Direct binding of cyclin D to the retinoblastoma gene product (pRb) and pRb phosphorylation by the cyclin D-dependent kinase CDK4.

@article{Kato1993DirectBO,
  title={Direct binding of cyclin D to the retinoblastoma gene product (pRb) and pRb phosphorylation by the cyclin D-dependent kinase CDK4.},
  author={Jun‐ya Kato and Hitoshi Matsushime and Scott W Hiebert and Mark E. Ewen and Charles J. Sherr},
  journal={Genes \& development},
  year={1993},
  volume={7 3},
  pages={
          331-42
        }
}
The product (pRb) of the retinoblastoma gene (RB-1) prevents S-phase entry during the cell cycle, and inactivation of this growth-suppressive function is presumed to result from pRb hyperphosphorylation during late G1 phase. Complexes of the cyclin-dependent kinase, cdk4, and each of three different D-type cyclins, assembled in insect Sf9 cells, phosphorylated a pRb fusion protein in vitro at sites identical to those phosphorylated in human T cells. Only D-type cyclins activated cdk4 enzyme… Expand
G1 cyclins control the retinoblastoma gene product growth regulation activity via upstream mechanisms.
  • L. Horton, Y. Qian, D. Templeton
  • Biology, Medicine
  • Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research
  • 1995
TLDR
Using in vivo expression systems, it is shown that cyclins A, E, D1, D2, and D3 each function to phosphorylate and inactivate pRb, and that coexpression of G1 cyclins and kinases represses pRB-mediated growth inhibition in Saos-2 cells. Expand
Functional interactions of the retinoblastoma protein with mammalian D-type cyclins
TLDR
All D-type cyclins do not function equivalently, and one of them plays a major role in reversing the cycle-blocking function of a known tumor suppressor. Expand
DNA tumor virus oncoproteins and retinoblastoma gene mutations share the ability to relieve the cell's requirement for cyclin D1 function in G1
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A model for an autoregulatory feedback loop mechanism that regulates both the expression of the cyclin D1 gene and the activity of pRB, thereby contributing to a G1 phase checkpoint control in cycling mammalian cells is proposed. Expand
A cyclin D1/cyclin-dependent kinase 4 binding site within the C domain of the retinoblastoma protein.
TLDR
A mutation in the C domain of Rb, L901Q, has been identified that completely abolishes cdk4/D1 phosphorylation of the isolated C domain and suggests a conservation of this C domain binding motif for cyclin D1/cdk4 kinase among the Rb family of proteins. Expand
Cyclin D1 is dispensable for G1 control in retinoblastoma gene-deficient cells independently of cdk4 activity
TLDR
Evidence is provided for an upstream control function of cyclin D1/cdk4, and a downstream role for pRB, in the order of events regulating transition through late G1 phase of the mammalian cell division cycle. Expand
Expression of Cyclin E Renders Cyclin D-CDK4 Dispensable for Inactivation of the Retinoblastoma Tumor Suppressor Protein, Activation of E2F, and G1-S Phase Progression*
TLDR
CDK2-cyclin E, without prior CDK4- cyclin D activity, can phosphorylate and inactivate pRb, activate E2F, and induce DNA synthesis, as assayed by E2f activation, cyclin A expression, and S phase progression. Expand
Disruption of the cyclin D/cyclin-dependent kinase/INK4/retinoblastoma protein regulatory pathway in human neuroblastoma.
TLDR
Results suggest that neuroblastoma cells may bypass the cell cycle block imposed by constitutive expression of wild-type p16INK4a in novel ways, but the mechanism(s) responsible for disruption of p16ink4a inhibitory activity in the remaining cell lines is unknown. Expand
Cyclin-dependent kinase-2 (Cdk2) forms an inactive complex with cyclin D1 since Cdk2 associated with cyclin D1 is not phosphorylated by Cdk7-cyclin-H.
TLDR
It is strongly suggested that Cdk2 forms a stable complex with cyclin D1 but is not activated because the Cdk 2 molecule in the complex is not phosphorylated by Cdk7-cyclin-H and the phosphorylation of Cdk1, an active form, does not bind to cyclinD1. Expand
Gi Cyclins Control the Retinoblastoma Gene Product Growth Regulation Activity via Upstream Mechanisms 1
Inactivation of the retinoblastoma gene produd (pRb) occurs concomitant with the appearance of its hyperphosphorylated form in mid to late G1 . Multiple cyclin/CDK complexes are implicated in theExpand
Regulation of the retinoblastoma protein-related p107 by G1 cyclin complexes.
TLDR
It is shown that phosphorylation of the pRb-related p107 results in the loss of the ability to associate with E2F-4, a transcription factor with growth-promoting and oncogenic activity, and that the activity of p107 is regulated by phosphorylated through D-type cyclins. Expand
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