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Henry Jay Forman

Researcher at University of Southern California

Publications -  314
Citations -  27464

Henry Jay Forman is an academic researcher from University of Southern California. The author has contributed to research in topics: Glutathione & Oxidative stress. The author has an hindex of 73, co-authored 307 publications receiving 24061 citations. Previous affiliations of Henry Jay Forman include University of Alabama at Birmingham & University of Kansas.

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Glutathione: overview of its protective roles, measurement, and biosynthesis.

TL;DR: The purpose here is to provide a brief overview of some of the important aspects of glutathione metabolism as part of this special issue that will provide a more comprehensive review of the state of knowledge regarding this essential molecule.
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Measuring reactive oxygen and nitrogen species with fluorescent probes: challenges and limitations.

TL;DR: A critical analysis of the challenges and limitations of the most widely used fluorescent probes for detecting and measuring reactive oxygen and nitrogen species and proposed guidelines that will help present and future researchers with regard to the optimal use of selected fluorescent probes and interpretation of results are presented.
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Oxidants as stimulators of signal transduction

TL;DR: Reactive oxygen species may be second messengers for transcription factor activation, apoptosis, bone resorption, cell growth, and chemotaxis as well as the mechanisms of the oxidant-stimulation of signal transduction are discussed.
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Reactive oxygen species and cell signaling: respiratory burst in macrophage signaling.

TL;DR: One of the subunits of the phagocyte NAD PH oxidase is now recognized as a member of a family of NADPH oxidases, or NOX, present in cells other than phagocytes, present at the plasma membrane from resident plasma membrane and cytosolic protein components.
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Cellular glutathione and thiols metabolism.

TL;DR: It is the aim that this commentary will lead the reader to appreciate that studies investigating the signaling for and regulation of thiol metabolism must never be generalized, and that perturbations in any of step ofThioredoxin and glutathione metabolism may have etiological roles in genetically, virally, and environmentally borne pathologies.