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Joy Joseph

Researcher at Medical College of Wisconsin

Publications -  136
Citations -  15240

Joy Joseph is an academic researcher from Medical College of Wisconsin. The author has contributed to research in topics: Oxidative stress & Apoptosis. The author has an hindex of 61, co-authored 136 publications receiving 13748 citations.

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Mitochondrial metabolism and ROS generation are essential for Kras-mediated tumorigenicity

TL;DR: It is reported that the major function of glucose metabolism for Kras-induced anchorage-independent growth, a hallmark of transformed cells, is to support the pentose phosphate pathway.
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Mitochondria-Targeted Triphenylphosphonium-Based Compounds: Syntheses, Mechanisms of Action, and Therapeutic and Diagnostic Applications

TL;DR: The physicochemical basis for mitochondrial accumulation of lipophilic cations, synthetic chemistry strategies to target compounds to mitochondria, mitochondrial probes, and sensors, and examples of mitochondrial targeting of bioactive compounds are described.
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Superoxide reacts with hydroethidine but forms a fluorescent product that is distinctly different from ethidium: potential implications in intracellular fluorescence detection of superoxide.

TL;DR: It is shown that superoxide generated in several enzymatic or chemical systems oxidizes HE to a fluorescent product that is totally different from ethidium, which could have implications in intracellular detection and imaging of superoxide.
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Doxorubicin induces apoptosis in normal and tumor cells via distinctly different mechanisms. intermediacy of H(2)O(2)- and p53-dependent pathways.

TL;DR: A newly discovered mechanistic difference in DOX-induced apoptotic cell death in normal versus tumor cells will be useful in developing drugs that selectively mitigate the toxic side effects of DOX without affecting its antitumor action.
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Mitochondrial Complex III ROS Regulate Adipocyte Differentiation

TL;DR: It is reported that primary human mesenchymal stem cells undergoing differentiation into adipocytes display an early increase in mitochondrial metabolism, biogenesis, and reactive oxygen species (ROS) generation, and this increase was dependent on mTORC1 signaling.