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Related Concept Videos

Duplication of Chromatin Structure02:05

Duplication of Chromatin Structure

The process of chromosome duplication during cell division requires genome-wide disruption and re-assembly of chromatin. The chromatin structure must be accurately inherited, reassembled, and maintained in the daughter cells to ensure lineage propagation.
The basic unit of the chromatin is the nucleosome, consisting of DNA wrapped around octameric histone proteins and short stretches of linker DNA separating individual nucleosomes. The histone proteins within the nucleosome have their...
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...
Inheritance of Chromatin Structures03:17

Inheritance of Chromatin Structures

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 DNA...
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...
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 Immunoprecipitation- ChIP02:36

Chromatin Immunoprecipitation- ChIP

Chromatin immunoprecipitation, or ChIP, is an antibody-based technique used to identify sites on DNA that bind to transcription factors of interest or histone proteins. It also helps determine the type of histone modifications such as acetylation, phosphorylation, or methylation.
Types of ChIP
ChIP can be divided into two types - X-ChIP and N-ChIP. X-ChIP involves in vivo cross-linking of histones and regulatory proteins to DNA, fragmenting the DNA by sonication, and isolating the protein-DNA...

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Related Experiment Video

Updated: Jun 20, 2026

In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
09:20

In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells

Published on: July 23, 2010

Papillomavirus interaction with cellular chromatin.

Jianxin You1

  • 1Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA. jianyou@mail.med.upenn.edu

Biochimica Et Biophysica Acta
|September 30, 2009
PubMed
Summary
This summary is machine-generated.

High-risk human papillomavirus (HPV) hijacks host cell division by attaching to mitotic chromosomes, ensuring its episomes are passed to daughter cells. This viral strategy promotes persistent infection and cervical cancer progression.

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Related Experiment Videos

Last Updated: Jun 20, 2026

In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
09:20

In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells

Published on: July 23, 2010

A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions
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A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions

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Chromatin Extraction from Frozen Chimeric Liver Tissue for Chromatin Immunoprecipitation Analysis
09:26

Chromatin Extraction from Frozen Chimeric Liver Tissue for Chromatin Immunoprecipitation Analysis

Published on: March 23, 2021

Area of Science:

  • Molecular Biology
  • Virology
  • Cancer Research

Background:

  • High-risk human papillomavirus (HPV) is the leading cause of cervical cancer.
  • Persistent HPV infection relies on maintaining viral genomes as episomes that replicate with host DNA.
  • The HPV life cycle is intrinsically linked to the differentiation of host squamous epithelium.

Purpose of the Study:

  • To review the role of host chromatin in the papillomavirus life cycle.
  • To examine how HPV subverts host chromatin for viral propagation and malignant progression.
  • To explore HPV-host chromatin interactions for insights into viral mechanisms and chromatin regulation.

Main Methods:

  • Literature review of existing studies on HPV and host chromatin interactions.
  • Analysis of viral strategies for episome maintenance and replication.
  • Examination of chromatin remodeling factors in HPV infection and pathogenesis.

Main Results:

  • Papillomaviruses use host mitotic chromosomes for episome transmission during cell division.
  • HPV subverts host chromatin-remodeling factors to enhance viral transcription and genome propagation.
  • Association with host chromatin creates a cellular environment favoring viral survival and cancer development.

Conclusions:

  • Understanding HPV-host chromatin interactions is crucial for deciphering the viral life cycle and chromatin regulation.
  • This interaction provides a model for studying other episomal DNA tumor viruses.
  • Targeting these interactions may offer novel therapeutic strategies for HPV-induced cancers.