phorbol/sarcoma

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Suppression of phorbol myristate acetate-triggering of macrophage H2O2 release by sarcoma 180 originating factor.

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A high molecular weight proteinaceous factor in the cell extract of sarcoma 180 (S-180) was found to inhibit phorbol myristate acetate (PMA)-triggering of macrophage H2O2 release. This factor (S-180 factor) was stable at 56 C for 1 hr and resistant to ultraviolet-irradiation. The S-180 factor

Regulation of a ribosomal protein S6 kinase activity by the Rous sarcoma virus transforming protein, serum, or phorbol ester.

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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

Effect of phorbol ester on growth of tumors induced by Rous sarcoma virus and on pp60src kinase activity in these tumors.

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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

Alteration of phenotype of 'regressor' avian sarcoma cells following treatment with phorbol ester.

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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

Differential effects of phorbol ester on tumor cells induced by avian sarcoma virus.

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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

Increased efficiency of phorbol ester-induced lytic reactivation of Kaposi's sarcoma-associated herpesvirus during S phase.

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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

Induction of transcription from the long terminal repeat of Moloney murine sarcoma provirus by UV-irradiation, x-irradiation, and phorbol ester.

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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

Phorbol myristate induces apoptosis of taxol-resistant sarcoma cells in vitro.

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Taxol was found to induce polyploidization and apoptosis in cultured methylcholanthrene-induced sarcoma cells (Meth-A cells), but some of the cells in G1 phase were not affected. We refer to these cells as taxol-resistant cells. Phorbol 12-myristate 13-acetate (PMA), a protein kinase C (PKC)

Keratinocytes blocked in phorbol ester-responsive early stage of terminal differentiation by sarcoma viruses.

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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

Ultrastructure of Kaposi's sarcoma-associated herpesvirus (KSHV)/human herpesvirus-8 (HHV-8) in a primary effusion lymphoma cell line treated with tetradecanoyl phorbol acetate (TPA).

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The ultrastructure of Kaposi's sarcoma-associated herpesvirus (KSHV)/human herpesvirus-8 (HHV-8) has not yet been fully elucidated, although some findings have been reported using primary effusion lymphoma (PEL) cell lines, KS-1, harboring no Epstein-Barr virus (EBV) coinfection. In the present

Early activation of the Kaposi's sarcoma-associated herpesvirus RTA, RAP, and MTA promoters by the tetradecanoyl phorbol acetate-induced AP1 pathway.

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Kaposi's sarcoma-associated herpesvirus (KSHV) maintains a latent infection in primary effusion lymphoma (PEL) cells, but treatment with tetradecanoyl phorbol acetate (TPA) can trigger the full lytic-cycle replication in some of these cells. During lytic-cycle replication, the KSHV-encoded

Phorbol ester, serum, and rous sarcoma virus transforming gene product induce similar phosphorylations of ribosomal protein S6.

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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

Effect of phorbol myristate acetate on cultured tumor cells derived from different stages of avian sarcoma virus (ASV)-induced neoplastic growth.

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We have investigated the action of the tumor promoter phorbol 12-myristate-13-acetate (PMA) on avian sarcoma cells cultured from avian sarcoma virus (ASV)-induced tumors at various stages of growth and on normal chicken embryo fibroblasts (CEF). We found that exposure to PMA (30 ng/ml) led to

Decrease in collagen production in normal and Rous sarcoma virus-transformed chick embryo fibroblasts induced by phorbol myristate acetate.

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The effect of the potent tumor promoter phorbol 12-myristate 13-acetate (PMA) on collagen synthesis, a differentiated property of chick embryo fibroblasts, was examined. Collagen synthesis, as measured by the rate of formation of [3H]hydroxyproline from [3H]proline, was found to be decreased in

In vitro and in vivo studies of murine sarcoma cells after prolonged treatment with promoting phorbol ester TPA.

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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

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