The targeted disruption of the MYPT1 gene results in embryonic lethality

被引：37

作者：

Okamoto, R

Ito, M

Suzuki, N

Kongo, M

Moriki, N

Saito, H

Tsumura, H

Imanaka-Yoshida, K

Kimura, K

Mizoguchi, A

Hartshorne, D

Nakano, T

机构：

[1] Mie Univ, Sch Med, Dept Internal Med 1, Tsu, Mie 5148507, Japan

[2] Mie Univ, Life Sci Res Ctr, Funct Genom Inst, Tsu, Mie 5148507, Japan

[3] Mie Univ, Sch Med, Dept Pathol, Tsu, Mie 5148507, Japan

[4] Mie Univ, Sch Med, Dept Anat, Tsu, Mie 5148507, Japan

[5] Univ Arizona, Muscle Biol Grp, Tucson, AZ 85721 USA

来源：

TRANSGENIC RESEARCH | 2005年 / 14卷 / 03期

关键词：

embryonic lethality; knockout mouse; myosin phosphatase; MYPT1;

D O I：

10.1007/s11248-005-3453-3

中图分类号：

Q5 [生物化学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：337 / 340

页数：4

共 9 条

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