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provides coniferyl ferulate(CAS#:41328-75-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
The analysis of DNA methylation at CpG dinucleotides has become a major research focus due to its regulatory role in numerous biological processes, but the requisite need for assays which amplify bisulfite-converted DNA represents a major bottleneck due to the unique design constraints imposed on bisulfite-PCR primers. Moreover, a review of the literature indicated no available software solutions which accommodated both high-throughput primer design, support for multiplex amplification assays, and primer-dimer prediction. In response, the tri-modular software package PrimerSuite was developed to support bisulfite multiplex PCR applications. This software was constructed to (i) design bisulfite primers against multiple regions simultaneously (PrimerSuite), (ii) screen for primer-primer dimerizing artefacts (PrimerDimer), and (iii) support multiplex PCR assays (PrimerPlex). Moreover, a major focus in the development of this software package was the emphasis on extensive empirical validation, and over 1300 unique primer pairs have been successfully designed and screened, with over 94% of them producing amplicons of the expected size, and an average mapping efficiency of 93% when screened using bisulfite multiplex resequencing. The potential use of the software in other bisulfite-based applications such as methylation-specific PCR is under consideration for future updates. This resource is freely available for use at PrimerSuite website (www.primer-suite.com).
PrimerSuite: A High-Throughput Web-Based Primer Design Program for Multiplex Bisulfite PCR
Jennifer Lu,1,2,* Andrew Johnston,1,2,* Philippe Berichon,1,2 Ke-lin Ru,1,2 Darren Korbie,a,1,2,* and Matt Traub,1,2,3
Many important decisions involve outcomes that are either probabilistic or delayed. Based on similarities in decision preferences, models of decision making have postulated that the same psychological processes may underlie decisions involving probabilities (i.e., risky choice) and decisions involving delay (i.e., intertemporal choice). Equivocal behavioral evidence has made this hypothesis difficult to evaluate. However, a combination of functional neuroimaging and behavioral data may allow identification of differences between these forms of decision making. Here, we used functional magnetic resonance imaging (fMRI) to examine brain activation in subjects making a series of choices between pairs of real monetary rewards that differed either in their relative risk or their relative delay. While both sorts of choices evoked activation in brain systems previously implicated in executive control, we observed clear distinctions between these forms of decision making. Notably, choices involving risk evoked greater activation in posterior parietal and lateral prefrontal cortices, whereas choices involving delay evoked greater activation in the posterior cingulate cortex and the striatum. Moreover, activation of regions associated with reward evaluation predicted choices of a more-risky option, whereas activation of control regions predicted choices of more-delayed or less-risky options. These results indicate that there are differences in the patterns of brain activation evoked by risky and intertemporal choices, suggesting that the two domains utilize at least partially distinct sets of cognitive processes.
risk, delay, utility, posterior parietal cortex, intraparietal sulcus, choice
The neural substrates of probabilistic and intertemporal decision making
Bethany J. Weber1 and Scott A. Huettel1,2
2009 Oct 9.
Transforming growth factor-beta (TGF-β) is a pleiotropic cytokine with important effects on processes such as fibrosis, angiogenesis, and immunosupression. Using bioinformatics, we identified SMAD2, one of the mediators of TGF-β signaling, as a predicted target for a microRNA, microRNA-155 (miR-155). MicroRNAs are a class of small non-coding RNAs that have emerged as an important class of gene expression regulators. miR-155 has been found to be involved in the regulation of the immune response in myeloid cells. Here, we provide direct evidence of binding of miR-155 to a predicted binding site and the ability of miR-155 to repress SMAD2 protein expression. We employed a lentivirally transduced monocyte cell line (THP1-155) containing an inducible miR-155 transgene to show that endogenous levels of SMAD2 protein were decreased after sustained overexpression of miR-155. This decrease in SMAD2 led to a reduction in both TGF-β-induced SMAD-2 phosphorylation and SMAD-2-dependent activation of the expression of the CAGA12LUC reporter plasmid. Overexpression of miR-155 altered the cellular responses to TGF-β by changing the expression of a set of genes that is involved in inflammation, fibrosis, and angiogenesis. Our study provides firm evidence of a role for miR-155 in directly repressing SMAD2 expression, and our results demonstrate the relevance of one of the two predicted target sites in SMAD2 3′-UTR. Altogether, our data uncover an important role for miR-155 in modulating the cellular response to TGF-β with possible implications in several human diseases where homeostasis of TGF-β might be altered.
Gene Expression, Immunology, Macrophage, MicroRNA, SMAD Transcription Factor, Transforming Growth Factor β (TGF-β), Angiogenesis, Fibrosis, miR-155
MicroRNA-155 Targets SMAD2 and Modulates the Response of Macrophages to Transforming Growth Factor-β*An external file that holds a picture, illustration, etc. Object name is sbox.jpg
Fethi Louafi,1 Rocio T. Martinez-Nunez, and Tilman Sanchez-Elsner2
2010 Dec 31;