Molecular motors

By M. Schliwa, G. Woehlke. 2003

8,134 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Computational Biology & Bioinformatics

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Citations in the corpus

Molecular Docking and Structure-Based Drug Design Strategies (2015, background): “Human aldose reductase (ALR2) is a NADPH-dependent oxidoreductase that catalyzes the reduction of glucose to sorbitol [217].”
New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis (2018, background): “Large amounts of ROS are generated during AGEs formation [7], and oxidized AGEs activate receptor for AGEs (RAGE) to stimulate NADPH oxidase-1, which contribute to ROS production in diabetes [28].”
Diabetes and mitochondrial function: role of hyperglycemia and oxidative stress. (2006, background): “Hyperglycemia resulting from uncontrolled glucose regulation is widely recognized as the causal link between diabetes and diabetic complications (Giardino et al., 1996; Brownlee, 2001).”
Diabetic Nephropathy: Mechanisms of Renal Disease Progression (2008, background): “Rotenone, an inhibitor of electron transport, blocks the DCFsensitive ROS generation, and the fact that a similar effect is observed by overexpression of mitochondrial MnSOD or uncoupling protein-1 (UCP-1) supports this notion (5, 32).”
Diabetic neuropathy: mechanisms to management. (2008, background): “4, when excess glucose is shunted through alternative metabolic pathways such as the fructose-6-phosphate or diacylglycerol, the signaling intermediates and modified transcription factors lead to increases in TGFβ and NFκB (Brownlee, 2001).”
Diabetes associated cell stress and dysfunction: role of mitochondrial and non‐mitochondrial ROS production and activity (2007, background): “The increase of O2− production in pancreatic β-cells in response to elevated glucose metabolism may result in activation of NADPH oxidase via increased lipid derived signalling molecules, such as DAG, and subsequent activation of PKC as described above (Morgan et al. 2007).”
Postprandial hyperglycemia and diabetes complications: is it time to treat? (2005, background): “Recent studies demonstrate that hyperglycemia induces an overproduction of superoxide by the mitochondrial electron-transport chain (58).”
Increased oxidative stress in obesity: implications for metabolic syndrome, diabetes, hypertension, dyslipidemia, atherosclerosis, and cancer. (2013, background): “[54] Brownlee M.”
T cell lipid peroxidation induces ferroptosis and prevents immunity to infection (2015, background): “, 1995), type 2 diabetes (Brownlee, 2001), atherosclerosis (Galkina and Ley, 2009), and neurodegeneration (Lin and Beal, 2006).”