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Related Concept Videos

Enzyme Inhibition01:30

Enzyme Inhibition

Inhibitors are molecules that reduce enzyme activity by binding to the enzyme. In a normally functioning cell, enzymes are regulated by a variety of inhibitors. Drugs and other toxins can also inhibit enzymes. Some inhibitors bind to the enzyme’s active site, while others inhibit enzymatic activity by binding to other sites on the protein structure.
Indirect-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:29

Indirect-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship

Indirect-acting cholinergic agonists are agents that interact with the acetylcholinesterase enzyme in the synaptic cleft, preventing the breakdown of acetylcholine into choline and acetate. Consequently, the concentration of acetylcholine in the synaptic cleft increases. These agonists can be classified into reversible and irreversible inhibitors based on their duration of action.
Reversible inhibitors display short to medium durations of action. Short-acting agents include simple alcohols with...
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...
Feedback Inhibition00:46

Feedback Inhibition

Biochemical reactions are occurring constantly in cells, converting starting substances to different products, usually with the help of enzymes that speed the reactions. Without enzymes, it would take far too long for most reactions to occur to be useful to the cell!
Indirect-Acting Cholinergic Agonists: Mechanism of Action01:18

Indirect-Acting Cholinergic Agonists: Mechanism of Action

Indirect-acting cholinergic agonists work by interacting with an enzyme called acetylcholinesterase (AChE) in the synaptic cleft. They can be reversible or irreversible inhibitors and have different effects on the enzyme.
Reversible inhibitors like edrophonium bind to a specific part of the enzyme called the anionic catalytic site. They form noncovalent bonds, which means they are not strongly attached to the enzyme. This creates a temporary and less stable enzyme–inhibitor complex, leading to...

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Related Experiment Video

Updated: Jul 13, 2026

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
09:19

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo

Published on: February 6, 2015

Itch inhibition regulates chemosensitivity in vitro.

T M Hansen1, M Rossi, J P Roperch

  • 1Medical Research Council, Toxicology Unit, Hodgkin Building, P.O. Box 138, Leicester University, Lancaster Road, Leicester LE1 9HN, UK.

Biochemical and Biophysical Research Communications
|July 21, 2007
PubMed
Summary

Inhibiting Itch, a protein regulating DNA damage response, enhances cancer drug effectiveness. This finding is particularly relevant for cancers with mutated or absent p53, suggesting Itch as a potential therapeutic target.

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10:24

NMR-Based Activity Assays for Determining Compound Inhibition, IC50 Values, Artifactual Activity, and Whole-Cell Activity of Nucleoside Ribohydrolases

Published on: June 30, 2019

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Biochemistry

Background:

  • Itch is a ubiquitin E3 ligase crucial for managing proteins involved in genotoxic stress response.
  • Itch targets tumor suppressors p73 and p63 for degradation via ubiquitylation.
  • The role of Itch in cancer therapy, especially in p53-deficient tumors, requires further investigation.

Purpose of the Study:

  • To investigate the effect of Itch depletion on apoptosis induced by chemotherapeutic drugs.
  • To determine the significance of Itch levels in cancers with altered p53 status.
  • To explore the therapeutic potential of targeting Itch in cancer treatment.

Main Methods:

  • RNA interference (RNAi) was used to deplete Itch expression.
  • Apoptosis assays were performed on cells treated with chemotherapeutic drugs.
  • Experiments involved both cell lines and fibroblasts from Itch-deficient mice.
  • Reintroduction of Itch was performed in Itch-deficient mouse fibroblasts.

Main Results:

  • Depletion of Itch significantly increased apoptosis in response to chemotherapeutic agents.
  • Cells lacking functional p53 exhibited heightened sensitivity to Itch depletion.
  • Restoring Itch expression in deficient cells reduced cell death following DNA damage.
  • Itch deficiency potentiates the efficacy of chemotherapy drugs.

Conclusions:

  • Itch plays a critical role in regulating cell death pathways following DNA damage.
  • Targeting Itch could enhance the effectiveness of current chemotherapeutic strategies, particularly in p53-mutated cancers.
  • Inhibition of Itch presents a promising pharmacological approach for cancer therapy.