Zalfia A Darieva

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REF cells transformed by oncogenes E1A and cHa-ras reveal high and constitutive DNA-binding activity of AP-1 factor lacking in c-Fos protein. Consistently, the transcription of c-fos gene has been found to be downregulated. To elucidate the mechanisms of c-fos downregulation in E1A+cHa-ras transformants, we studied the levels of activity of ERK, JNK/SAPK(More)
Proteins of Ras family play an important role in regulation of cell growth and proliferation, and their mutations can lead to growth factor-independent proliferation due to constitutive activity of various signal transduction cascades. In the present work, we studied the activity of ERK, JNK and p38 MAP-kinase cascades in rat embryo fibroblast cells(More)
Changes in the levels of mRNAs encoding ion transporters (ATP1B1, NHE1, NKCC1), beta-actin, GAPDH, regulators of proliferation and apoptosis (p53, Bcl-2) and kinase hSGK, involved in cell water regulation, were studied using RT PCR in the peripheral human lymphocytes activated with phytohemagglutinin for 4-24 h. The common, "grouped", effect that was found(More)
DNA binding activity and intracellular distribution of transcription factor NF-kappa B in primary embryo fibroblast (REF) cells transformed by the complementing oncogenes E1A plus cHa-ras have been studied. By means of a gel retardation assay with a regulatory element kappa B, we showed that DNA binding activity of NF-kappa B increased upon transformation.(More)
In view of recent studies showing that cell proliferation of E1Aad5+c-Ha-ras-transformed fibroblasts cannot be regulated by growth factors and phorbol eaters in contrast to normal and E1Aad5-immortalized cell lines, the present work was undertaken to examine the role of protein kinase C (PKC) in the mitogenic signal transduction machinery in rat embryonal(More)
The ability of growth factors (GF) to stimulate proliferation of rat embryo fibroblast (REF) lines immortalized by E 1A oncogene and transformed by complementing E 1A and c-Ha-ras oncogenes (mutant form) was studied. Unlike untreated REF, those immortalized by E 1A oncogene required less serum and GF to proliferate. Proliferation could be stimulated by(More)
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