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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.
X-chromosome...
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Epigenetic Regulation01:46

Epigenetic Regulation

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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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Related Experiment Video

Updated: Nov 25, 2025

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
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Epigenetic Analysis in Ewing Sarcoma.

Jeremy M Simon1,2,3, Nicholas C Gomez4

  • 1Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.

Methods in Molecular Biology (Clifton, N.J.)
|December 16, 2020
PubMed
Summary
This summary is machine-generated.

This study details computational methods for analyzing chromatin data in Ewing sarcoma. It provides a pipeline for understanding how the EWSR1-FLI1 fusion protein drives cancer by altering gene expression.

Keywords:
ATAC-SeqBioinformaticsChIP-seqEWSR1-FLI1EpigeneticsEwing sarcomaH3K27acNext-generation sequencing

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Area of Science:

  • Oncology
  • Genomics
  • Computational Biology

Background:

  • Ewing sarcoma is a highly malignant bone tumor driven by specific chromosomal translocations.
  • The EWSR1-FLI1 fusion protein, a common translocation product, alters gene expression by targeting specific genomic loci.
  • Understanding EWSR1-FLI1's chromatin interactions is crucial for deciphering its oncogenic mechanisms.

Purpose of the Study:

  • To provide a detailed protocol for analyzing genome-wide transcription factor binding and chromatin accessibility data in Ewing sarcoma.
  • To outline computational tools and statistical methods for processing and interpreting ChIP-seq and ATAC-seq data.
  • To establish a framework for molecular biologists to analyze Ewing sarcoma genomic and epigenomic data.

Main Methods:

  • Data quality control and adapter trimming.
  • Reference genome alignment.
  • Identification and annotation of transcription factor binding sites (ChIP-seq) and accessible chromatin regions (ATAC-seq).
  • Motif discovery and data visualization.

Main Results:

  • A comprehensive computational pipeline for analyzing ChIP-seq and ATAC-seq data from Ewing sarcoma cells.
  • Demonstration of data processing steps including alignment, peak calling, and annotation.
  • Provision of real-world data examples for practical application.

Conclusions:

  • The described protocol enables robust analysis of genome-wide chromatin data in Ewing sarcoma.
  • This analytical platform facilitates the interpretation of EWSR1-FLI1's role in oncogenesis.
  • The methodology supports the development of personalized analytical pipelines for cancer research.