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The highly conserved coadapters CREB binding protein (CBP) and p300 form complexes with CREB as well as other DNA binding transcription factors to modulate chromatin remodeling and thus transcription. Human T-lymphotropic virus type 1 (HTLV-1) transcription is controlled, in part, by the CREB/ATF family of transcription factors which bind promoter sequences(More)
One of the early events in O2 chemoreception is inhibition of O2-sensitive K+ (KO2) channels. Characterization of the molecular composition of the native KO2 channels in chemosensitive cells is important to understand the mechanism(s) that couple O2 to the KO2 channels. The rat phaeochromocytoma PC12 clonal cell line expresses an O2-sensitive(More)
Human T-lymphotropic virus type 1 (HTLV-1) is a complex retrovirus encoding regulatory and accessory genes in four open reading frames (ORF I to IV) of the pX region. Emerging evidence indicates an important role for the pX ORF I-encoded accessory protein p12(I) in viral replication, but its contribution to viral pathogenesis remains to be defined. p12(I)(More)
Human T-lymphotropic virus type 1 (HTLV-1), a complex retrovirus, causes adult T-cell lymphoma/leukemia and is linked to a variety of immune-mediated disorders. The roles of proteins encoded in the pX open reading frame (ORF) II gene region in HTLV-1 replication or in mediating virus-associated diseases remain to be defined. A nucleus-localizing 30-kDa(More)
Human T lymphotropic virus type 1 (HTLV-1) is a complex retrovirus containing regulatory and accessory genes encoded in four open reading frames (ORF I-IV) of the pX region. It is not clear what role pX ORFs I and II-encoded proteins have in the pathogenesis of the lymphoproliferative diseases associated with HTLV-1 infection. The conserved ORF I encodes(More)
Animal research has shown that reinforcement is substantially less effective when it is delayed, but in studies of human motor learning delays in providing feedback typically have much less effect. One possible explanation is that in human research participants know the response to be learned and can thus focus on it during the delay; that is not the case(More)
failure of antigen production is more likely to be due to genetic change associated with incomplete penetrance than to genetic loss. An alternative or additional possibility cannot, however, be excluded-that exuberant cell division causes dilution of a particulate cytoplasmic factor responsible for the formation of the antigen. Loss of organ-specific(More)
Human hypercalcemia-inducing renal tumors have been established as xenografts in nude mice and nude rats. Animals bearing these tumors became cachexic and hypercalcemic and these changes could be reversed by excision of xenograft tumors. Metabolic studies carried out in nude rats suggested that the hypercalcemia-inducing factor was effecting renal excretion(More)
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