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Related Concept Videos

Histone Modification02:32

Histone Modification

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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
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone...
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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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Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3...
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Inheritance of Chromatin Structures03:17

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Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying...
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Heterochromatin02:38

Heterochromatin

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The extent of chromatin compaction can be studied by staining chromatin using specific DNA binding dyes. Under the microscope, the dense-compacted regions that take up more dye are called heterochromatin. Heterochromatin is further classified into two forms – constitutive heterochromatin and facultative heterochromatin.
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Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
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IDH1, Histone Methylation, and So Forth.

Virginie Penard-Lacronique1, Olivier A Bernard1

  • 1INSERM U1170, 94805 Villejuif, France; Equipe Labellisée Ligue Nationale Contre le Cancer, Paris, France; Université Paris Sud, Université Paris-Saclay, 94720 Le Kremlin-Bicêtre, France; Gustave Roussy, Université Paris-Saclay, 94805 Villejuif, France.

Cancer Cell
|August 10, 2016
PubMed
Summary
This summary is machine-generated.

Isocitrate dehydrogenase (IDH) mutations alter cell methylation, driving cancers. A new study reveals IDH1 mutations may reduce Atm expression by inhibiting H3K9 demethylases, a potential early step in cancer development.

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Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Isocitrate dehydrogenase (IDH) mutations are linked to various hematological and neuronal malignancies.
  • These mutations are known to cause abnormal DNA and histone methylation patterns.
  • Aberrant epigenetic modifications are critical drivers of cancer development.

Purpose of the Study:

  • To investigate the specific molecular mechanisms by which IDH mutations contribute to cellular transformation.
  • To explore the potential link between IDH1 mutations and the regulation of Atm expression.
  • To identify early molecular events in oncogenesis driven by IDH mutations.

Main Methods:

  • Analysis of IDH mutant cell lines and patient samples.
  • Assays to measure DNA and histone methylation.
  • Investigation of histone demethylase activity and H3K9 methylation levels.
  • Quantitative analysis of Atm gene and protein expression.

Main Results:

  • IDH1 mutations were found to significantly reduce Atm expression.
  • This reduction in Atm expression was correlated with the inhibition of H3K9 demethylases.
  • The study suggests a direct mechanistic link between IDH1 mutations and decreased Atm levels.
  • Epigenetic alterations mediated by IDH1 mutations impact key tumor suppressor pathways.

Conclusions:

  • IDH1 mutations may initiate cellular transformation by reducing Atm expression through H3K9 demethylase inhibition.
  • This finding provides a potential molecular explanation for the oncogenic role of IDH1 mutations.
  • Targeting this pathway could offer new therapeutic strategies for IDH-mutant cancers.