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Expression of Kaposi's sarcoma-associated herpesvirus (KSHV) lytic genes is thought to be essential for the establishment and progression of KSHV-induced diseases. The inefficiency of lytic reactivation in various in vitro systems hampers the study of lytic genes in the context of whole virus. We
The long terminal repeat (LTR) of Moloney murine sarcoma virus (Mo-MuSV) was used as a model system to study the stress response of mammalian cells to physical carcinogens. The chloramphenicol acetyltransferase (CAT) gene was inserted between two Mo-MuSV LTRs, and the LTR-CAT-LTR construct was used
It has been suggested that the initiation step in mouse skin carcinogenesis involves an alteration in epidermal-differentiation, as mouse basal keratinocytes exposed to initiators resist the arrest of cell growth that is normally associated with the induction of terminal differentiation by calcium
Murine sarcoma cell line (L-1) treated with promoting phorbol ester (TPA) showed decreased content and activity of protein kinase C (PKC) as measured by Western blotting and histone phosphorylation methods. The PKC depleted line (L-1R) produced bigger, tumors after s.c. transplantation into
Protein kinase capable of phosphorylating 40S ribosomal protein S6 on serine residues has been detected in chicken embryo fibroblasts. This activity appears to be regulated in direct response to expression of pp60v-src in chicken embryo fibroblasts infected with a temperature-sensitive
The inoculation of Rous sarcoma virus (RSV) into chickens results in the induction of tumors which usually grow progressively for several weeks and then regress. We have found that the direct injection of phorbol myristate acetate into growing RSV-induced sarcomas resulted in accelerated tumor
Tumor cells which are cultured from the regressor phase of avian sarcoma virus (ASV)-induced tumor growth are deficient with respect to ability to produce progeny transforming virus. In addition, such cells are relatively unreactive with anti-viral antibody and are unable to elaborate, into the
Avian sarcoma virus-induced tumors usually grow progressively for several weeks and then regress. We have injected phorbol myristate acetate (PMA) directly into tumors in an effort to stimulate neoplastic growth. The results show instead that PMA exerted an inhibitory effect in this regard and, in
The addition of phorbol 12-myristate 13-acetate (PMA), a potent tumor promoter, to serum-starved quiescent chicken embryo fibroblasts (CEF) or C127 murine cells resulted in increased phosphorylation of 40S ribosomal protein S6. The effect of PMA on S6 phosphorylation in quiescent CEF was
Kaposi's sarcoma-associated herpesvirus (KSHV) establishes latent infections in lymphocytes and endothelial cells, and latent infection is closely linked to tumorigenesis. As few viral markers are expressed during latency, compounds that can safely and efficiently increase lytic gene expression in
BACKGROUND
Iatrogenic immunosuppressed patients are at increased risk for development of various cancers that comprise Kaposi's sarcoma (KS).
METHODS
To investigate the direct impact of immunosuppressive agents on Kaposi's sarcoma-associated herpesvirus (KSHV) and KS development, we quantified the
Kaposi sarcoma-associated herpesvirus (KSHV) is associated with KS, primary effusion lymphoma (PEL), and multicentric Castleman disease. Reactivation of KSHV in latently infected cells and subsequent plasma viremia occur before the development of KS. Intracellular signaling pathways involved in KSHV
Epidemiological studies strongly suggest that a newly discovered herpesvirus, Kaposi's sarcoma associated-herpesvirus (KSHV/HHV8), is the likely infectious cause of Kaposi's sarcoma (KS). Identification of this agent suggests the possibility that existing anti-herpesvirus chemotherapeutics have
Alterations in patterns of protein phosphorylation after exposure to phorbol esters were compared in chicken embryo fibroblasts and KD cells (a human fibroblast line) by two-dimensional gel electrophoresis. A substantial increase in phosphorylation was observed of a major, markedly acidic protein of
The effects of the tumor promotor, 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA), on the intra- and extracellular distribution of transferrin receptors and rates of iron uptake were studied in normal developing myogenic cells and myogenic cells transformed with a temperature-sensitive