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CDK2 — RHOA
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Saito et al., Thyroid 2001
:
Thyrotropin ( TSH ) -initiated cell cycle progression from G1 to S phase in FRTL-5 thyroid cells requires serum, insulin, or insulin-like growth factor 1 (IGF-1) and involves activation of 3-hydroxy-3-methylglutaryl-CoA reductase, geranylgeranylation of
RhoA , p27Kip1 degradation, and
activation of
cyclin dependent kinase (cdk) 2
Teramoto et al., Oncogene 2003
:
For example, H-Ras V12 upregulated osteopontin and Akt 1, and H-Ras and
RhoA stimulated cyclin G1,
cyclin dependent kinase 8, cyclin A2 and HMGI-C, while Rac1 QL and Cdc42 QL upregulated extracellular matrix and cell adhesion proteins such as alpha-actinin 4, procollagen type I and V and neuropilin
Hu et al., J Biol Chem 1999
:
In this report, we have demonstrated that, in IIC9 cells,
RhoA regulates cyclin
E/CDK2 activity, which is required for p27 ( Kip ) degradation ... In the absence of serum, expression of constitutively active
RhoA ( 63 )
resulted in significant stimulation of cyclin
E/CDK2 activity and degradation of p27 ( Kip ) ... In addition, expression of dominant negative
RhoA blocked serum induced cyclin
E/CDK2 activity and p27 ( Kip ) degradation