Topic
Cell synchronization
About: Cell synchronization is a research topic. Over the lifetime, 435 publications have been published within this topic receiving 12070 citations.
Papers published on a yearly basis
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Papers
TL;DR: The expression of cyclins D, E, A and B1 provides new cell cycle landmarks that can be used to subdivide the cell cycle into several distinct subcompartments and the point of cell cycle arrest by many antitumor agents can be estimated with better accuracy in relation to these compartments compared to the traditional subdivision into four cell cycle phases.
Abstract: Cyclins are key components of the cell cycle progression machinery. They activate their partner cyclin-dependent kinases (CDKs) and possibly target them to respective substrate proteins within the cell. CDK-mediated phosphorylation of specific sets of proteins drives the cell through particular phases or checkpoints of the cell cycle. During unperturbed growth of normal cells, the timing of expression of several cyclins is discontinuous, occurring at discrete and well-defined periods of the cell cycle. Immunocytochemical detection of cyclins in relation to cell cycle position (DNA content) by multiparameter flow cytometry has provided a new approach to cell cycle studies. This approach, like no other method, can be used to detect the unscheduled expression of cyclins, namely, the presentation of G1 cyclins by cells in G2/M and of G2/M cyclins by G1 cells, without the need for cell synchronization. Such unscheduled expression of cyclins B1 and A was seen when cell cycle progression was halted, e.g., after synchronization at the G1/S boundary by inhibitors of DNA replication. The unscheduled expression of cyclins B1 or E, but not of A, was also observed in some tumor cell lines even when their growth was unperturbed. Likewise, whereas the expression of cyclins D1 or D3 in nontumor cells was restricted to an early section of G1, the presentation of these proteins in many tumor cell lines also was seen during S and G2/M. This suggests that the partner kinase CDK4 (which upon activation by D-type cyclins phosphorylates pRB committing the cell to enter S) is perpetually active throughout the cell cycle in these tumor lines. Expression of cyclin D also may serve to discriminate G0 vs. G1 cells and, as an activation marker, to identify the mitogenically stimulated cells entering the cell cycle. Differences in cyclin expression make it possible to discriminate between cells having the same DNA content but residing at different phases such as in G2 vs. M or G2/M of a lower DNA ploidy vs. G1 cells of a higher ploidy. The expression of cyclins D, E, A and B1 provides new cell cycle landmarks that can be used to subdivide the cell cycle into several distinct subcompartments. The point of cell cycle arrest by many antitumor agents can be estimated with better accuracy in relation to these compartments compared to the traditional subdivision into four cell cycle phases. The latter applications, however, pertain only to normal cells or to tumor cells whose phenotype is characterized by scheduled expression of cyclins. As sensitive and specific indicators of the cell's proliferative potential, the cyclins, in particular D-type cyclins, are expected to be key prognostic markers in neoplasia. © 1996 Wiley-Liss, Inc.
231 citations
TL;DR: This chapter describes the methods that permit the isolation of cell populations that are unique with respect to their position within the division cycle and presents the protocols for synchronization of continuously dividing cells by either imposing a metabolic block or by centrifugal elutriation.
Abstract: Publisher Summary This chapter describes the methods that permit the isolation of cell populations that are unique with respect to their position within the division cycle. It presents the protocols for synchronization of continuously dividing cells by either imposing a metabolic block or by centrifugal elutriation. To understand how eukaryotic cells grow and divide, it is important to identify and characterize the molecular components controlling entry into and execution of the two major events of the cell cycle, S and M phase. The most widely used methods to synchronize cells in the G 1 to S phase interval are starvation in methionine-free media or culturing cells in the presence of mimosine, hydroxyurea, aphidicolin, or excess thymidine. Cell synchronization by centrifugal elutriation does not cause perturbations in either, the biochemistry of the cell or the subsequent progression of cells through the cell cycle. Since this technology exploits the difference in the volume of cells as a function of their position in the cell cycle, it allows the separation of an asynchronous cell population into fractions enriched in G 1 , S, and G 2 /M phase cells.
216 citations
TL;DR: A review of cell synchronization methods that involve less perturbation of biological systems, such as serum deprivation, contact inhibition, and centrifugal elutriation have a significant advantage.
Abstract: Understanding the molecular and biochemical basis of cellular growth and division involves the investigation of regulatory events that most often occur in a cell-cycle phase-dependent fashion. Studies examining cell-cycle regulatory mechanisms and progression invariably require cell-cycle synchronization of cell populations. Thus, many methods have been established to synchronize cells at specific phases of the cell cycle. Several of the common methods involve pharmacological agents, which act at various points throughout the cell cycle. Because of adverse cellular perturbations resulting from many of the synchronizing drugs used, other synchrony methods that involve less perturbation of biological systems, such as serum deprivation, contact inhibition, and centrifugal elutriation have a significant advantage. The advantages and disadvantages of these cell synchronization methods are discussed in this review.
216 citations
TL;DR: It is proposed that rux functions as a negative regulator of G1 progression in the developing eye by encoding a novel protein of 335 amino acids that is suppressed by mutations in genes that promote cell cycle progression and enhanced by mutations that promote differentiation.
196 citations
TL;DR: RO-3306 represents a new molecular tool for studying CDK1 function in human cells that reversibly arrests proliferating human cells at the G2/M phase border and provides a novel means for cell cycle synchronization.
Abstract: Chemical agents for cell cycle synchronization have greatly facilitated the study of biochemical events driving cell cycle progression. G1, S and M phase inhibitors have been developed and used widely in cell cycle research. However, currently there are no effective G2 phase inhibitors and synchronization of cultured cells in G2 phase has been challenging. Recently, a selective CDK1 inhibitor, RO-3306, has been identified that reversibly arrests proliferating human cells at the G2/M phase border and provides a novel means for cell cycle synchronization. A single-step protocol using RO-3306 permits the synchronization of >95% of cycling cancer cells in G2 phase. RO-3306 arrested cells enter mitosis rapidly after release from the G2 block thus allowing for isolation of mitotic cells without microtubule poisons. RO-3306 represents a new molecular tool for studying CDK1 function in human cells.
192 citations
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Performance Metrics
| Year | Papers |
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| 2025 | 2 |
| 2024 | 6 |
| 2023 | 10 |
| 2022 | 15 |
| 2021 | 10 |
| 2020 | 10 |