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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein.
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

Phase II biotransformation reactions are essential for detoxifying and eliminating xenobiotics, including many pharmaceutical compounds. These reactions typically involve conjugation, the covalent attachment of polar endogenous groups such as glucuronic acid, sulfate, methyl, or acetyl moieties to functional groups introduced during Phase I metabolism. The resulting conjugates are more water-soluble, enabling efficient renal or biliary excretion.The major classes of Phase II enzymes include...
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Drug Metabolism: Phase II Reactions

Phase II reactions are essential for the detoxification and elimination of drugs from the body. These reactions involve the conjugation of parent drugs or their phase I metabolites with endogenous molecules, resulting in more hydrophilic drug conjugates. The primary conjugation reactions in this phase are sulfation and glucuronidation. Both sulfation and glucuronidation typically produce biologically inactive metabolites. However, in some cases involving prodrugs, active metabolites may be...

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Related Experiment Video

Updated: May 7, 2026

Resin-Assisted Capture Coupled with Isobaric Tandem Mass Tag Labeling for Multiplexed Quantification of Protein Thiol Oxidation
07:16

Resin-Assisted Capture Coupled with Isobaric Tandem Mass Tag Labeling for Multiplexed Quantification of Protein Thiol Oxidation

Published on: June 21, 2021

USP2a alters chemotherapeutic response by modulating redox.

B Benassi1, M Marani, M Loda

  • 1Unit of Radiation Biology and Human Health, ENEA-Casaccia, Rome, Italy.

Cell Death & Disease
|September 28, 2013
PubMed
Summary

The ubiquitin-specific protease 2a (USP2a) enzyme promotes chemoresistance in prostate cancer cells by increasing glutathione levels, which reduces oxidative stress and prevents apoptosis. Targeting c-Myc or miR-34b/c may reverse this drug resistance.

Related Experiment Videos

Last Updated: May 7, 2026

Resin-Assisted Capture Coupled with Isobaric Tandem Mass Tag Labeling for Multiplexed Quantification of Protein Thiol Oxidation
07:16

Resin-Assisted Capture Coupled with Isobaric Tandem Mass Tag Labeling for Multiplexed Quantification of Protein Thiol Oxidation

Published on: June 21, 2021

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Altered ubiquitination is a hallmark of cancer cells.
  • USP2a, a deubiquitinating enzyme, is overexpressed in prostate cancer and acts as an oncogene.
  • USP2a targets c-Myc through the miR-34b/c cluster, contributing to its oncogenic functions.

Purpose of the Study:

  • To investigate the role of USP2a in conferring drug resistance in prostate cancer cells.
  • To elucidate the molecular mechanisms by which USP2a mediates chemoresistance, focusing on oxidative stress and apoptosis.

Main Methods:

  • Overexpression of USP2a in immortalized and transformed prostate cells.
  • Treatment with chemotherapeutic agents (cisplatin, doxorubicin, taxanes).
  • Measurement of reactive oxygen species (ROS) production, mitochondrial membrane potential (ΔΨ), and apoptosis.
  • Assessment of glutathione (GSH) levels and c-Myc/miR-34b/c expression.

Main Results:

  • USP2a overexpression confers resistance to cisplatin, doxorubicin, and taxanes.
  • USP2a reduces drug-induced oxidative stress by decreasing ROS production and stabilizing mitochondrial membrane potential.
  • USP2a inhibits p38 activation and apoptosis.
  • USP2a increases intracellular GSH content via miR-34b/c-mediated c-Myc regulation, thereby interfering with oxidative stress cascades.

Conclusions:

  • USP2a plays a critical role in promoting chemoresistance in prostate cancer.
  • USP2a confers resistance by enhancing the antioxidant capacity through the GSH/c-Myc/miR-34b/c pathway.
  • Targeting c-Myc and/or miR-34b/c represents a potential strategy to overcome USP2a-mediated chemoresistance.