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ChREBP regulates fructose-induced glucose production independently of insulin signaling.
Obese, insulin-resistant states are characterized by a paradoxical pathogenic condition in which the liver appears to be selectively insulin resistant. Specifically, insulin fails to suppress glucoseExpand
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Intestinal, but not hepatic, ChREBP is required for fructose tolerance.
Increased sugar consumption is a risk factor for the metabolic syndrome including obesity, hypertriglyceridemia, insulin resistance, diabetes, and nonalcoholic fatty liver disease (NAFLD).Expand
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Activating Autophagy as a Therapeutic Strategy for Parkinson’s Disease
Parkinson’s disease is a progressive neurodegenerative disease characterized by Lewy body pathology of which the primary constituent is aggregated misfolded alpha-synuclein protein. Currently, thereExpand
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Beta-adrenergic receptors are critical for weight loss but not for other metabolic adaptations to the consumption of a ketogenic diet in male mice
Objective We have previously shown that the consumption of a low-carbohydrate ketogenic diet (KD) by mice leads to a distinct physiologic state associated with weight loss, increased metabolic rate,Expand
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Pharmacokinetics and pharmacodynamics of a single dose Nilotinib in individuals with Parkinson's disease
Nilotinib is a broad‐based tyrosine kinase inhibitor with the highest affinity to inhibit Abelson (c‐Abl) and discoidin domain receptors (DDR1/2). Preclinical evidence indicates that NilotinibExpand
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Multikinase Abl/DDR/Src Inhibition Produces Optimal Effects for Tyrosine Kinase Inhibition in Neurodegeneration
Background and objectivesInhibition of Abelson (Abl) tyrosine kinase as a therapeutic target has been gaining attention in neurodegeneration. Post-mortem Alzheimer’s and Parkinson’s disease brainsExpand
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Discoidin Domain Receptor 1 is a therapeutic target for neurodegenerative diseases.
The role of Discoidin Domain Receptors (DDRs) is poorly understood in neurodegeneration. DDRs are upregulated in Alzheimer's and Parkinson's disease, and DDRs knockdown reduces neurotoxic proteinExpand
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Author’s Reply to Segura-Aguilar: Autophagosome maturation not autophagy induction is impaired in neurodegeneration
The letter to the editor by Juan Segura-Aguilar [1] commenting on the manuscript by Fowler and Moussa titled ‘‘Activating autophagy as a therapeutic strategy for Parkinson’s disease’’ [2] isExpand
4564 Nilotinib alters microRNAs that regulate specific autophagy and ubiquitination genes in the cerebrospinal fluid of Parkinson’s patients
OBJECTIVES/GOALS: Our preclinical data demonstrate that the principal effects of nilotinib, a multi-tyrosine kinase inhibitor, in models of neurodegeneration is clearance of misfolded proteins viaExpand