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Related Concept Videos

Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Epigenetic Regulation01:37

Epigenetic Regulation

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...
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Histone Modification02:32

Histone Modification

The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone deacetylase,...
Histone Modification02:32

Histone Modification

The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone deacetylase,...
CRISPR01:59

CRISPR

Genome editing technologies allow scientists to modify an organism’s DNA via the addition, removal, or rearrangement of genetic material at specific genomic locations. These types of techniques could potentially be used to cure genetic disorders such as hemophilia and sickle cell anemia. One popular and widely used DNA-editing research tool that could lead to safe and effective cures for genetic disorders is the CRISPR-Cas9 system. CRISPR-Cas9 stands for Clustered Regularly Interspaced Short...

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Updated: May 10, 2026

Epigenetic Engineering of K562 Cells: Dual-Vector Episomal Strategy for Stable Targeted DNA Methylation using dCas9-DNMT3A and -HDAC1 Fusion Proteins
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Succinate: a new epigenetic hacker.

Ming Yang1, Patrick J Pollard

  • 1Cancer Biology and Metabolism Group, Nuffield Department of Medicine, Henry Wellcome Building for Molecular Physiology, University of Oxford, Oxford OX3 7BN, UK.

Cancer Cell
|June 15, 2013
PubMed
Summary
This summary is machine-generated.

Succinate dehydrogenase gene mutations cause DNA hypermethylation in paragangliomas. This epigenetic silencing affects neuroendocrine differentiation by inhibiting key demethylase enzymes.

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CRISPR Epigenome Editing in Human Cells using Plasmid DNA Transfection and mRNA Nucleofection Delivery

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Area of Science:

  • Oncology
  • Epigenetics
  • Biochemistry

Background:

  • Epigenetic reprogramming is a hallmark of human cancers.
  • Paragangliomas are rare tumors that can arise from specific nerve cells.

Purpose of the Study:

  • To investigate the role of DNA hypermethylation in paragangliomas with succinate dehydrogenase (SDH) gene mutations.
  • To understand the molecular mechanisms linking SDH mutations to epigenetic alterations and tumor development.

Main Methods:

  • Analysis of DNA methylation patterns in paragangliomas.
  • Investigation of succinate accumulation and its effect on demethylase activity.
  • Assessment of neuroendocrine differentiation markers.

Main Results:

  • SDH-mutated paragangliomas exhibit widespread DNA hypermethylation.
  • Succinate accumulation due to SDH mutations inhibits 2-oxoglutarate-dependent histone and DNA demethylases.
  • Epigenetic silencing mediated by demethylase inhibition impacts neuroendocrine differentiation.

Conclusions:

  • Succinate accumulation is a key driver of epigenetic alterations in SDH-mutated paragangliomas.
  • Inhibition of demethylase activity leads to aberrant gene silencing and affects tumor cell differentiation.
  • Targeting epigenetic pathways may offer therapeutic strategies for these tumors.