Publications by authors named "Pavel S Grudinkin"
Article Synopsis
- High doses of epidermal growth factor (EGF) can paradoxically trigger cell death (apoptosis) in A431 epidermoid carcinoma cells that overexpress EGF receptors, despite EGF being known to promote cell growth.
- The study reveals that the activation of the STAT1 transcription factor is vital for EGF-induced apoptosis in these cells.
- Researchers found that the p38 MAP kinase pathway is crucial in this process, as inhibiting it reduced both the growth-inhibiting and pro-apoptotic effects of EGF by decreasing the phosphorylation of STAT1, specifically on tyrosine 701.
EGF in high concentrations has a growth-inhibitory effect on human epidermoid carcinoma cells A431. The transcription factor STAT1 is the most probable candidate for mediating this effect. In the present study, we demonstrated a strong reduction of the expression level of STAT1 in EGF-resistant sub-clones of A431 cells.
View Article and Find Full Text PDFAntioxidant protein Peroxiredoxin V (PrxV) is located in mitochondria and peroxisomes but is also present in the nucleus. Here, we show that nuclear PrxV associates with coilin-containing bodies suggesting possible interaction of this protein with transcription complexes. We also studied etoposide-induced phosphorylation of histone H2AX (gamma-H2AX) in human cells in which PrxV activity was downregulated (knockdown, KD-clones) or compromised by overexpression of redox-negative (RD) protein.
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