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High-probability grants
According to our matching algorithm, Thurl E. Harris is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2014 — 2018 |
Harris, Thurl E. |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Role of Oxidized Neutral Lipids in Adipocyte Function
Project Summary/Abstract Obesity is now a pandemic that will have significant impact on our current health care system. A common theme in obese individuals that progress towards diabetes is insulin resistance. A critical question in the field asks how obesity impairs insulin sensitivity as a first step in progression to type 2 diabetes mellitus. The mammalian Target of Rapamycin Complexes (mTORC1) and 2 are multisubunit kinase complexes responsible for integrating multiple aspects of nutrient and growth factor signaling to regulate cellular anabolic processes such as cell growth, and translation. We have found that during catecholamine-induced lipolysis in fat cells the mTOR complexes are dissociated and thereby inhibited. While investigating the mechanism by which this occurs we made the novel discovery of a new class of oxidized neutral lipids that are responsible. While oxidized phospholipids have been implicated as component of lipoproteins responsible for initiating cardiovascular disease, our findings suggest that oxidized neutral lipids may analogously be responsible for adipocyte dysfunction. Completion of these aims will: 1.) define oxidized neutral lipids as novel inputs regulating mTOR complex activity, 2.) discover new strategies for inhibiting both mTOR complexes, 3.) describe the mechanism whereby catecholamines inhibit glucose uptake by adipocytes.
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1 |
2020 — 2021 |
Harris, Thurl E. |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Regulation of Lipin Phosphatidic Acid Phosphatase Activity
Project Summary/Abstract It has been more than 50 years since Eugene Kennedy described/identified phosphatidic acid phosphatase (PAP) activity. This enzymatic activity unified what is now known as the Kennedy pathway of phosphatidylcholine synthesis. The genes encoding PAP, termed Lipin 1-3, sit at an important branch point in the Kennedy pathway of glycerolipid synthesis. Unlike the remainder of the enzymes in the triacylglycerol synthesis pathway, the lipins are cytosolic proteins that translocate from the cytosol to their site of action at internal membranes. Loss of function alleles of lipin family members results in profound metabolic and inflammatory disturbances in both mice and humans, and lipin polymorphisms are linked to a number of metabolic conditions. But while genetics has demonstrated the importance of these enzymes in health and disease, precisely how they are regulated is still poorly defined. Elucidating the mechanisms and pathways controlling lipin family activity will provide insight into glycerolipid biosynthesis and the pathophysiological consequences when it is disrupted, and will open new avenues for pharmacological interventions for these diseases. This proposal undertakes a rigorous and comprehensive examination of lipin 1 regulation with the goal of understanding how its PAP activity is biochemically controlled. We will characterize the effects of two kinases on lipin 1 PAP activity and stability and identify how these regulatory events occur. In addition, we will determine how dysregulation of lipin PAP activity impacts cellular function, particularly neutral and phospholipid synthesis. Given the striking phenotypes displayed by genetic alterations in the lipins, accomplishing these aims will yield important insights into lipid biosynthetic pathways as well as clinically relevant pathologies.
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1 |