The cyclopentenone 15-deoxy-delta 12,14-prostaglandin J2 binds to and activates H-Ras

The cyclopentenone 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) induces cell proliferation and mitogen-activated protein kinase activation. Here, we describe that these effects are mediated by 15d-PGJ(2)-elicited H-Ras activation. We demonstrate that this pathway is specific for H-Ras throu...

Descripción completa

Detalles Bibliográficos
Autores: Oliva-Martinez, Jose Luis, Pérez-Sala, Dolores, Castrillo, Antonio, Martinez, Natalia, Cañada, F Javier, Boscá, Lisardo, Rojas-Cabañeros, Jose Maria
Tipo de recurso: artículo
Fecha de publicación:2003
País:España
Institución:Instituto de Salud Carlos III (ISCIII)
Repositorio:Repisalud
Idioma:inglés
OAI Identifier:oai:repisalud.isciii.es:20.500.12105/26115
Acceso en línea:https://hdl.handle.net/20.500.12105/26115
Access Level:acceso abierto
Palabra clave:Mitogen-activated protein kinase
Cell proliferation
Posttranslational modification
3T3 Cells
Amino Acid Sequence
Animals
Binding Sites
COS Cells
Cell Division
Cysteine
Gene Expression Regulation
Genes, ras
In Vitro Techniques
MAP Kinase Signaling System
Mice
Molecular Sequence Data
Mutagenesis, Site-Directed
Mutation
Prostaglandin D2
Protein Binding
Recombinant Proteins
ras Proteins
Descripción
Sumario:The cyclopentenone 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) induces cell proliferation and mitogen-activated protein kinase activation. Here, we describe that these effects are mediated by 15d-PGJ(2)-elicited H-Ras activation. We demonstrate that this pathway is specific for H-Ras through the formation of a covalent adduct of 15d-PGJ(2) with Cys-184 of H-Ras, but not with N-Ras or K-Ras. Mutation of C184 inhibited H-Ras modification and activation by 15d-PGJ(2), whereas serum-elicited stimulation was not affected. These results describe a mechanism for the activation of the Ras signaling pathway, which results from the chemical modification of H-Ras by formation of a covalent adduct with cyclopentenone prostaglandins.