Neuron
ArticleA brain-specific transcription activator
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FosB and ΔFosB expression in brain regions containing differentially susceptible dopamine neurons following acute neurotoxicant exposure
2016, Brain ResearchCitation Excerpt :A bicinchoninic acid assay was used to determine protein concentrations, samples were diluted to equal amounts of protein and used for Western blot analyses. Nuclear extractions were performed based on methods reported by Karunakaran and Ravindranath (2009) and Korner et al. (1989). Mice were killed by decapitation; the brain was removed, placed in cold PBS, and sectioned with a razor blade using a Zivic brain matrix.
A proteomics approach for identification of single strand DNA-binding proteins involved in transcriptional regulation of mouse μ opioid receptor gene
2008, Molecular and Cellular ProteomicsCitation Excerpt :Thus, gene activity must be modulated via sequence-specific enhancer- and/or silencer-binding proteins to produce restricted patterns of expression in the nervous system. Tissue- or cell-specific regulatory factors (24, 41–44) presumably modulate the ability of ubiquitous factors (such as hnRNP K and the αCPs examined in this study or the other unidentified factors) to regulate Oprm1 promoter activity. Our findings may promote a better understanding of the molecular mechanisms underlying Oprm1 expression.
NF-κB functions in the nervous system: From development to disease
2006, Biochemical PharmacologyCitation Excerpt :An additional factor may rely on the κB site sequence itself, which determines the selectivity of the interaction with coactivators [36]. Interactions between NF-κB and cAMP response element binding protein (CBP) [37–39] have indeed been described in neurons, and might explain the reports of κB-binding complexes distinct from bona fide NF-κB family members in grey matter extracts [40], developing cortex [41], cerebellum or primary cell cultures from microglia and neurons [42]. A possible interference between the NF-κB and Sp1 transcription factors nevertheless remains, as regards the binding to subsets of κB sites in neurons [43–45].
Molecular basis underlying the poly C binding protein 1 as a regulator of the proximal promoter of mouse μ-opioid receptor gene
2006, Brain ResearchCitation Excerpt :For example, a shift of hnRNP K from nucleus to cytoplasm altered its function role from a transcription regulator (Michelotti et al., 1996) to a silencer of LOX mRNA translation (Makeyev and Liebhaber, 2002). Finally, to restrict the MOR gene expression to the certain subsets of neuronal cells in the brain, MOR promoter activity must be modulated by tissue/cell-specific factors (Schoenherr and Anderson, 1995; Pecorino et al., 1991; Korner et al., 1989; Solecki et al., 1997; Kovarik et al., 1993; Ogata et al., 1998; Oosterhuis and van der Hoorn, 1999; Kim et al., 2004), which may alter the cooperativity of PCBP domains and therefore modulate the ability of PCBP to regulate the MOR promoter activity. The domain cooperativity of PCBP may further provide a means of fine tuning for control of MOR gene expression in neurons.