1  through both the glycolytic pathway and the hexose monophosphate shunt.

2 stion of heat-killed yeast and by subsequent hexose-monophosphate shunt activation using nitroblue te

3 -beta deficiency would impair glycolysis and hexose monophosphate shunt activities leading to reducti

4 pyrimidines, but also from inhibition of the hexose monophosphate shunt activity in young erythrocyte

5 glycolysis 25-120% and the activity of their hexose monophosphate shunt (HMPS) 100-600%, reaching a p

6                These changes suggest reduced hexose monophosphate shunt (HMS) activity.

7 G-6-PDase), the rate-controlling step of the hexose monophosphate shunt (HMS), is located near the ce

8 GDase), which are the first two steps of the hexose monophosphate shunt (HMS).

9 ific isocitrate dehydrogenase (Idp2p) or the hexose monophosphate shunt is essential for growth with

10  conditions that do not favor the use of the hexose monophosphate shunt (Luzzatto et al.).

11 ng-chain fatty acid metabolites, and reduced hexose monophosphate shunt metabolites in the resistant

12                          The activity of the hexose monophosphate shunt pathway in isolated rat retin

13 triphosphate (ATP), lactic acid content, the hexose monophosphate shunt pathway, aldose reductase act

14 e proteins, or enzymes in the glycolytic and hexose monophosphate shunt pathways.

15 tivating NADPH oxidase, or by inhibiting the hexose monophosphate shunt that generates NADPH from glu

16       Biochemical analysis revealed that the hexose monophosphate shunt was compromised in Gsr-defici

17 roduction was also blocked by inhibiting the hexose monophosphate shunt, which regenerates the NADPH

18                            Inhibition of the hexose monophosphate shunt, which utilizes glucose to re