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Your search keyword '"Mónika, Vecsernyés"' showing total 2 results
Start Over Author "Mónika, Vecsernyés" Publisher wiley
2 results on '"Mónika, Vecsernyés"'

1. Urocortin stimulates the ERK1/2 signaling pathway and the proliferation of HeLa cells via CRF receptor 1

Author

Bálint Balogh, Mónika Vecsernyés, Alexandra Stayer‐Harci, Gergely Berta, Oktávia Tarjányi, and György Sétáló Jr

Subjects
cell proliferation, E2F‐1, ERK1/2, MEK, HeLa, urocortin, Biology (General), QH301-705.5
Abstract

Corticotropin‐releasing factor (CRF) stimulates adrenocorticotropic hormone (ACTH) secretion from the pituitary gland and is an essential regulator of the hypothalamic–pituitary–adrenocortical axis. Isoforms of CRF receptor are known to mediate the effects of urocortin stress ligands on the regulation of stress responses, anxiety, and feeding behavior; however, urocortin stress ligands also influence cell proliferation. In view of the tumor‐promoting capacity of prolonged stress, here we investigated (a) the effect of urocortin on cell proliferative signaling via extracellular signal‐regulated kinase 1/2, (b) the expression and cellular distribution of the specific CRF receptor isoforms, and (c) the intracellular localization of phosphorylated ERK1/2 in HeLa cells. Stimulation of cell proliferation was observed in the presence of 10 nm urocortin. Our data also suggest that MAP kinase MEK, the transcription factors E2F‐1 and p53, and PKB/Akt are involved in this process. These findings may have therapeutic relevance for the targeted treatment of various malignancies.

Published
2023
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2. The effects of a mutant p53 protein on the proliferation and differentiation of PC12 rat phaeochromocytoma cells

Author

Zsolt Fábián, Marianna Pap, Mónika Vecsernyés, and József Szeberényi

Subjects
MAPK/ERK pathway, Cell cycle checkpoint, p38 mitogen-activated protein kinases, Cell, Mutant, Endogeny, Biology, PC12 Cells, Biochemistry, Nerve Growth Factor, medicine, Animals, Humans, Phosphorylation, Extracellular Signal-Regulated MAP Kinases, Molecular Biology, Cell Proliferation, Neurons, Kinase, Cell Differentiation, Cell Biology, Rats, Cell biology, Enzyme Activation, Enhancer Elements, Genetic, medicine.anatomical_structure, nervous system, Mitogen-Activated Protein Kinases, Tumor Suppressor Protein p53
Abstract

PC12 rat phaeochromocytoma cells show neuronal differentiation upon NGF treatment. NGF induces prolonged activation of the Ras/Raf/MEK/ERK pathway in which the 42/44 kDa mitogen-activated protein kinases (MAPKs), ERK 1 and 2 are thought to be the key mediators of the differentiation signals. Activation of ERKs leads to the increased transcription of early response genes resulting in cell cycle arrest. Upon NGF treatment the p53 protein, the most commonly mutated tumor suppressor in human cancers, translocates to the nucleus and may play a role in the mediation of NGF-induced cell cycle arrest and neuronal differentiation. Here we demonstrate that in PC12 cells expressing both wild-type and V143A mutant p53 proteins (p143p53PC12 cells), p53-mediated biological responses are critically influenced. p143p53PC12 cells are not able to cease their proliferation and begin their neuronal differentiation program upon NGF treatment. The presence of mutant p53 also reduces the DNA-binding activity of endogenous p53 and disturbs the regulatory machinery of p53 including both the phosphorylation of ERK 1/2, p38 and SAPK/JNK MAP kinases and itself. J. Cell. Biochem. 99: 1431–1441, 2006. © 2006 Wiley-Liss, Inc.

Published
2006
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