The ERK1/2 mitogen-activated protein kinase pathway as a master regulator of the G1- to S-phase transition

1,152 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Mitochondrial metabolism and ROS generation are essential for Kras-mediated tumorigenicity (2010, background): “The ERK MAPKs are regulated by the upstream MEK kinase (MAPK kinase) and at low levels induce cellular proliferation but at high levels cause growth arrest (18).”
The Ras-ERK and PI3K-mTOR Pathways: Cross-talk and Compensation (2011, background): “Confoundingly, non-physiological hyper-activation of Ras-ERK signaling can induce the expression of CDK (cyclin-dependent kinase) inhibitors and trigger cell cycle arrest [5].”
Mechanisms and pathways of growth failure in primordial dwarfism. (2011, background): “Expression of Cdk inhibitors p21 and p27 is also inhibited, along with maintenance of transcriptional repression of a variety of anti-proliferative genes (Yamamoto et al. 2006; Meloche and Pouyssegur 2007).”
Targeting the Mitogen-Activated Protein Kinase RAS-RAF Signaling Pathway in Cancer Therapy (2012, background): “Once activated, ERK1/ERK2 broadly phosphorylate several nuclear and cytoplasmic effector genes involved in diverse cellular responses such as cell proliferation, survival, differentiation, motility and angiogenesis [19-21].”
Oxidative Stress in Aging Human Skin (2015, background): “The tumor suppressor Rb is then in a complex with the E2F transcription factors, resulting in an inhibition of E2F target genes and a cell cycle arrest [343,345–351].”