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MAP Kinases and Prostate Cancer

Gonzalo Rodríguez‐BerrigueteDepartment of Cell Biology and Genetics, University of Alcalá, Alcalá de Henares, 28871 Madrid, SpainBenito FraileDepartment of Cell Biology and Genetics, University of Alcalá, Alcalá de Henares, 28871 Madrid, SpainPilar Martínez-OnsurbeDepartment of Pathology, Príncipe de Asturias Hospital, Alcalá de Henares, 28806 Madrid, SpainGabriel OlmedillaDepartment of Pathology, Príncipe de Asturias Hospital, Alcalá de Henares, 28806 Madrid, SpainRicardo PaniaguaDepartment of Cell Biology and Genetics, University of Alcalá, Alcalá de Henares, 28871 Madrid, SpainMar RoyuelaDepartment of Cell Biology and Genetics, University of Alcalá, Alcalá de Henares, 28871 Madrid, Spain
2011en
ABI

Аннотация

The three major mitogen-activated protein kinases (MAPKs) p38, JNK, and ERK are signal transducers involved in a broad range of cell functions including survival, apoptosis, and cell differentiation. Whereas JNK and p38 have been generally linked to cell death and tumor suppression, ERK plays a prominent role in cell survival and tumor promotion, in response to a broad range of stimuli such as cytokines, growth factors, ultraviolet radiation, hypoxia, or pharmacological compounds. However, there is a growing body of evidence supporting that JNK and p38 also contribute to the development of a number of malignances. In this paper we focus on the involvement of the MAPK pathways in prostate cancer, including the less-known ERK5 pathway, as pro- or antitumor mediators, through their effects on apoptosis, survival, metastatic potential, and androgen-independent growth.

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