Inhibition of pRb phosphorylation and cell-cycle progression by a 20-residue peptide from p16CDKN2/INK4A

@article{Fhraeus1996InhibitionOP,
  title={Inhibition of pRb phosphorylation and cell-cycle progression by a 20-residue peptide from p16CDKN2/INK4A},
  author={Robin F{\aa}hraeus and Jes{\'u}s M. Paramio and Kathryn L. Ball and Sonia La{\'i}n and David Philip Lane},
  journal={Current Biology},
  year={1996},
  volume={6},
  pages={84-91}
}

Transduced p16INK4a peptides inhibit hypophosphorylation of the retinoblastoma protein and cell cycle progression prior to activation of Cdk2 complexes in late G1.

It is concluded that cyclin D:Cdk4/6 activity is required for early G1 phase cell cycle progression up to, but not beyond, activation of cyclin E:C DK2 complexes at the restriction point and is thus nonredundant with cyclin Cdk2 in late G1.

Induction of p21WAF1/CIP1and Inhibition of Cdk2 Mediated by the Tumor Suppressor p16INK4a

It is indicated that p21-mediated inhibition of cdk2 contributes to the cell cycle arrest imposed by p16 and is a potential point of cooperation between the p16/pRB and p14ARF/p53 tumor suppressor pathways.

Structure of the cyclin-dependent kinase inhibitor p19Ink4d

The structure of the p19Ink4d protein, determined by NMR spectroscopy, indicates that most mutations to the p16Ink 4a gene, which result in loss of function, are due to incorrectly folded and/or insoluble protein.

Structural Analysis of the Inhibition of Cdk4 and Cdk6 by p16INK4a through Molecular Dynamics Simulations

Results from molecular dynamics simulations provide a better understanding of the role of the T-loop conformation, a fragment of Cdks, and the way the ATP binding-site is distorted upon binding of p16INK4a.

Structural basis for inhibition of the cyclin-dependent kinase Cdk6 by the tumour suppressor p16INK4a

Tumour-derived mutations in INK4a and Cdk4 map to interface contacts, solidifying the role of CDK binding and inhibition in the tumour suppressor activity of p16INK4a.

Inhibition of cyclin-dependent kinase 4 (Cdk4) by fascaplysin, a marine natural product.

Fascaplysin will prove to be a useful tool in studying the consequence of Cdk4 inhibition, especially in cells containing inactivated p16, and caused G1 arrest and prevented pRb phosphorylation at sites implicated as being specific for Cdk 4 kinase.

Selective in vivo and in vitro effects of a small molecule inhibitor of cyclin-dependent kinase 4.

The specificity of CINK4 for Cdk4 raises the possibility that this small molecule or one with a similar structure could have therapeutic value and slows tumor growth in vivo.

Role of cell cycle control and cyclin-dependent kinases in breast cancer.

The regulation of cell cycle and proliferation has been extensively studied in the last few years and a consensus paradigm of cell cycle regulation has been developed [1,2]. According to this
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