Research tools are urgently needed to elucidate the specificities of NMO and MS due to their clinical similarity at the early stage of the diseases. Herein, using high-field-strength MRI we characterized the optic nerve and spinal cord lesions in 2D2(tg) mice (MOG 35-55 specific TCR). Specifically, early Blood-brain Barrier breakdown was observed in 86% of the 2D2(tg) mice, while the majority of mice showed little to no brain lesions.
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January 2012
Although the mechanisms that regulate CYP4F genes have been and are currently being studied in a number of laboratories, the specific mechanisms for the regulation of these genes are not yet fully understood. This study shows that nuclear factor κB of the light-chain-enhancer in activated B cells (NF-κB) can inhibit CYP4F11 expression in human liver carcinoma cell line (HepG2) as summarized below. Tumor necrosis factor-α (TNF-α), a proinflammatory cytokine, has been shown to activate NF-κB signaling while also activating the c-Jun NH(2)-terminal kinase (JNK) signaling pathway.
View Article and Find Full Text PDFMechanisms regulating CYP4F genes remain under investigation, although characterization of CYP4F regulatory modalities would facilitate the discovery of new drug targets. This present study shows that all-trans- and 9-cis-retinoic acids can inhibit CYP4F11 expression in human keratinocyte-derived HaCaT cells. Transrepression of many genes by retinoic acids is mediated by interactions between retinoid receptors and the activator protein 1 (AP-1) complex.
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