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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.
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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...
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Mechanisms of Retrovirus-induced Cancers

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In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
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Published on: July 23, 2010

Papillomavirus E6 and E7 proteins and their cellular targets.

Trisha M Wise-Draper1, Susanne I Wells

  • 1Division of Hematology/Oncology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center and The University of Cincinnati College of Medicine, Cincinnati, Ohio 45229, USA.

Frontiers in Bioscience : a Journal and Virtual Library
|November 6, 2007
PubMed
Summary

High-risk human papillomaviruses (HPVs) cause cancers by expressing E6 and E7 oncogenes. These proteins interact with cellular targets to drive cell cycle dysregulation and promote carcinogenesis.

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

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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

Area of Science:

  • Oncology
  • Virology
  • Cell Biology

Background:

  • Mucosal human papillomaviruses (HPVs) infect epithelial cells, causing benign to malignant lesions.
  • HPV-associated malignancies include cervical, anogenital, and some head and neck cancers.
  • High-risk HPVs mediate carcinogenesis, while low-risk types cause benign lesions.

Purpose of the Study:

  • To summarize current insights into the interactions of HPV E6 and E7 oncogenes with cellular targets.
  • To elucidate how these interactions stimulate viral life cycle, disrupt cell cycle control, and promote cancer development.

Main Methods:

  • Review of existing literature on HPV oncogene function and cellular interactions.
  • Analysis of the mechanisms by which E6 and E7 proteins interfere with tumor suppressor pathways.

Main Results:

  • Expression of high-risk HPV E6 and E7 oncogenes is sufficient for keratinocyte immortalization and cancer initiation.
  • E6 and E7 proteins lack intrinsic enzymatic activity but function via interactions with cellular proteins, including tumor suppressors.
  • High levels of E6/E7 are a hallmark of HPV-positive cancers, indicating their role as key transformation stimuli.

Conclusions:

  • HPV E6 and E7 proteins are critical viral-derived drivers of HPV-mediated carcinogenesis.
  • Understanding E6/E7 interactions with cellular proteins is crucial for developing targeted cancer therapies.