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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

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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.
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Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
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NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
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Anaphase Promoting Complex00:50

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...

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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
12:26

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Published on: May 3, 2018

Cyclin D1 is a NF-κB corepressor.

María F Rubio1, Pablo N Larrosa Fernandez, Cecilia V Alvarado

  • 1Laboratorio de Biología Molecular y Apoptosis, Instituto de Investigaciones Médicas Alfredo Lanari (IDIM-CONICET), Universidad de Buenos Aires, Combatientes de Malvinas 3150, C1427ARO Buenos Aires, Argentina.

Biochimica Et Biophysica Acta
|February 7, 2012
PubMed
Summary

Cyclin D1 (CD1) inhibits NF-κB activity, but RAC3 can reverse this effect. The balance of CD1 and RAC3 expression influences tumor cell proliferation, impacting cancer progression.

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Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors

Published on: October 26, 2015

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Nuclear factor-kappa B (NF-κB) is a key regulator of gene expression.
  • Cyclin D1 (CD1) and RAC3 are proteins involved in cell cycle regulation and transcriptional activity.

Purpose of the Study:

  • To investigate the regulatory role of Cyclin D1 (CD1) on NF-κB transcriptional activity.
  • To understand how RAC3 influences the interaction between CD1 and NF-κB.

Main Methods:

  • Investigated the effect of CD1 on NF-κB activity in tumoral and non-tumoral cells.
  • Utilized transfection to over-express CD1 and RAC3 individually and simultaneously.
  • Analyzed protein expression patterns in relation to the cell cycle.

Main Results:

  • CD1 was found to inhibit NF-κB transcriptional activity via a corepressor function.
  • Over-expression of RAC3 reverted the inhibitory effect of CD1 on NF-κB.
  • Individual over-expression of CD1 or RAC3 enhanced cell proliferation, while simultaneous over-expression inhibited it.
  • RAC3 and CD1 expression patterns are cell-cycle regulated with distinct peaks.

Conclusions:

  • The relative amounts and expression timing of CD1 and RAC3 are critical in modulating tumor cell proliferation.
  • These oncogenes can influence the balance of tumor growth in response to external signals.