Use of gene targeting for compromising energy homeostasis in neuro-muscular tissues: The role of sarcomeric mitochondrial creatine kinase

被引：44

作者：

Steeghs, K

Heerschap, A

deHaan, A

Ruitenbeek, W

Oerlemans, F

vanDeursen, J

Perryman, B

Pette, D

Bruckwilder, M

Koudijs, J

Jap, P

Wieringa, B

机构：

[1] UNIV NIJMEGEN, FAC MED SCI, DEPT CELL BIOL & HISTOL, NL-6500 HB NIJMEGEN, NETHERLANDS

[2] UNIV NIJMEGEN, FAC MED SCI, DEPT DIAGNOST RADIOL, NL-6500 HB NIJMEGEN, NETHERLANDS

[3] VRIJE UNIV AMSTERDAM, DEPT MUSCLE & EXERCISE PHYSIOL, NL-1081 BT AMSTERDAM, NETHERLANDS

[4] UNIV NIJMEGEN, FAC MED SCI, DEPT PAEDIAT, NL-6500 HB NIJMEGEN, NETHERLANDS

[5] ST JUDE CHILDRENS RES HOSP, DEPT GENET, MEMPHIS, TN 38101 USA

[6] UNIV COLORADO, HLTH SCI CTR, DIV CARDIOL, DENVER, CO 80262 USA

[7] UNIV KONSTANZ, DEPT BIOL, D-7834 CONSTANCE, GERMANY

来源：

JOURNAL OF NEUROSCIENCE METHODS | 1997年 / 71卷 / 01期

关键词：

creatine kinase; mitochondria; gene targeting; energy homeostasis; muscle physiology; oxidative phosphorylation;

D O I：

10.1016/S0165-0270(96)00124-0

中图分类号：

Q5 [生物化学];

学科分类号：

071010 ; 081704 ;

摘要：

We have introduced a single knock-out mutation in the mitochondrial creatine kinase gene (ScCKmit) in the mouse germ line via targeted mutagenesis in mouse embryonic stem (ES) cells. Surprisingly, ScCKmit -/- muscles, unlike muscles of mice with a deficiency of cytosolic M-type creatine kinase (M-CK -/-; Van Deursen et al, (1993) Cell 74, 621-631), display no altered morphology, performance or oxidative phosphorylation capacity. Also, the levels of high energy phosphate metabolites were essentially unaltered in ScCKmit mutants, Our results challenge some of the present concepts about the strict coupling between CKmit function and aerobic respiration.

引用

页码：29 / 41

页数：13

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