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Gene therapy for murine glycerol kinase deficiency: importance of murine ortholog.

Abstract：

:A glycerol kinase (Gyk) knock-out (KO) mouse model permits improved understanding of glycerol kinase (GK) deficiency (GKD) pathogenesis, however, early death of affected mice limits its utility. The purpose of this work was to delay death of affected males to investigate thoroughly their phenotypes. An adenoviral vector carrying the human (Adeno-XGK) or mouse (Adeno-XGyk) GK gene was injected into KO mice within 24 h of birth. Adeno-XGK did not change KO mouse survival time despite liver GK activity greater than 100% of wild type. However, Adeno-XGyk improved KO mouse survival time greater than two-fold. These investigations demonstrate that gene replacement therapy for Gyk KO mice is more efficacious using murine Gyk than human GK. These studies expand our understanding of GKD pathogenesis in the murine model, and show that while murine GKD is more severe than in humans, GKD mice have similar metabolic disturbances to affected humans with hypoglycemia and acidemia.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Kuwada N,Nagano K,MacLennan N,Havens J,Kumar M,Dipple KM,McCabe ER

doi

10.1016/j.bbrc.2005.07.066

subject

Has Abstract

pub_date

2005-09-16 00:00:00

pages

247-55

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(05)01519-6

journal_volume

335

pub_type

杂志文章

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