These results indicate that kinesthesia is the product of cooperative integration processes in which the final percept strongly depends on the experimental conditions as well as sensorial preferences. The observed changes in the relative contribution of each input across experimental conditions likely reflect reliability-dependent weights. (c) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.”
“The human T-cell leukemia virus type 1 (HTLV-1)

Tax oncoprotein actively shuttles between buy GSK621 the nucleus, where it interacts with transcriptional and splicing regulatory proteins, and the cytoplasm, where it activates NF-kappa B. Posttranslational modifications of Tax such as ubiquitination regulate its subcellular localization and hence its function; however, the regulation of Tax trafficking and NF-kappa B activation by host factors is poorly understood. By screening a deubiquitinating (DUB) enzyme small interfering RNA (siRNA) library, we identified the metalloprotease

STAM-binding protein-like 1 (STAMBPL1) as a positive regulator of Tax-mediated NF-kappa B activation. Overexpression of wild-type STAMBPL1, but not a catalytically inactive mutant, enhanced Tax-mediated NF-kappa B activation, whereas silencing of STAMBPL1 with siRNA impaired Tax activation of both the canonical and non-canonical NF-kappa B signaling pathways. STAMBPL1 regulated Tax-induced NF-kappa B signaling indirectly by controlling Tax nuclear/cytoplasmic transport and was required for DNA damage-induced Tax nuclear export. Together, these results reveal that the deubiquitinase Cediranib (AZD2171) www.selleckchem.com/products/ipi-549.html STAMBPL1 is a key regulator of Tax trafficking and function.”
“The half-a-tetratricopeptide (HAT) repeat motif is of interest because it is found exclusively in proteins that are involved in RNA metabolism. Little is known about structure-function relationships in this class of repeat motif. Here, we present the results of a combined bioinformatics, modeling and mutagenesis study of the HAT domain of Utp6. We have derived

a new HAT consensus, delineated its structure-defining residues and, by homology modeling, have placed these residues in a structural context. By considering only HAT motifs from Utp6 proteins, we identified residues that are shared by, and unique to, only this subset of HAT motifs, suggesting a key functional role. Employing both random and directed mutagenesis of the HAT domain in yeast Utp6, we have identified residues whose mutation results in loss of function. By examining these residues in the context of the homology model, we have delineated those that act by perturbing structure and those that more likely have a direct effect on function. Importantly, the residues we predict to have a direct effect on function map together on the tertiary structure, thus defining a potential functional interaction surface.