A mouse model of galactose-1-phosphate uridyl transferase deficiency
Related Experiment Video
Updated: Oct 23, 2026

Measuring Glucose Uptake in Drosophila Models of TDP-43 Proteinopathy
Published on: August 3, 2021
N D Leslie1, K L Yager, P D McNamara
1Division of Human Genetics Children's Hospital Research Foundation, Cincinnati, Ohio 45229, USA.
Abstract:
Galactose-1-phosphate uridyl transferase (GALT) deficiency causes classical galactosemia in humans. Mice deficient in this enzyme were created by gene targeting. GALT-deficient mice develop biochemical features similar to those seen in humans with GALT deficiency, but fail to develop the pattern of acute toxicity seen in newborns with classical galactosemia. This study suggests that alternative routes of galactose metabolism are important in the pathogenesis of galactosemia.
Related Concept Videos
Mouse Models of Cancer Study
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...
Glucose Transporters
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:

