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Michelle S. Johnson

Researcher at University of Alabama at Birmingham

Publications -  62
Citations -  3952

Michelle S. Johnson is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Mitochondrion & Oxidative stress. The author has an hindex of 29, co-authored 56 publications receiving 3277 citations.

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2ME2 inhibits tumor growth and angiogenesis by disrupting microtubules and dysregulating HIF.

TL;DR: These data establish 2ME2 as a small molecule inhibitor of HIF-1 and provide a mechanistic link between the disruption of the MT cytoskeleton and inhibition of angiogenesis.
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A review of the mitochondrial and glycolytic metabolism in human platelets and leukocytes: Implications for their use as bioenergetic biomarkers

TL;DR: How the utilization of glycolysis and oxidative phosphorylation differs in platelets and leukocytes is described and how they can be used in patient populations is discussed.
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Methods for defining distinct bioenergetic profiles in platelets, lymphocytes, monocytes, and neutrophils, and the oxidative burst from human blood

TL;DR: The measurement of cellular bioenergetics in isolated human monocytes, lymphocytes, and platelets, including the oxidative burst from neutrophils and monocytes from individual donors are demonstrated and suggest that selection of cell type from blood cells is critical for assessing bioenergetic dysfunction and redox biology in translational research.
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Prevention of diabetic nephropathy in Ins2(+/)⁻(AkitaJ) mice by the mitochondria-targeted therapy MitoQ.

TL;DR: The hypothesis that mitochondrially targeted therapies may be beneficial in the treatment of diabetic nephropathy is supported and a relatively unexplored aspect of mitochondrial ROS signalling in the control of fibrosis is highlighted.
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Inhibition of autophagy with bafilomycin and chloroquine decreases mitochondrial quality and bioenergetic function in primary neurons

TL;DR: A significant impact of bafilomycin and chloroquine on cellular bioenergetics and metabolism consistent with decreased mitochondrial quality associated with inhibition of autophagy is demonstrated.