When purified from persistent infections, the genomes of most human polyomaviruses contain single enhancers. However, when isolated from productively infected cells from immunocompromised individuals, the genomes of several polyomaviruses contain duplicated enhancers that promote a number of polyoma-based diseases. The mechanism(s) that gives rise to the duplicated enhancers in the polyomaviruses is, however, not known.
View Article and Find Full Text PDFThe present treatment of childhood T-cell leukemias involves the systemic administration of prokaryotic L-asparaginase (ASNase), which depletes plasma Asparagine (Asn) and inhibits protein synthesis. The mechanism of therapeutic action of ASNase is poorly understood, as are the etiologies of the side-effects incurred by treatment. Protein expression from genes bearing Asn homopolymeric coding regions (N-hCR) may be particularly susceptible to Asn level fluctuation.
View Article and Find Full Text PDFThe STAT6 (signal transducer and activator of transcription 6) protein facilitates T-helper cell 2 (Th2) mediated responses that control IgE-mediated atopic diseases such as asthma. We have identified compounds that bind to STAT6 and inhibit STAT6 tyrosine phosphorylation induced by IL-4. In the bronchial epithelial cell line BEAS-2B, compound (R)-84 inhibits the secretion of eotaxin-3, a chemokine eliciting eosinophil infiltration.
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