Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Initiation of Translation02:33

Initiation of Translation

Initiating translation is complex because it involves multiple molecules. Initiator tRNA, ribosomal subunits, and eukaryotic initiation factors (eIFs) are all required to assemble on the initiation codon of mRNA. This process consists of several steps that are mediated by different eIFs.
First, the initiator tRNA must be selected from the pool of elongator tRNAs by eukaryotic initiation factor 2 (eIF2). The initiator tRNA (Met-tRNAi) has conserved sequence elements including modified bases at...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Differentiation-independent Activation of HPV Genome Replication by the lncRNA DINO.

bioRxiv : the preprint server for biology·2026
Same author

Characterization of patient-derived HPV16 E6 and E7 variant alleles.

Journal of virology·2026
Same author

Inactivation of the RB1 and PTPN14 tumor suppressors cooperatively enables the carcinogenic activity of the human papillomavirus E7 oncoprotein.

bioRxiv : the preprint server for biology·2026
Same author

The HPV101 E7 protein shares host cellular targets and biological activities with high-risk HPV16 E7.

Tumour virus research·2024
Same author

What are the essential determinants of human papillomavirus carcinogenesis?

mBio·2024
Same author

Correction for Rasmussen et al., "Virology-the path forward".

Journal of virology·2024

Related Experiment Video

Updated: Jul 4, 2026

Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
13:41

Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus

Published on: March 8, 2012

Human papillomavirus type 16 E7 oncoprotein associates with E2F6.

Margaret E McLaughlin-Drubin1, Kyung-Won Huh, Karl Münger

  • 1Department of Medicine, Infectious Diseases Division, The Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

Journal of Virology
|June 27, 2008
PubMed
Summary

Human papillomavirus (HPV) E7 protein disrupts E2F6

Area of Science:

  • Molecular biology
  • Virology
  • Cell cycle regulation

Background:

  • Papillomavirus replication is linked to epithelial cell differentiation.
  • Human papillomavirus (HPV) E7 protein drives aberrant cell cycle progression.
  • E2F6 acts as a repressor, slowing S-phase entry.

Purpose of the Study:

  • Investigate HPV E7's interaction with E2F6.
  • Determine if viral oncoproteins can inactivate E2F6's repressive function.
  • Understand the role of E2F6 inactivation in HPV-infected cells.

Main Methods:

  • Co-immunoprecipitation assays to detect protein interactions.
  • Western blotting to assess protein levels and activity.
  • Immunofluorescence staining to visualize protein localization and complex formation.

More Related Videos

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

RNAscope for In situ Detection of Transcriptionally Active Human Papillomavirus in Head and Neck Squamous Cell Carcinoma
10:26

RNAscope for In situ Detection of Transcriptionally Active Human Papillomavirus in Head and Neck Squamous Cell Carcinoma

Published on: March 11, 2014

Related Experiment Videos

Last Updated: Jul 4, 2026

Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
13:41

Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus

Published on: March 8, 2012

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

RNAscope for In situ Detection of Transcriptionally Active Human Papillomavirus in Head and Neck Squamous Cell Carcinoma
10:26

RNAscope for In situ Detection of Transcriptionally Active Human Papillomavirus in Head and Neck Squamous Cell Carcinoma

Published on: March 11, 2014

Main Results:

  • HPV E7 proteins associate with and inactivate E2F6's transcriptional repression.
  • Simian virus 40 T antigen and adenovirus E1A also interact with and inactivate E2F6.
  • E7-expressing cells exhibit reduced E2F6/polycomb complex staining, partly due to E7-E2F6 association.

Conclusions:

  • Viral oncoproteins, including HPV E7, subvert E2F6-mediated cellular defense mechanisms.
  • Inactivation of E2F6 by HPV E7 may lead to prolonged S-phase competence in infected cells.
  • E2F6's role in polycomb complexes and cell fate maintenance is disrupted by viral infection.