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Cyclooxygenase inhibitors regulate the expression of a TGF-beta superfamily member that has proapoptotic and antitumorigenic activities.
TLDR
The increased NAG-1 expression by NSAIDs provides a suitable explanation for COX-independent apoptotic effects of NSAIDs in cultured cells, and its regulation by COX inhibitors may provide new clues for explaining their proapoptotic and antitumorigenic activities. Expand
High levels of GDF15 in thalassemia suppress expression of the iron regulatory protein hepcidin
TLDR
It is suggested that GDF15 overexpression arising from an expanded erythroid compartment contributes to iron overload in thalassemia syndromes by inhibiting hepcidin expression. Expand
The horseradish peroxidase-catalyzed oxidation of 3,5,3',5'-tetramethylbenzidine. Free radical and charge-transfer complex intermediates.
TLDR
A theoretical analysis of the oxidation of 3,5,3',5'-tetramethylbenzidine is presented, including a determination of the extinction coefficients and equilibrium constant for the nonradical species. Expand
Role of reactive oxygen species in LPS‐induced production of prostaglandin E2 in microglia
TLDR
Results suggest that ROS play a regulatory role in the expression of COX‐2 and the subsequent production of PGE2 during the activation process of microglia and suggest a potential therapeutic intervention strategy for the treatment of inflammation‐mediated neurodegenerative diseases. Expand
The diverse roles of nonsteroidal anti-inflammatory drug activated gene (NAG-1/GDF15) in cancer.
TLDR
Laboratory and clinical evidence suggest that NAG-1, like other TGF-β family members, may have different or pleiotropic functions in the early and late stages of carcinogenesis and may serve as a potential biomarker for the diagnosis and prognosis of cancer. Expand
Prostaglandin H synthase and xenobiotic oxidation.
TLDR
In vivo investigations support the importance of the peroxidase and peroxyl radical systems in both activation and detoxification of chemicals in extrahepatic tissues. Expand
Cyclooxygenase Inhibitors Induce the Expression of the Tumor Suppressor Gene EGR-1, Which Results in the Up-Regulation of NAG-1, an Antitumorigenic Protein
TLDR
NSAIDs induce the expression of EGR-1, a tumor suppressor gene, providing a novel mechanism to explain, in part, the antitumorigenic properties of some NSAIDs. Expand
Resveratrol enhances the expression of non-steroidal anti-inflammatory drug-activated gene (NAG-1) by increasing the expression of p53.
TLDR
It is demonstrated that resveratrol induces NAG-1 expression and apoptosis in a concentration-dependent manner, and it is shown that the p53 binding sites within the promoter region of NAG, a member of the transforming growth factor-beta (TGF-beta) superfamily, play a pivotal role to control NAG -1 expression by resver atrol. Expand
Expression of NAG-1, a Transforming Growth Factor-β Superfamily Member, by Troglitazone Requires the Early Growth Response Gene EGR-1*
TLDR
The results suggest that EGR-1 induction is a unique property ofTGZ, but is independent of PPARγ activation, and the up-regulation of NAG-1 may provide a novel explanation for the antitumorigenic property of TGZ. Expand
Activation of mitogen-activated protein kinases by arachidonic acid and its metabolites in vascular smooth muscle cells.
TLDR
The results suggest that 15-HETE, a 15-lipoxygenase product of arachidonic acid, at least in part, mediates the arachidsonic acid effect on MAP kinases; and protein kinase C appears to be important in arachIDonic acid activation of MAP kin enzymes in VSMC. Expand
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