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

نویسندگان

  • K Steeghs
  • A Heerschap
  • A de Haan
  • W Ruitenbeek
  • F Oerlemans
  • J van Deursen
  • B Perryman
  • D Pette
  • M Brückwilder
  • J Koudijs
  • P Jap
  • B Wieringa
چکیده

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.

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عنوان ژورنال:
  • Journal of neuroscience methods

دوره 71 1  شماره 

صفحات  -

تاریخ انتشار 1997