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Related Concept Videos

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,...
Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

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.
Compact chromatin makes reprogramming difficult. Enzymes, such as histone demethylases and acetyltransferases, are often added during reprogramming to loosen the chromatin, making the DNA more accessible to transcription factors. Molecules that inhibit histone...
Spreading of Chromatin Modifications02:25

Spreading of Chromatin Modifications

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.
Writers
The writer is an enzyme that can...
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...

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Related Experiment Video

Updated: Jul 19, 2026

Assessing Cardiomyocyte Subtypes Following Transcription Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts
09:29

Assessing Cardiomyocyte Subtypes Following Transcription Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts

Published on: March 22, 2017

Multiple chromatin modifications important for gene expression changes in cardiac hypertrophy.

A J Bingham1, L Ooi, I C Wood

  • 1Institute of Membrane and Systems Biology, University of Leeds, Leeds LS2 9JT, UK.

Biochemical Society Transactions
|November 1, 2006
PubMed
Summary

Cardiac hypertrophy, an enlargement of heart muscle cells, can lead to heart failure. Researchers identified the transcription factor REST as a key repressor of genes reactivated during this condition.

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Epigenetic Regulation of Cardiac Differentiation of Embryonic Stem Cells and Tissues
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Epigenetic Regulation of Cardiac Differentiation of Embryonic Stem Cells and Tissues

Published on: June 3, 2016

Quantitative Analysis of Chromatin Proteomes in Disease
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Quantitative Analysis of Chromatin Proteomes in Disease

Published on: December 28, 2012

Related Experiment Videos

Last Updated: Jul 19, 2026

Assessing Cardiomyocyte Subtypes Following Transcription Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts
09:29

Assessing Cardiomyocyte Subtypes Following Transcription Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts

Published on: March 22, 2017

Epigenetic Regulation of Cardiac Differentiation of Embryonic Stem Cells and Tissues
13:03

Epigenetic Regulation of Cardiac Differentiation of Embryonic Stem Cells and Tissues

Published on: June 3, 2016

Quantitative Analysis of Chromatin Proteomes in Disease
08:11

Quantitative Analysis of Chromatin Proteomes in Disease

Published on: December 28, 2012

Area of Science:

  • Cardiology
  • Molecular Biology
  • Gene Regulation

Background:

  • Cardiac hypertrophy involves myocyte growth due to increased heart workload.
  • Excessive cardiac hypertrophy is linked to heart failure.
  • Hypertrophy is characterized by the re-expression of fetal genes.

Purpose of the Study:

  • To elucidate the mechanisms behind fetal gene re-expression in cardiac hypertrophy.
  • To identify key regulatory factors involved in hypertrophic gene expression.

Main Methods:

  • Investigated gene expression changes in cardiac hypertrophy.
  • Focused on the role of transcription factors in regulating hypertrophic genes.

Main Results:

  • Identified the transcription factor REST (repressor element 1-silencing transcription factor) as a crucial repressor.
  • REST plays a significant role in silencing genes during normal cardiac function that are reactivated in hypertrophy.

Conclusions:

  • REST is a key molecular player in preventing the pathological re-expression of fetal genes during cardiac hypertrophy.
  • Understanding REST's function may offer therapeutic targets for heart failure related to hypertrophy.