• Publications
  • Influence
Epac- and Ca2+-controlled Activation of Ras and Extracellular Signal-regulated Kinases by Gs-coupled Receptors*
The data indicated that Gs-coupled receptors can activate H-Ras and subsequently the mitogen-activated protein kinases ERK1/2 by a Ca2+-activated Ras-GEF, possibly RasGRP1, mediated by cAMP-activated Epac proteins, which then lead via Rap2B and PLC-ϵ stimulation to [Ca2+]i increase.
Direct stimulation of receptor‐controlled phospholipase D1 by phospho‐cofilin
It is demonstrated that muscarinic receptor‐mediated stimulation of phospholipase D1 (PLD1) is controlled by LIM‐kinase, slingshot phosphatase as well as 14‐3‐3ζ, and requires phosphorylatable cofilin, and suggested that phospho‐cofilin by its stimulatory effect on PLD1 may control a large variety of cellular functions.
Antiestrogens induce transforming growth factor beta-mediated immunosuppression in breast cancer.
Evidence is offered that antiestrogen induces immunosuppression in the tumor microenvironment, through a TGFbeta-dependent mechanism that may contribute to the development of antiestrogens resistance in breast cancer.
Rap2B-Dependent Stimulation of Phospholipase C-ε by Epidermal Growth Factor Receptor Mediated by c-Src Phosphorylation of RasGRP3
ABSTRACT Receptor tyrosine kinase regulation of phospholipase C-ε (PLC-ε), which is under the control of Ras-like and Rho GTPases, was studied with HEK-293 cells endogenously expressing PLC-coupled
Heat Shock Protein HSP27 Secretion by Ovarian Cancer Cells Is Linked to Intracellular Expression Levels, Occurs Independently of the Endoplasmic Reticulum Pathway and HSP27's Phosphorylation Status,
It is demonstrated that HSP27 secretion by OVCAR-3 and SK-OV-3 cells depends on intracellular H SP27 concentrations and is independent of the endoplasmic reticulum secretory pathway and HSP 27 phosphorylation.
Peroxiredoxin Expression of Human Osteosarcoma Cells Is Influenced by Cold Atmospheric Plasma Treatment.
Antioxidant supplementation with NAC increases proliferation of CAP-treated osteosarcoma cells, implicating an involvement of redox signalling and indicating CAP affects redox homeostasis.
Cold Atmospheric Plasma Treatment Induces Anti-Proliferative Effects in Prostate Cancer Cells by Redox and Apoptotic Signaling Pathways
Investigation of the impact of CAP on cellular proliferation and consecutive molecular response mechanisms in established prostate cancer cell lines found relatively short treatments with CAP were sufficient to induce a significant inhibition of cancer proliferation, as observed for the first time in urogenital cancer.
Detection and Quantification of Nuclear Morphology Changes in Apoptotic Cells by Fluorescence Microscopy and Subsequent Analysis of Visualized Fluorescent Signals.
A computerized method for apoptosis detection and quantification using images of fluorescent dye-stained cell nuclei is presented, able to routinely assess apoptosis by a fast, highly reproducible low-cost technique.
Cytochrome P450 17A1 inhibitor abiraterone attenuates cellular growth of prostate cancer cells independently from androgen receptor signaling by modulation of oncogenic and apoptotic pathways.
It is demonstrated, that abiraterone treatment significantly decreased cell growth, AR expression, and AR activity of AR-positive LNCaP cells, and may play a more global role in PC progression control than originally hypothesized.