Transient deactivation of ERK signalling is sufficient for stable entry into G0 in primary avian fibroblasts

Current Biology

Volumn 10, Issue 18, 2000, Pages 1119-1122

  Black, E J ^a   Clark, W ^a   Gillespie, D A F ^b  

^a BEATSON INSTITUTE FOR CANCER RESEARCH   (United Kingdom)

^b UNIVERSITY OF GLASGOW   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

EID: 0034699348     PISSN: 09609822     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0960-9822(00)00699-0     Document Type: Article

References (15)

1. Mitogen-activated protein kinases p42mapk and p44mapk are required for fibroblast proliferation
2. Nuclear translocation of p42/p44 mitogen-activated protein kinase is required for growth factor-induced gene expression and cell cycle entry
3. Activation of MAP kinase kinase is necessary and sufficient for PC12 differentiation and for transformation of NIH 3T3 cells
4. Raf-induced proliferation or cell cycle arrest is determined by the level of Raf activity with arrest mediated by p21Cip1
5. Two co-existing mechanisms for nuclear import of MAP kinase: Passive diffusion of a monomer and active transport of a dimer
6. Growth factor-induced p42/p44 MAPK nuclear translocation and retention requires both MAPK activation and neosynthesis of nuclear anchoring proteins
7. Immunological characterization of avian MAP kinases: Evidence for nuclear localization
8. Transformation by v-Jun prevents cell cycle exit and promotes apoptosis in the absence of serum growth factors
9. Signal transduction through MAP kinase cascades
10. Cell cycle-dependent activation of Ras
11. Integrin signaling and cell growth control
12. Growth factor activation of MAP kinase requires cell adhesion
13. A synthetic inhibitor of the mitogen-activated protein kinase cascade
14. Activated MEK stimulates expression of AP-1 components independently of phosphatidylinositol 3-kinase (PI3-kinase) but requires a PI3-kinase signal To stimulate DNA synthesis
15. Oncogenes, growth factors and phorbol esters regulate Raf-1 through common mechanisms