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Jeffrey M. Peters

Researcher at Pennsylvania State University

Publications -  217
Citations -  21665

Jeffrey M. Peters is an academic researcher from Pennsylvania State University. The author has contributed to research in topics: Peroxisome proliferator-activated receptor & Receptor. The author has an hindex of 74, co-authored 214 publications receiving 20405 citations. Previous affiliations of Jeffrey M. Peters include Lawrence Livermore National Laboratory & National Institutes of Health.

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Targeted disruption of peroxisomal proliferator-activated receptor β (δ) results in distinct gender differences in mouse brain phospholipid and esterified FA levels

TL;DR: The data suggest that PPARβ is involved in maintaining FA and phospholipid levels in adult female mouse brain and provide strong evidence that suggests a role for PPAR β in brain peroxisomal acyl-CoA utilization.
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Peroxisome proliferator-activated receptors (PPAR) and the mitochondrial aldehyde dehydrogenase (ALDH2) promoter in vitro and in vivo

TL;DR: Data indicate that ALDH2 is not part of the battery of lipid metabolizing enzymes and proteins regulated by PPARalpha, and in vitro translated PPARs bound the ALDH NRRE with high affinity.
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Targeting Peroxisome Proliferator-Activated Receptor-β/δ (PPARβ/δ) for Cancer Chemoprevention

TL;DR: Whether PPARβ/δ is suitable to target with natural and/or synthetic agonists or antagonists for cancer chemoprevention is hindered because of the uncertainty in the mechanism of action and role in carcinogenesis.
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Ligand activation of peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) inhibits cell growth in a mouse mammary gland cancer cell line

TL;DR: Results from this study show that proliferation of the C20 mouse mammary gland cancer cell line is inhibited by ligand activation of PPARbeta/delta due in part to increased apoptosis.
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Peroxisome proliferator‐activated receptor‐β/δ inhibits human neuroblastoma cell tumorigenesis by inducing p53‐ and SOX2‐mediated cell differentiation

TL;DR: Observations demonstrate that activating or over‐expressing PPARβ/δ induces cell differentiation through p53‐ and SOX2‐dependent signaling pathways in neuroblastoma cells and tumors and suggests that combinatorial activation of both RARα and PPARα may be suitable as an alternative therapeutic approach for RA‐resistant neuroblastomas patients.