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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

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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.
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Epigenetic Regulation01:46

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

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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
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Chromatin Modification in iPS Cells01:32

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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
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Spreading of Chromatin Modifications02:25

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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
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Genomic Imprinting and Inheritance02:30

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Diploid organisms inherit genetic material through chromosomes from both parents. Copies of the same gene are known as alleles. In most cases, both alleles are simultaneously expressed and allow various cellular processes to function optimally. If one of the alleles is missing or mutated, the expression of the other allele can compensate; however, this is not true for all genes.
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Related Experiment Video

Updated: Apr 11, 2026

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
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Dynamic changes in DNA methylation in ischemic tolerance.

Robert Meller1, Andrea Pearson1, Roger P Simon2

  • 1Translational Stroke Program, Neuroscience Institute, Morehouse School of Medicine , Atlanta, GA , USA.

Frontiers in Neurology
|June 2, 2015
PubMed
Summary
This summary is machine-generated.

Investigating DNA methylation in neuronal cultures reveals dynamic changes following ischemic conditions. These epigenetic alterations may offer new therapeutic targets for neuroprotection against stroke.

Keywords:
ChIP-seqDNA methylationischemiaischemic tolerancepreconditioningstroke

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Area of Science:

  • Neuroscience
  • Epigenetics
  • Molecular Biology

Background:

  • Epigenetic mechanisms, such as DNA methylation, are crucial for regulating gene expression.
  • Understanding how these mechanisms respond to ischemic events is vital for developing neuroprotective strategies.
  • Ischemic tolerance models provide insights into cellular responses to reduced blood flow.

Purpose of the Study:

  • To investigate the dynamic patterns of DNA methylation in neuronal cultures subjected to ischemic conditions.
  • To identify specific genomic regions and chromosomal locations affected by DNA methylation changes during ischemic preconditioning and tolerance.

Main Methods:

  • Utilized methyl-DNA enrichment and ChIP-sequencing (ChIP-seq) to profile DNA methylation patterns.
  • Employed an established in vitro model of ischemic tolerance using oxygen and glucose deprivation (OGD) in neuronal cultures.
  • Analyzed global and regional DNA methylation changes at various time points following different ischemic insults.

Main Results:

  • Observed a significant decrease in global DNA methylation across all tested ischemic conditions (preconditioning, harmful ischemia, and ischemic tolerance).
  • Identified a smaller subset of hypermethylated regions, with distinct chromosomal localization and concentration on specific genomic areas.
  • Demonstrated highly dynamic temporal profiles of both DNA hypomethylation and hypermethylation in response to ischemia.

Conclusions:

  • The study reveals dynamic and widespread changes in DNA methylation in neurons following ischemic insults.
  • These dynamic epigenetic alterations highlight potential novel therapeutic targets for neuroprotection.
  • Further research into these methylation patterns could lead to strategies to mitigate neuronal damage from stroke.