D. C. Liemburg-Apers

发表

Mitochondrial hyperpolarization during chronic complex I inhibition is sustained by low activity of complex II, III, IV and V.

J. Smeitink, Aleksandra Wojtala, M. Wieckowski, 2014, Biochimica et biophysica acta.

University of Birmingham Mitochondrial hyperpolarization during chronic complex I inhibition is sustained by low activity of complex II, III, IV and V

J. Smeitink, Aleksandra Wojtala, M. Wieckowski, 2014 .

Interactions between mitochondrial reactive oxygen species and cellular glucose metabolism

P. Willems, W. Koopman, S. Grefte, 2015, Archives of Toxicology.

Mitochondrial dysfunction in primary human fibroblasts triggers an adaptive cell survival program that requires AMPK-α.

B. Viollet, R. Rodenburg, J. Fransen, 2015, Biochimica et biophysica acta.

The role of glucose in oxidative phosphorylation dysfunctional myoblasts

D. C. Liemburg-Apers, 2016 .

Acute stimulation of glucose influx upon mitoenergetic dysfunction requires LKB1, AMPK, Sirt2 and mTOR–RAPTOR

J. Smeitink, P. Willems, W. Koopman, 2016, Journal of Cell Science.

Mitoenergetic Dysfunction Triggers a Rapid Compensatory Increase in Steady-State Glucose Flux.

F. Russel, P. Willems, W. Koopman, 2015, Biophysical journal.

Quantitative Glucose and ATP Sensing in Mammalian Cells

J. Smeitink, R. Brock, P. Willems, 2011, Pharmaceutical Research.

Mitochondrial hyperpolarization during chronic complex I inhibition is sustained by low activity of complex II, III, IV and V.

J. Smeitink, Aleksandra Wojtala, M. Wieckowski, 2014, Biochimica et biophysica acta.

Mitochondrial dysfunction in primary human fibroblasts triggers an adaptive cell survival program that requires AMPK-α.

B. Viollet, R. Rodenburg, J. Fransen, 2015, Biochimica et biophysica acta.