Related Experiment Video

Updated: Jul 19, 2026

Inducible and Reversible Dominant-negative (DN) Protein Inhibition
08:35

Inducible and Reversible Dominant-negative (DN) Protein Inhibition

Published on: January 7, 2019

Expression of the Nd1 gene is down-regulated by doxorubicin at post-transcriptional level

Yasuyuki Takamori1, Yuji Matsudo, Lisa Fujimura

  • 1Departments of Developmental Genetics (H2), Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.

International Journal of Molecular Medicine
|October 4, 2006
PubMed

Insights

Doxorubicin chemotherapy reduces Nd1 gene expression in various organs and cell types. This suggests doxorubicin may decrease Nd1 mRNA stability, impacting protein levels.

Area of Science:

  • Molecular Biology
  • Pharmacology
  • Cardiology

Background:

  • Doxorubicin is a key anti-neoplastic agent.
  • Cardiotoxicity is a significant side effect of doxorubicin treatment.
  • Previous studies linked doxorubicin to decreased Nd1 gene expression in the heart.

Purpose of the Study:

  • To investigate the effect of doxorubicin on Nd1 expression across different organs and cell types.
  • To explore the mechanism behind doxorubicin-induced reduction in Nd1 mRNA levels.

Main Methods:

  • Administered doxorubicin to mice and cultured cell lines (NIH3T3).
  • Analyzed Nd1 gene and mRNA expression in various tissues and cells.
  • Utilized Nd1-transgenic mice and Nd1-transfectants.
  • Assessed the impact of cycloheximide on doxorubicin-induced Nd1 mRNA reduction.

Main Results:

  • Doxorubicin treatment reduced Nd1 expression in multiple organs and cultured cells.
  • Exogenous Nd1 mRNA levels were also decreased in transgenic models.
  • Cycloheximide treatment inhibited the doxorubicin-induced reduction of Nd1 mRNA in NIH3T3 cells.

Conclusions:

  • Doxorubicin treatment broadly impacts Nd1 expression beyond the heart.
  • The findings suggest doxorubicin specifically reduces Nd1 mRNA stability.
  • This mechanism may contribute to doxorubicin's side effects.

More Related Videos

Establishing Cell Lines Overexpressing DR3 to Assess the Apoptotic Response to Anti-mitotic Therapeutics12:28

Establishing Cell Lines Overexpressing DR3 to Assess the Apoptotic Response to Anti-mitotic Therapeutics

Published on: January 11, 2019

Related Concept Videos

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

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...
What is Gene Expression?01:36

What is Gene Expression?

A gene is a stretch of DNA that serves as the blueprint for functional RNAs and proteins. Since DNA is comprised  of nucleotides and proteins are comprised of amino acids, a mediator is required to convert the information encoded in DNA into proteins. This mediator is the messenger RNA (mRNA). mRNA copies the blueprint from DNA by a process called transcription. In eukaryotes, transcription occurs in the nucleus by complementary base-pairing with the DNA template. The mRNA is then processed and...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR activation may...