Cyclin B-cdk1
Cyclin B-cdk1 - Related Videos
13:15
Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
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Cited by 5 •
2016
Here, we outline how to study mitochondrial localization of a (cell cycle) kinase, and how to determine its sub-mitochondrial location as well as potential mitochondrial substrates/targets. Forced expression of proteins into the mitochondria provides a useful tool for studying the functional consequences of mitochondrial localization of a protein of interest.
10:54
Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations
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Cited by 2 •
2012
Metaphase to anaphase transition is triggered through anaphase-promoting complex (APC/C)-dependent ubiquitination and subsequent destruction of cyclin B. Here, we established a system which, following pulse-chase labeling, allows monitoring cyclin B proteolysis in entire cell populations and facilitates the detection of interference by the mitotic checkpoint.
12:26
Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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Cited by 10 •
2018
Cyclin-dependent kinase 1 (Cdk1) is activated in the G2 phase of the cell cycle and regulates many cellular pathways. Here, we present a protocol for an in vitro kinase assay with Cdk1, which allows the identification of Cdk1-specific phosphorylation sites for establishing cellular targets of this important kinase.
02:37
Restarting Stalled Replication Forks
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2020
DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...
01:45
Positive Regulator Molecules
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2019
To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated. Internal regulatory checkpoints ensure that a cell’s size, energy reserves, and DNA quality and completeness are sufficient to advance through the cell cycle. At these checkpoints, positive and negative regulators promote or inhibit a cell’s continuation through the cell cycle. Positive regulators include two protein groups that allow cells to pass through regulatory...
FAQs
Activation depends on a balance between opposing regulators. Wee1 and Myt1 kinases place inhibitory phosphates on CDK1, whereas Cdc25 phosphatases remove those phosphates. Cyclin B accumulation during G2 supplies the binding partner for CDK1, and Cdc25-mediated removal of inhibition permits the complex to phosphorylate proteins that initiate mitotic events.
These enzymes create a regulatory gate that controls when the Cyclin B-CDK1 complex can act. Wee1 and Myt1 restrain CDK1 through inhibitory phosphorylation, while Cdc25 reverses that modification. Their opposing activities connect Cyclin B accumulation with the timing of mitotic entry, helping prevent premature activation of processes required for chromosome and nuclear reorganization.
Active Cyclin B-CDK1 phosphorylates several proteins that drive major structural changes in the cell. These targets promote chromosome condensation, spindle assembly, and nuclear envelope breakdown, coordinating distinct features of mitosis. The complex therefore links a regulatory activation event to the physical remodeling required for chromosome segregation and cell division.
Mitotic exit follows activation of the anaphase-promoting complex/cyclosome, which triggers Cyclin B degradation. Removing Cyclin B changes the state of the CDK1 regulatory circuit after its mitotic activities have occurred. This transition helps terminate the phosphorylation program associated with mitosis and supports progression out of the mitotic phase.
Cyclin B accumulation during G2, inhibitory phosphorylation of CDK1, Cdc25 activity, and later Cyclin B degradation provide distinct points for examining the circuit. Mitotic consequences such as chromosome condensation, spindle assembly, and nuclear envelope breakdown offer functional readouts. Together, these observations connect molecular regulation with cell-cycle progression.
Studying this pathway helps researchers relate molecular cell-cycle control to checkpoint function, developmental transitions, and genomic stability. Because abnormal CDK1 regulation can contribute to uncontrolled cell proliferation, the circuit also provides context for understanding how failures in mitotic control may affect biological systems. Its sequential regulators make it useful for tracing transitions through cell division.