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Related Concept Videos

GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
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Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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Amplifying Signals via Enzymatic Cascade

When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze the...
Inhibition of Cdk Activity02:34

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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...
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Anaphase Promoting Complex

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Related Experiment Video

Updated: Jul 6, 2026

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells
08:47

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells

Published on: May 1, 2020

PPARgamma ligands suppress the feedback loop between E2F2 and cyclin-E1.

Yoko Komatsu1, Ichiaki Ito, Mitsutoshi Wayama

  • 1Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba Science City, Ibaraki 305-8572, Japan.

Biochemical and Biophysical Research Communications
|March 22, 2008
PubMed
Summary

The PPARgamma ligand troglitazone halts colon cancer cell cycle progression by downregulating E2F2 and cyclin-E1. This mechanism inhibits the Rb protein pathway, offering a novel therapeutic target for colon cancer.

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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Last Updated: Jul 6, 2026

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Published on: May 1, 2020

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors
10:33

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

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Peroxisome proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor involved in peroxisome proliferation.
  • PPARgamma ligands have been shown to suppress cell cycle progression, but the underlying mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the mechanism by which the PPARgamma ligand troglitazone inhibits cell cycle progression in colon cancer cells.
  • To determine the role of E2F2, cyclin-E1, and Rb protein in troglitazone-induced cell cycle arrest.

Main Methods:

  • LS174T colon cancer cells were treated with troglitazone.
  • Cell cycle progression was analyzed.
  • Gene expression levels of CDK inhibitor (p18), Wnt signaling pathway components, E2F2, and cyclin-E1 were assessed using GeneChip and RT-PCR analyses.

Main Results:

  • Troglitazone inhibited the G1/S transition in LS174T colon cancer cells.
  • Troglitazone did not affect p18 expression or the Wnt signaling pathway.
  • Troglitazone decreased mRNA levels of E2F2 and cyclin-E1, leading to reduced Rb protein phosphorylation and suppression of E2F2 transcriptional activity.

Conclusions:

  • Troglitazone-induced colon cancer cell cycle arrest is mediated by the downregulation of E2F2 and cyclin-E1.
  • The study proposes a mechanism involving the suppression of a feedback loop comprising E2F2, cyclin-E1, and Rb protein.
  • This finding suggests a potential therapeutic strategy for colon cancer targeting the PPARgamma pathway.