Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Phase II Reactions: Acetylation Reactions01:24

Phase II Reactions: Acetylation Reactions

400
Acetylation, a phase II biotransformation reaction, introduces an acetyl group to drugs or their metabolites. Acetyltransferase enzymes facilitate this reaction, which resembles α-amino acid conjugation due to the addition of a functional group to the drug molecule.
The substrates for acetylation are typically drugs or their metabolites with an amino, sulfonamide, or hydrazine functional group. Acetylation can occur at several points in the drug molecule, including primary, secondary, and...
400
Transcription Attenuation in Prokaryotes02:42

Transcription Attenuation in Prokaryotes

16.2K
Transcriptional attenuation occurs when RNA transcription is prematurely terminated due to the formation of a terminator mRNA hairpin structure.  Bacteria use these hairpins to regulate the transcription process and control the synthesis of several amino acids including histidine, lysine, threonine, and phenylalanine. Transcription attenuation takes place in the non-coding regions of mRNA.
There are several different mechanisms used to attenuate transcription. In ribosome mediated...
16.2K
Stringent Response in E. coli01:23

Stringent Response in E. coli

69
Bacterial growth is closely tied to nutrient availability, with cells proliferating exponentially under favorable conditions and entering a stationary phase when resources become scarce. This transition is mediated by a regulatory mechanism known as the stringent response, which allows bacteria to adapt to nutrient deprivation by modulating gene expression and metabolic activity.During nutrient scarcity, intracellular amino acid levels decline. It results in the accumulation of uncharged tRNAs...
69
The Unfolded Protein Response01:37

The Unfolded Protein Response

5.2K
The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
5.2K
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

2.6K
Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
2.6K
RNA Editing02:23

RNA Editing

9.2K
RNA editing is a post-transcriptional modification where a precursor mRNA (pre-mRNA) nucleotide sequence is changed by base insertion, deletion, or modification. The extent of RNA editing varies from a few hundred bases, in mitochondrial DNA of trypanosomes, to a just single base, in nuclear genes of mammals. Even a single base change in the pre-mRNA can convert a codon for one amino acid into the codon for another amino acid or a stop codon. This type of re-coding can significantly affect the...
9.2K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

A phosphorylated variant of the mast/stem cell growth factor receptor KIT is upregulated in dorsal root ganglia of Friedreich ataxia.

Histology and histopathology·2026
Same author

Designing Reversible Photoswitching Azobenzene-Modified Nucleotide for Controlling Biological Function.

Journal of the American Chemical Society·2025
Same author

In Vivo Ribosome-Amplified MetaBOlism, RAMBO, Effect Observed by Real Time Pulse Chase, RTPC, NMR Spectroscopy.

Biochemistry·2025
Same author

Ribosome External Electric Field Regulates Metabolic Enzyme Activity: The RAMBO Effect.

The journal of physical chemistry. B·2024
Same author

Characterization of m6A Modifiers and RNA Modifications in Uterine Fibroids.

Endocrinology·2024
Same author

Characterization of the mIF4G Domains in the RNA Surveillance Protein Upf2p.

Current issues in molecular biology·2024

Related Experiment Video

Updated: Sep 29, 2025

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons
10:50

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons

Published on: April 24, 2021

1.1K

Epitranscriptomic Reprogramming Is Required to Prevent Stress and Damage from Acetaminophen.

Sara Evke1,2, Qishan Lin2,3,4, Juan Andres Melendez1,2

  • 1Nanobioscience Constellation, College of Nanoscale Science and Engineering, SUNY Polytechnic Institute, Albany, NY 12203, USA.

Genes
|March 25, 2022
PubMed
Summary
This summary is machine-generated.

Acetaminophen (APAP) alters RNA modifications, impacting gene regulation. The writer Alkylation Repair Homolog 8 (Alkbh8) is crucial for managing these epitranscriptomic changes and cellular response to APAP toxicity.

Keywords:
Alkbh8RNA modificationacetaminophenepitranscriptomicstress responsetRNA

More Related Videos

Measurements of Physiological Stress Responses in C. Elegans
10:36

Measurements of Physiological Stress Responses in C. Elegans

Published on: May 21, 2020

14.2K
Efficient Transcriptionally Controlled Plasmid Expression System for Investigation of the Stability of mRNA Transcripts in Primary Alveolar Epithelial Cells
10:49

Efficient Transcriptionally Controlled Plasmid Expression System for Investigation of the Stability of mRNA Transcripts in Primary Alveolar Epithelial Cells

Published on: March 6, 2020

6.2K

Related Experiment Videos

Last Updated: Sep 29, 2025

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons
10:50

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons

Published on: April 24, 2021

1.1K
Measurements of Physiological Stress Responses in C. Elegans
10:36

Measurements of Physiological Stress Responses in C. Elegans

Published on: May 21, 2020

14.2K
Efficient Transcriptionally Controlled Plasmid Expression System for Investigation of the Stability of mRNA Transcripts in Primary Alveolar Epithelial Cells
10:49

Efficient Transcriptionally Controlled Plasmid Expression System for Investigation of the Stability of mRNA Transcripts in Primary Alveolar Epithelial Cells

Published on: March 6, 2020

6.2K

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Toxicology

Background:

  • Epitranscriptomic marks regulate gene expression in response to various conditions.
  • The impact of pharmaceutical toxins on the epitranscriptome is largely unknown.
  • Acetaminophen (APAP) is a common drug with known toxic effects.

Purpose of the Study:

  • To investigate how APAP induces epitranscriptomic reprogramming.
  • To define the role of Alkylation Repair Homolog 8 (Alkbh8) in APAP-induced epitranscriptomic changes.
  • To understand the link between epitranscriptomic modifications and APAP toxicity.

Main Methods:

  • Comparison of wildtype and Alkbh8-deficient mouse livers following APAP administration.
  • Analysis of liver damage markers and selenoprotein levels.
  • Profiling of multiple epitranscriptomic marks on tRNAs (transfer RNAs).

Main Results:

  • APAP increased liver toxicity and damage markers while decreasing selenoprotein levels in Alkbh8-deficient mice compared to wildtype.
  • APAP induced widespread changes in liver tRNA epitranscriptome modifications, including mcm5U, i6A, Ψ, and m1A.
  • Alkbh8 deficiency resulted in broad epitranscriptomic dysregulation in response to APAP, indicating its central role.

Conclusions:

  • Alkbh8 is a key regulator of the epitranscriptomic response to APAP toxicity.
  • Epitranscriptomic modifications and translational regulation are critical in cellular responses to APAP.
  • The epitranscriptome plays a significant role in how the body responds to pharmaceutical challenges.