Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.5.2 (NQO1)
 6,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Doublecortin-immunoreactive (DCX+) cells were detected across the allo- and neo-cortical regions in the adult guinea pig cerebrum, localized to layer II specifically at its border with layer I. The density of labeled cells declined with age, whereas no apparent apoptotic activity was detectable over the cortex including layer II. DCX+ cells varied in somal size, labeling intensity, nuclear appearance, and complexity of processes. These cells were often arranged in clusters with cells of similar morphology sometimes packed tightly together. They exhibited complete colocalization with polysialylated neural cell adhesion molecule (PSA-NCAM) and neuron-specific type III beta-tubulin (TuJ1). Medium to large-sized DCX+ cells had well-developed neuritic processes, and expressed neuron-specific nuclear protein (NeuN). Large mature-looking cells with weak DCX reactivity invariably displayed heavy NeuN reactivity, implicating a transitional stage of these labeled cells. These "transitional" cells also consistently exhibited weak reactivity for gamma-aminobutyric acid (GABA), glutamate decarboxylase (GAD67), beta-nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) and neuronal nitric oxide synthase (nNOS), suggestive of them being young GABAergic/nitrinergic interneurons. Our data indicate that DCX+ cells exist widely in the adult guinea pig cerebral cortex, with a predominant localization in upper layer II. The morphological variation and differential expression of neuronal markers in these cells implicate that they might be developing neurons, and that they are probably differentiating into GABAergic interneurons. This population of cells might be involved in interneuron plasticity in the adult mammalian cerebral cortex.
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PMID:Doublecortin-expressing cells are present in layer II across the adult guinea pig cerebral cortex: partial colocalization with mature interneuron markers. 1837 31

In previous studies, we observed that cells treated with aminochrome obtained by oxidizing dopamine with oxidizing agents dramatically changed cell morphology, thus posing the question if such morphological changes were dependent on aminochrome or the oxidizing agents used to produce aminochrome. Therefore, to answer this question, we have now purified aminochrome on a CM-Sepharose 50-100 column and, using NMR studies, we have confirmed that the resulting aminochrome was pure and that it retained its structure. Fluorescence microscopy with calcein-AM and transmission electron microscopy showed that RCSN-3 cells presented an elongated shape that did not change when the cells were incubated with 50 muM aminochrome or 100 muM dicoumarol, an inhibitor of DT-diaphorase. However, the cell were reduced in size and the elongated shape become spherical when the cells where incubated with 50 muM aminochrome in the presence of 100 muM dicoumarol. Under these conditions, actin, alpha-, and beta-tubulin cytoskeleton filament networks became condensed around the cell membrane. Actin aggregates were also observed in cells processes that connected the cells in culture. These results suggest that aminochrome one-electron metabolism induces the disruption of the normal morphology of actin, alpha-, and beta-tubulin in the cytoskeleton, and that DT-diaphorase prevents these effects.
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PMID:Aminochrome induces disruption of actin, alpha-, and beta-tubulin cytoskeleton networks in substantia-nigra-derived cell line. 2008 99

Pregestational diabetes mellitus (PGDM) enhances the risk of fetal neurodevelopmental defects. However, the mechanism of hyperglycaemia-induced neurodevelopmental defects is not fully understood. In this study, several typical neurodevelopmental defects were identified in the streptozotocin-induced diabetes mouse model. The neuron-specific class III beta-tubulin/forkhead box P1-labelled neuronal differentiation was suppressed and glial fibrillary acidic protein-labelled glial cell lineage differentiation was slightly promoted in pregestational diabetes mellitus (PGDM) mice. Various concentrations of glucose did not change the U87 cell viability, but glial cell line-derived neurotrophic factor expression was altered with varying glucose concentrations. Mouse maternal hyperglycaemia significantly increased Tunel(+) apoptosis but did not dramatically affect PCNA(+) cell proliferation in the process. To determine the cause of increased apoptosis, we determined the SOD activity, the expression of Nrf2 as well as its downstream anti-oxidative factors NQO1 and HO1, and found that all of them significantly increased in PGDM fetal brains compared with controls. However, Nrf2 expression in U87 cells was not significantly changed by different glucose concentrations. In mouse telencephalon, we observed the co-localization of Tuj-1 and Nrf2 expression in neurons, and down-regulating of Nrf2 in SH-SY5Y cells altered the viability of SH-SY5Y cells exposed to high glucose concentrations. Taken together, the data suggest that Nrf2-modulated antioxidant stress plays a crucial role in maternal hyperglycaemia-induced neurodevelopmental defects.
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PMID:Effects of oxidative stress on hyperglycaemia-induced brain malformations in a diabetes mouse model. 2749 68