UV-induced activation of AP-1 involves obligatory extranuclear steps including Raf-1 kinase.
AUTOR(ES)
Radler-Pohl, A
RESUMO
Irradiation of cells with ultraviolet light (UV) leads to modifications of c-Jun resembling those elicited by phorbol esters or oncogenes, and to enhanced transcription of AP-1-dependent genes. The UV-induced signal also triggers activation of Raf-1 and MAP-2 kinases. A dominant-negative Raf-1 kinase mutant strongly interferes with both phorbol ester and UV-induced AP-1 activation, indicating obligatory involvement of identical components in cytoplasmic signal transduction. Thus, from a presumably nuclear site of energy absorption, a signal needs to be transmitted to the cytoplasm in order to achieve activation of a nuclear transcription factor. Further, signals elicited from different primary sites merge prior to or at the level of activation of Raf-1 kinase.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=413301Documentos Relacionados
- The proteasome regulates the UV-induced activation of the AP-1-like transcription factor Gcn4
- Role of Gab1 in UV-Induced c-Jun NH2-Terminal Kinase Activation and Cell Apoptosis
- Role of diacylglycerol-regulated protein kinase C isotypes in growth factor activation of the Raf-1 protein kinase.
- Raf-1 and p21v-ras cooperate in the activation of mitogen-activated protein kinase.
- UV-induced DNA damage is an intermediate step in UV-induced expression of human immunodeficiency virus type 1, collagenase, c-fos, and metallothionein.