Stress and apoptosis signaling research group
Members of the group:
Dr. Bátor Judit senior lecturer
Brandt Barbara assistant professor
Les Hajnalka assistant professor
Kele-Morvai Petra lab technician
Németh Marica assistant professor
Schipp Renáta research fellow
Dr. Varga Judit senior lecturer
Research area:
Nitric oxide (NO), as a secondary messenger, has wide-range intra- and intercellular signaling effects. These effects are highly dose-dependent: at low concentrations, it influences cell proliferation (stimulating it in very low, but inhibiting it in a little higher concentration), while at higher doses it causes cellular stress (nitrosative stress), which can lead to cell death, apoptosis, or even necrosis. The NO dose required to induce cell death depends on the cell type. We use sodium nitroprusside (SNP) as a NO donor.
Our research group investigates the role of the Ras protein family and the p53 protein in NO-induced signaling processes using modified PC12 cell lines. It is also worth noting that cell death induced by high-dose SNP treatment can be prevented or mitigated by pretreatment with lower, non-toxic doses of SNP. Extracellular vesicles released from cells following SNP treatment, known as exosomes, may play a role in this process. We have extended our research to various human tumor cell lines; for example, in melanoma cell lines, we investigate protein activation changes that mediate the antiproliferative and proapoptotic effects of SNP.
The best-known effect of anisomycin is its potential to inhibit protein synthesis, thereby causing cellular stress and apoptosis. Studies using a cell line expressing mutant p53 protein have revealed that the p53 protein plays a significant role in mediating this effect.
Glioblastoma multiforme (GBM) is the most common brain tumor, with an extremely low average survival rate. Chemotherapy with temozolomide (TMZ) is used during treatment, but it is ineffective in some patients. In our research, we work with GBM cell lines and investigate the possible molecular mechanisms resulting in TMZ resistance. Our goal is to induce apoptosis in these cell lines by activating alternative signaling pathways.
In GBM and PC12 cells, we also investigate the role of the CREB transcription factor in endoplasmic reticulum stress and apoptosis. Our goal is to determine by what manner CREB overexpression affects cell survival following ethanol treatment.