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

Epigenetic Regulation01:37

Epigenetic Regulation

3.5K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
3.5K
Epigenetic Regulation01:46

Epigenetic Regulation

28.8K
Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
28.8K
Epigenetic Regulation01:46

Epigenetic Regulation

24.1K
24.1K
Apoptosis01:30

Apoptosis

12.2K
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
12.2K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

6.2K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.2K
Phase II Reactions: Methylation Reactions01:17

Phase II Reactions: Methylation Reactions

921
Methylation is a phase II biotransformation process involving the attachment of a methyl group to a substrate. Enzymes known as methyltransferases orchestrate this reaction.
The mechanism of methylation unfolds in two stages. The first stage sees a methyltransferase enzyme facilitating the transfer of a methyl group from S-adenosylmethionine (SAM) to the substrate, forming S-adenosylhomocysteine (SAH). The second stage involves further metabolism of SAH into homocysteine, which can be recycled...
921

You might also read

Related Articles

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

Sort by
Same author

Inhibiting biofilm growth on ammonium salt-functionalized or fluorinated voice prostheses silicone.

Applied microbiology and biotechnology·2026
Same author

Correction: The potent human CAR activator CITCO is a non-genotoxic hepatic tumour-promoting agent in humanised constitutive androstane receptor mice but not in wild-type animals.

Archives of toxicology·2026
Same author

Assessment of biofilm growth on voice prostheses using a tracheoesophageal fistula simulator.

Otolaryngologia polska = The Polish otolaryngology·2026
Same author

Multiplexed P21/MCM-2 Detection Predicts Relapse and May Identify Tyrosine Kinase Inhibitor-Resistant Patients in Clear Cell Renal Cell Carcinoma.

Cancer research communications·2026
Same author

Source-dependent temporal toxicity and transcriptomic remodeling by urban ultrafine particles: Megacity - suburban comparison in aging olfactory-brain interface.

The Science of the total environment·2026
Same author

Long-Read Spatial Transcriptomics of Patient-Derived Clear Cell Renal Cell Carcinoma Organoids Identifies Heterogeneity and Transcriptional Remodelling Following NUC-7738 Treatment.

Cancers·2026

Related Experiment Video

Updated: May 6, 2026

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
09:42

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images

Published on: September 7, 2017

10.4K

Apoptosis and DNA methylation.

Huan X Meng1, James A Hackett, Colm Nestor

  • 1MRC Human Genetics Unit, IGMM, Western General Hospital, Edinburgh EH4 2XU, UK. richard.meehan@hgu.mrc.ac.uk.

Cancers
|November 12, 2013
PubMed
Summary
This summary is machine-generated.

Epigenetic alterations in DNA methylation can trigger apoptosis, impacting genome integrity. This study explores links between DNA methyltransferases, methyl-CpG binding proteins, and apoptosis, including the evolutionary origins of MBD4 and TDG.

More Related Videos

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
06:07

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors

Published on: August 5, 2022

2.5K
Immunohistochemical Detection of 5-Methylcytosine and 5-Hydroxymethylcytosine in Developing and Postmitotic Mouse Retina
07:50

Immunohistochemical Detection of 5-Methylcytosine and 5-Hydroxymethylcytosine in Developing and Postmitotic Mouse Retina

Published on: August 29, 2018

10.0K

Related Experiment Videos

Last Updated: May 6, 2026

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
09:42

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images

Published on: September 7, 2017

10.4K
Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
06:07

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors

Published on: August 5, 2022

2.5K
Immunohistochemical Detection of 5-Methylcytosine and 5-Hydroxymethylcytosine in Developing and Postmitotic Mouse Retina
07:50

Immunohistochemical Detection of 5-Methylcytosine and 5-Hydroxymethylcytosine in Developing and Postmitotic Mouse Retina

Published on: August 29, 2018

10.0K

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Genomics

Background:

  • Epigenetic mechanisms, including DNA and histone methylation, are crucial for maintaining gene expression and cellular identity.
  • Dysregulation of methylation patterns is implicated in disease pathology and can activate cell death pathways.
  • Methyl-CpG binding proteins play key roles in interpreting DNA methylation marks.

Purpose of the Study:

  • To investigate the molecular pathways connecting DNA methyltransferases and methyl-CpG binding proteins to apoptosis.
  • To analyze the evolutionary origins of thymine DNA glycosylases MBD4 and TDG, which are specific for G/T mismatches.

Main Methods:

  • Bioinformatic analyses were employed to study the evolutionary history of MBD4 and TDG.
  • Literature review and pathway analysis to connect epigenetic modifiers with apoptotic signaling.

Main Results:

  • Perturbation of DNA and histone methylation patterns can lead to the activation of apoptotic pathways.
  • Bioinformatic analysis provides insights into the evolutionary trajectory of MBD4 and TDG.
  • Identified links between epigenetic regulation, DNA repair, and programmed cell death.

Conclusions:

  • Epigenetic dysregulation, particularly in methylation, is a significant factor in initiating apoptosis and compromising genome stability.
  • Understanding the evolution of DNA glycosylases like MBD4 and TDG offers insights into their roles in maintaining genome integrity.
  • Further research into these pathways could reveal therapeutic targets for diseases involving epigenetic alterations and apoptosis.