Repositorio Institucional
Repositorio Institucional
CONICET Digital
  • Inicio
  • EXPLORAR
    • AUTORES
    • DISCIPLINAS
    • COMUNIDADES
  • Estadísticas
  • Novedades
    • Noticias
    • Boletines
  • Ayuda
    • General
    • Datos de investigación
  • Acerca de
    • CONICET Digital
    • Equipo
    • Red Federal
  • Contacto
JavaScript is disabled for your browser. Some features of this site may not work without it.
  • INFORMACIÓN GENERAL
  • RESUMEN
  • ESTADISTICAS
 
Artículo

Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation

Dekanty, AndresIcon ; Sauane, Moira; Cárdenas, Belén; Coluccio Leskow, FedericoIcon ; Barrio, Marcela; Casala, Jorgelina; Paciencia, Mercedes; Rogers, Florencia; Coso, Omar AdrianIcon ; Piwien Pilipuk, GracielaIcon ; Rudlland, Philip S.; Jimenez de Asua, Luis Adan FelipeIcon
Fecha de publicación: 10/03/2006
Editorial: American Society For Biochemistry And Molecular Biology
Revista: Journal Of Biological Chemistry
ISSN: 0021-9258
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Medicina Critica y de Emergencia

Resumen

Leukemia inhibitory factor (LIF) and oncostatin M (OSM) induce DNA synthesis in Swiss 3T3 cells through common signaling mechanism(s), whereas other related cytokines such as interleukin-6 and ciliary neurotrophic factor do not cause this response. Induction of DNA replication by LIF or prostaglandin F2alpha (PGF2alpha) occurs, in part, through different signaling events. LIF and OSM specifically trigger STAT1 cytoplasmic to nuclear translocation, whereas PGF2alpha fails to do so. However, LIF and PGF2alpha can trigger increases in ERK1/2 activity, which are required for their mitogenic responses because U0126, a MEK1/2 inhibitor, prevents both ERK1/2 activation and induction of DNA synthesis by LIF or PGF2alpha treatment. PGF2alpha induces cyclin D expression and full phosphorylation of retinoblastoma protein. In contrast, LIF fails to promote increases in cyclin D mRNA/protein levels; consequently, LIF induces DNA synthesis without promoting full phosphorylation of retinoblastoma protein (Rb). However, both LIF and PGF2alpha increase cyclin E expression. Furthermore, LIF mitogenic action does not involve protein kinase C (PKC) activation, because a PKC inhibitor does not block this effect. In contrast, PKC activity is required for PGF2alpha mitogenic action. More importantly, the synergistic effect between LIF and PGF2alpha to promote S phase entry is independent of PKC activation. These results show fundamental differences between LIF- and PGF2alpha-dependent mechanism(s) that induce cellular entry into S phase. These findings are critical in understanding how LIF and other related cytokine-regulated events participate in normal cell cycle control and may also provide clues to unravel crucial processes underlying cancerous cell division.
Palabras clave: Lif , Pgf2alpha , Osm , Mapk
Ver el registro completo
 
Archivos asociados
Thumbnail
 
Tamaño: 478.5Kb
Formato: PDF
.
Descargar
Licencia
info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/18518
URL: http://www.jbc.org/content/281/10/6136.long
DOI: http://dx.doi.org/10.1074/jbc.M505839200
Colecciones
Articulos(IBYME)
Articulos de INST.DE BIOLOGIA Y MEDICINA EXPERIMENTAL (I)
Citación
Dekanty, Andres; Sauane, Moira; Cárdenas, Belén; Coluccio Leskow, Federico; Barrio, Marcela; et al.; Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation; American Society For Biochemistry And Molecular Biology; Journal Of Biological Chemistry; 28; 10; 10-3-2006; 6136-6143
Compartir
Altmétricas
 
Estadísticas
Visualizaciones: 109
Descargas: 130

Enviar por e-mail
Separar cada destinatario (hasta 5) con punto y coma.
  • Facebook
  • Twitter
  • Instagram
  • YouTube
  • Sound Cloud

Los contenidos del CONICET están licenciados bajo Creative Commons Reconocimiento 2.5 Argentina License

Ministerio
https://www.conicet.gov.ar/ - CONICET

Inicio

Explorar

  • Autores
  • Disciplinas
  • Comunidades

Estadísticas

Novedades

  • Noticias
  • Boletines

Ayuda

Acerca de

  • CONICET Digital
  • Equipo
  • Red Federal

Contacto

Godoy Cruz 2290 (C1425FQB) CABA – República Argentina – Tel: +5411 4899-5400 repositorio@conicet.gov.ar
TÉRMINOS Y CONDICIONES