Biomedical subjects

B Spira

Publications and source records attributed to B Spira.

23 records · Page 2Linked to original sources

PubMed1987

Altered pp60src kinase activity in regressing tumors induced by Rous sarcoma virus.

Tumors which are induced in chickens by Rous sarcoma virus (RSV) usually grow progressively for several weeks and then regress. pp60src kinase activity was found to be reduced in cultured tumor cells which derived from regressing sarcomas by 60-75% as compared to progressively growing neoplasms. We further found that a cellular pp89 which co-precipitated with pp60src was largely diminished in tumor cells derived from regressing as compared with progressively growing sarcomas. In contrast, immunoprecipitation analyses from membrane or cytosol fractions did not reveal any significant differences between these 2 types of tumor cells in distribution of pp60src. Moreover, partial proteolysis or isoelectric focussing of labelled immunoprecipitated pp60src did not reveal major differences between the 2 tumor cell types. These data indicate that the lack of pp89 cell binding to pp60src in regressing sarcoma cells correlates well with the diminution of the pp60src kinase activity in these cells, but does not affect the transport of pp60src to the plasma membrane.

Animals↗

PubMed1987

Inhibition of human lymphocyte mitogenesis by human and other retroviruses. Differential effect of interleukin-2 in restoration of responsiveness.

The addition of both live and ultraviolet-inactivated preparations of human T lymphotropic virus type I (HTLV-I) and HIV to cultures of human peripheral lymphocytes impeded the ability of these cells to respond to phytohaemagglutinin (PHA). This inhibition depended on the concentration of the virus and seemed due, in part at least, to interference with the generation of interleukin-2 (IL-2) activity in the PHA-stimulated cultures. However, the addition of exogenous IL-2 did not effectively restore the lymphocyte proliferative responsiveness of cells which had been co-incubated with these human retroviruses. Exposure to the viruses did not affect expression on co-incubated cells of the Tac antigen, an epitope of the IL-2 receptor, as determined by an indirect immunofluorescence assay. These results suggest that one mechanism through which human retroviruses may be able to impede cellular proliferative responsiveness is interference with the ability of target cells to respond to IL-2, even though IL-2 receptors continue to be expressed under the conditions tested.

Deltaretrovirus↗

PubMed1985

Inhibition by human T-lymphotropic virus (HTLV-I) of T-lymphocyte mitogenesis: failure of exogenous T-cell growth factor to restore responsiveness to lectin.

Various retroviruses, including human T-cell lymphotropic virus (HTLV-I) and avian sarcoma virus (ASV), can prevent coincubated human peripheral lymphocytes from responding efficiently to phytohaemagglutinin. Addition of high concentrations of T-cell growth factor (TCGF) activity usually overcomes this inhibition. However, such restoration of responsiveness does not occur in the case of HTLV-coincubated cells.

Avian Sarcoma Viruses↗

PubMed1984

Reversible interference with TCGF activity by virus particles.

Several types of virus particles including retroviruses and herpes viruses can impede the ability of human peripheral blood lymphocytes to respond to mitogenic stimuli. This is true even in the case of viruses that have been inactivated by u.v. light, indicating that the mechanisms involved are infection independent, at least in part. The observed inhibition could be shown to correlate with a reduced level of production of TCGF activity in the virus co-incubated cultures. In addition, these same viruses are apparently able to complex directly with TCGF activity and to render it biologically inactive. This was shown by allowing known quantities of virus to interact with TCGF activity for different periods of time, followed by centrifugation of any virus-TCGF complexes. This interference is reversible, however, and the dissociation of these virus-TCGF complexes by mild detergent, followed by viral centrifugation, yields TCGF activity in the supernatant.

Cells, Cultured↗

PubMedDate not supplied

Studies on pp60src and associated kinase activity in regressing tumors induced by Rous sarcoma virus.

Rous sarcoma virus induced chicken tumors usually grow progressively for several weeks and then regress. pp60src kinase activity was reduced in cultured tumor cells which derived from regressing sarcomas by 60-75% as compared to progressively-growing neoplasms. We have demonstrated the presence of inhibitory activity to pp60src kinase activity in extracts of regressing tumor cells. Such extracts were able to reduced by 60% the level of kinase activity found in progressively-growing tumors, as measured in a IgG phosphorylation assay. Immunoprecipitation analyses of membrane or cytosol fractions did not reveal any significant differences between these two types of tumor cells in distribution of pp60src. The pp60src kinase of progressively-growing tumor cells was more sensitive than that of "regressor" cells to inhibition by P1, P4 di-(adenosine-5') tetraphosphate (Ap4 A) and to heat inactivation. These results suggest that the reduction of pp60src kinase activity in regressing neoplasms might be due to the presence of inhibitors in such cells, but that the basal levels of activity which remain are relatively resistant to further perturbation by heat and/or chemical antagonists.

Animals↗