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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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Eukaryotic Transcription Inhibitors01:52

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Certain biochemical processes, such as embryonic development and cell growth regulation, depend on the repression of specific genes. DNA binding proteins known as eukaryotic transcription inhibitors regulate the repression of gene expression in eukaryotes. The presence of these inhibitors at the required location and time in the cell is triggered by the presence of hormones and additional signals from other cells.
Eukaryotic transcription inhibitors usually contain two distinct domains, a...
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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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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.
Constitutive heterochromatin: It is a highly compact region of chromatin that is mostly concentrated in the centromere and telomere. Unlike euchromatin, the amino acid at...
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Spreading of Chromatin Modifications

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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.
Writers
The writer...
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Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

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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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GATA-3-dependent Gene Transcription is Impaired upon HDAC Inhibition.

Xiangrong Geng1, Chenguang Wang1, Suhaib Abdelrahman1

  • 1Department of Internal Medicine, Division of Hematology and Oncology, University of Michigan, Ann Arbor, Michigan.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|January 2, 2024
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Histone deacetylase inhibitors (HDACi) reprogram T-cell lymphoma by increasing GATA-3 acetylation, impairing its DNA binding and gene regulation. This mechanism offers new therapeutic strategies for GATA-3-driven lymphomas.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Cutaneous T-cell lymphoma (CTCL) often shows poor response to chemotherapy.
  • The transcription factor GATA-3 is oncogenic and highly expressed in T-cell neoplasms.
  • GATA-3 function is regulated by posttranslational acetylation.

Purpose of the Study:

  • To investigate how histone deacetylase inhibitors (HDACi) affect the transcriptional landscape in CTCL.
  • To understand the role of GATA-3 acetylation in HDACi treatment response.

Main Methods:

  • Chromatin immunoprecipitation sequencing (ChIP-seq) and RNA sequencing were integrated.
  • Analyses were performed on CTCL cell line models and primary CTCL specimens.
  • Samples were treated with clinically available HDACi.

Main Results:

  • HDACi treatment caused significant transcriptional reprogramming in CTCL.
  • Increased GATA-3 acetylation was observed upon HDACi exposure.
  • HDACi-induced GATA-3 acetylation impaired DNA binding and target gene regulation.

Conclusions:

  • HDACi attenuate the transcriptional landscape in CTCL by targeting GATA-3 acetylation.
  • Findings elucidate the mechanism of action for HDACi in CTCL.
  • Results support the use of HDACi in GATA-3-driven lymphoproliferative neoplasms.