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Martine I. Darville

Researcher at Université libre de Bruxelles

Publications -  21
Citations -  1953

Martine I. Darville is an academic researcher from Université libre de Bruxelles. The author has contributed to research in topics: Transcription factor & Nitric oxide synthase. The author has an hindex of 20, co-authored 21 publications receiving 1894 citations. Previous affiliations of Martine I. Darville include Vrije Universiteit Brussel & VU University Amsterdam.

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Inhibition of cytokine-induced NF-kappaB activation by adenovirus-mediated expression of a NF-kappaB super-repressor prevents beta-cell apoptosis.

TL;DR: NF-kappaB activation, under in vitro conditions, has primarily a pro-apoptotic function in beta-cells, and beta-cell survival after IL-1beta + IFN-gamma treatment was significantly improved by IkappaB((SA)2) expression, mostly through inhibition of the apoptotic pathway.
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Activation of signal transducer and activator of transcription 3 protects cardiomyocytes from hypoxia/reoxygenation-induced oxidative stress through the upregulation of manganese superoxide dismutase.

TL;DR: The activation of STAT3 induces a protective effect on H/R-induced cardiomyocyte damage, mainly by inducting MnSOD, and the STAT3-mediated signal is proposed as a therapeutical target of ROS-inducedCardiomyocytes injury.
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Discovery of Gene Networks Regulating Cytokine-Induced Dysfunction and Apoptosis in Insulin-Producing INS-1 Cells

TL;DR: Changes in the expression of genes related to metabolism, signal transduction, and transcription factors at all time points studied indicate beta-cell attempts to adapt to the effects of continuous cytokine exposure and the role of NO for these modifications in gene expression is revealed.
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Regulation by cytokines of the inducible nitric oxide synthase promoter in insulin-producing cells

TL;DR: Investigation of the effects of cytokines on iNOS transcriptional regulation in both rat insulin-producing RINm5F cells and in primary FACS-purified rat beta cells unveiled the nature of the promoter binding sites necessary for iN OS expression in rodent beta cells.
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beta-cell apoptosis and defense mechanisms: lessons from type 1 diabetes.

TL;DR: Some of the cytokine-modified genes that may contribute to beta-cell survival or death are discussed, and it is suggested that the necrotic component in rodent islets is due to NO-induced mitochondrial impairment and consequent decreased ATP production, and human islets can complete the apoptotic program after the death signal delivered by cytokines.