosphatase responsible for the dephosphorylation of the regulatory light chain of myosin II. MYPT1, a target subunit of smooth and nonmuscle MP, is responsible for activation and regulation of MP. To identity the physiological roles of MP, we have generated MYPT1-deficient mice by gene targeting. The heterozygous mice showed no changes in expression levels of MYPT1 and no distinct phenotype compared to wild-type mice was observed. None of the F2 mice were homozygous for the MYPT1 deletion, indicating that the targeted disruption of the MYPT1 gene resulted in embryonic lethality. The point of embryonic lethality is before 7.5 dpc. These findings indicate that MYPT1 is essential for mouse embryogenesis. |
| Keywords: | Embryonic lethality Knockout mouse Myosin phosphatase MYPT1 |
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