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“me53 is an immediate-early/late gene found in all lepidopteran baculoviruses sequenced to date. Deletion of me53 results in a greater-than-1,000-fold reduction in budded-virus production in tissue culture (J. de Jong, B. M. Arif, D. A. Theilmann, and P. J. Krell, see more J. Virol. 83: 7440-7448, 2009). We investigated the localization of ME53 using an ME53 construct fused to green fluorescent protein (GFP). ME53: GFP adopted a primarily cytoplasmic distribution at early times postinfection and a primarily nuclear distribution at late times postinfection. Additionally, at late times ME53: GFP formed distinct

foci at the cell periphery. These foci colocalized with the major envelope fusion protein GP64 and frequently with VP39 capsid protein, suggesting that these cell membrane regions may represent viral budding sites. Deletion of vp39 did not influence the distribution of ME53: GFP; find more however, deletion of gp64 abolished ME53: GFP foci at the cell periphery, implying an association between ME53 and GP64. Despite the association

of ME53 and GP64, ME53 fractionated with the nucleocapsid only after budded-virus fractionation. Together these findings suggest that ME53 may be providing a scaffold that bridges the viral envelope and nucleocapsid.”
“Rationale A number of human and animal studies implicate GSK3 in the pathophysiology and genetics of schizophrenia. In general, the data suggest that phosphorylation levels of GSK3 beta are reduced in schizophrenia, resulting in increased GSK3 beta activity. Since selleck inhibitor GSK3 beta regulation is altered in schizophrenia, polymorphic variation in this gene may affect susceptibility to schizophrenia or treatment response.

Objective To analyze GSK3 beta genetic variants for association with schizophrenia and clozapine response.

Materials and methods We examined GSK3 beta markers in 185 matched case-control subjects, 85 small nuclear families, and 150 schizophrenia patients treated with clozapine for 6 months.

Results Three markers (rs7624540, rs4072520, and rs6779828) showed genotypic association with schizophrenia in the case-control

sample. We did not observe any family and clozapine response association with a specific allele, genotype, or haplotype.

Conclusions Our results suggest that GSK3 beta polymorphisms might be involved in schizophrenia risk but do not appear to play a significant role in clozapine response.”
“Antiplatelet therapies form the cornerstone of atherothrombosis prevention, reducing the morbidity and mortality associated with cardiovascular disease. Despite these benefits, there is still an unmet need for more effective and safer pharmacological agents. To expedite this process, biological platforms that better reflect the intravascular environment in humans will be required in order to shorten drug development time, enable better determination of dosing regimes, and aid in the design of clinical studies.