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CDK inhibitors: positive and negative regulators of G1-phase progression.
This work challenges previous assumptions about how the G1/S transition of the mammalian cell cycle is governed, helps explain some enigmatic features of cell cycle control that also involve the functions of the retinoblastoma protein (Rb) and the INK4 proteins, and changes the thinking about how either p16 loss or overexpression of cyclin D-dependent kinases contribute to cancer. Expand
Cancer Cell Cycles
- C. Sherr
- Biology, Medicine
- 6 December 1996
Genetic alterations affecting p16INK4a and cyclin D1, proteins that govern phosphorylation of the retinoblastoma protein and control exit from the G1 phase of the cell cycle, are so frequent in human cancers that inactivation of this pathway may well be necessary for tumor development. Expand
Inhibitors of mammalian G1 cyclin-dependent kinases.
Glycogen synthase kinase-3beta regulates cyclin D1 proteolysis and subcellular localization.
It is demonstrated that glycogen synthase kinase-3beta (GSK-3 beta) phosphorylates cyclin D1 specifically on Thr-286, thereby triggering rapid cyclinD1 turnover, which leads to proteasomal degradation of D1 and linked to phosphorylation and proteolytic turnover of cyclin L1 and its subcellular localization during the cell division cycle. Expand
The RB and p53 pathways in cancer.
Interconnecting signaling pathways controlled by RB and p53 are discussed, attempting to explain their potentially universal involvement in the etiology of cancer. Expand
Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization.
MEFs that survive myc overexpression sustain p53 mutation or ARF loss during the process of establishment and become immortal, and ARF regulates a p53-dependent checkpoint that safeguards cells against hyperproliferative, oncogenic signals. Expand
Tumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19 ARF
The INK4a tumor suppressor locus encodes growth inhibitory proteins that act upstream of the retinoblastoma protein and p53, and mice lacking p19ARF but expressing functional p16INK4a develop tumors early in life. Expand
The Pezcoller lecture: cancer cell cycles revisited.
- C. Sherr
- Biology, Medicine
- Cancer research
- 15 July 2000
Lesions in the p16--cyclin D-CDK4--Rb and ARF--Mdm2--p53 pathways occur so frequently in cancer, regardless of patient age or tumor type, that they appear to be part of the life history of most, if not all, cancer cells. Expand
p27Kip1, a cyclin-Cdk inhibitor, links transforming growth factor-beta and contact inhibition to cell cycle arrest.
Cyclin D2-Cdk4 complexes bind competitively to and down-regulate the activity of p27 and may thereby act in a pathway that reverses Cdk2 inhibition and enables G1 progression. Expand
Alternative reading frames of the INK4a tumor suppressor gene encode two unrelated proteins capable of inducing cell cycle arrest
The INK4a gene encodes an inhibitor of the cyclin D-dependent kinases CDK4 and CDK6 that blocks them from phosphorylating the retinoblastoma protein and prevents exit from the G1 phase of the cell cycle. Expand