D
David Beach
Researcher at Cold Spring Harbor Laboratory
Publications - 207
Citations - 56103
David Beach is an academic researcher from Cold Spring Harbor Laboratory. The author has contributed to research in topics: Cyclin-dependent kinase 1 & Cell cycle. The author has an hindex of 97, co-authored 204 publications receiving 54757 citations. Previous affiliations of David Beach include Howard Hughes Medical Institute & Max Planck Society.
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Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a
TL;DR: It is shown that expression of oncogenic ras in primary human or rodent cells results in a permanent G1 arrest, and that the onset of cellular senescence does not simply reflect the accumulation of cell divisions, but can be prematurely activated in response to an onCogenic stimulus.
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A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4
TL;DR: P16 seems to act in a regulatory feedback circuit with CDK4, D-type cyclins and retinoblastoma protein, and inhibits the catalytic activity of theCDK4/cyclin D enzymes.
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p21 is a universal inhibitor of cyclin kinases
Yue Xiong,Gregory J. Hannon,Gregory J. Hannon,Hui Zhang,Hui Zhang,David J. Casso,David J. Casso,Ryuji Kobayashi,David Beach,David Beach +9 more
TL;DR: It is found that over expression of p21 inhibits the activity of each member of the cyclin/CDK family, and this results indicate that p21 may be a universal inhibitor of cyclin kinases.
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An RNA-directed nuclease mediates post-transcriptional gene silencing in Drosophila cells
TL;DR: It is shown that ‘loss-of-function’ phenotypes can be created in cultured Drosophila cells by transfection with specific double-stranded RNAs, which coincides with a marked reduction in the level of cognate cellular messenger RNAs.
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pl5 INK4B is a potentia| effector of TGF-β-induced cell cycle arrest
Gregory J. Hannon,David Beach +1 more
TL;DR: A new member of the p16INK4 family is isolated, p15INK4B, which is induced ∼30-fold in human keratinocytes by treatment with TGF-β, suggesting that pi5 may act as an effector of T GF-β-mediated cell cycle arrest.