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Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...

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High-Throughput Cellular Profiling of Targeted Protein Degradation Compounds Using HiBiT CRISPR Cell Lines
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Multiple degradation pathways regulate versatile CIP/KIP CDK inhibitors.

Natalia G Starostina1, Edward T Kipreos

  • 1Department of Cellular Biology, University of Georgia, Athens, GA 30602, USA. ngs@uga.edu

Trends in Cell Biology
|December 14, 2011
PubMed
Summary
This summary is machine-generated.

The CIP/KIP cyclin-dependent kinase inhibitors (CKIs) regulate cell cycle, transcription, and apoptosis. This review details how ubiquitin ligase pathways control CKI degradation, influencing their diverse roles in cancer.

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12:26

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • The CIP/KIP family of cyclin-dependent kinase (CDK) inhibitors (CKIs) includes p21, p27, and p57.
  • These proteins inhibit CDK complexes crucial for cell cycle regulation.
  • CKIs also have independent roles in transcription, apoptosis, and cytoskeletal dynamics.

Purpose of the Study:

  • To review recent findings on how E3 ubiquitin ligase pathways regulate CKI degradation.
  • To elucidate the mechanisms controlling CKI subpopulations and their diverse functions.
  • To understand the dual role of CKIs in cancer suppression and promotion.

Main Methods:

  • Literature review of recent research on CKI regulation.
  • Analysis of data on ubiquitin ligase pathways targeting p21, p27, and p57.
  • Examination of distinct cellular compartments and functions of CKIs.

Main Results:

  • Multiple E3 ligases mediate the proteasomal degradation of p21, p27, and p57.
  • Specific E3 pathways differentially regulate CKI subpopulations.
  • This regulation impacts the diverse functions of CKIs, including their roles in cell cycle control and cancer.

Conclusions:

  • Distinct E3 ligase pathways are critical for controlling CKI activity and function.
  • Understanding these pathways is key to deciphering the complex roles of CKIs in cellular processes and disease.
  • Targeting E3-CKI interactions may offer therapeutic strategies for cancer.