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Cyclin

About: Cyclin is a research topic. Over the lifetime, 4628 publications have been published within this topic receiving 286340 citations. The topic is also known as: IPR039361 & Cyclin family.


Papers
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Journal ArticleDOI
18 Nov 1994-Cell
TL;DR: Phosphorylation of ~40~‘~’ by Clnl,Cln2-Cdc28 might trigger its ubiquitin- mediated degradation, thereby enabling the Cln-regulated kinases to control S phase entry indirectly.

2,736 citations

Journal Article
TL;DR: The results support the idea that WAF1/CIP1 is a critical downstream effector in the p53-specific pathway of growth control in mammalian cells.
Abstract: The tumor growth suppressor WAF1/CIP1 was recently shown to be induced by p53 and to be a potent inhibitor of cyclin-dependent kinases In the present studies, we sought to determine the relationship between the expression of WAF1/CIP1 and endogenous regulation of p53 function WAF1/CIP1 protein was first localized to the nucleus of cells containing wild-type p53 and undergoing G 1 arrest WAF1/CIP1 was induced in wild-type p53-containing cells by exposure to DNA damaging agents, but not in mutant p53 -containing cells The induction of WAF1/CIP1 protein occurred in cells undergoing either p53 -associated G 1 arrest or apoptosis but not in cells induced to arrest in G 1 or to undergo apoptosis through p53 -independent mechanisms DNA damage led to increased levels of WAF1/CIP1 in cyclin E-containing complexes and to an associated decrease in cyclin-dependent kinase activity These results support the idea that WAF1/CIP1 is a critical downstream effector in the p53 -specific pathway of growth control in mammalian cells

2,056 citations

Journal ArticleDOI
18 Jun 1993-Cell

2,017 citations

Journal ArticleDOI
TL;DR: 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.
Abstract: Cell-cell contact and TGF-beta can arrest the cell cycle in G1. Mv1Lu mink epithelial cells arrested by either mechanism are incapable of assembling active complexes containing the G1 cyclin, cyclin E, and its catalytic subunit, Cdk2. These growth inhibitory signals block Cdk2 activation by raising the threshold level of cyclin E necessary to activate Cdk2. In arrested cells the threshold is set higher than physiological cyclin E levels and is determined by an inhibitor that binds to cyclin E-Cdk2 complexes. A 27-kD protein that binds to and prevents the activation of cyclin E-Cdk2 complexes can be purified from arrested cells but not from proliferating cells, using cyclin E-Cdk2 affinity chromatography. p27 is present in proliferating cells, but it is sequestered and unavailable to interact with cyclin E-Cdk2 complexes. 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.

1,934 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023190
202284
2021113
2020120
2019107
201899