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Related Experiment Videos

Relationship between E1A binding to cellular proteins, c-myc activation and S-phase induction.

S Baluchamy1, N Sankar, A Navaraj

  • 1Department of Microbiology-Immunology Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.

Oncogene
|July 25, 2006
PubMed
Summary

Adenovirus E1A protein disrupts cell cycle by interacting with host proteins like p300 and retinoblastoma protein (pRb). This interaction leads to c-myc activation and S-phase entry, potentially causing cell transformation.

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Area of Science:

  • Cell biology
  • Molecular oncology
  • Virology

Background:

  • p300/CREB-binding protein (CBP) maintains G0/G1 cell cycle arrest by repressing c-myc.
  • Adenovirus E1A oncoprotein induces c-myc and S-phase entry in a p300-dependent manner.
  • E1A's S-phase induction relies on its ability to bind and inactivate host proteins, including p300/CBP.

Purpose of the Study:

  • To investigate the correlation between host protein binding to E1A's N-terminal region, c-myc activation, and S-phase induction.
  • To elucidate the roles of specific chromatin-associated proteins (pRb, p300, p400, PCAF) in E1A-mediated cellular changes.

Main Methods:

  • Infection of quiescent human cells with adenovirus (Ad) N-terminal E1A mutants.
  • Assaying c-myc and S-phase induction.

Related Experiment Videos

  • Mutational analysis of E1A to specifically disrupt binding to pRb, p300, p400, and PCAF.

    • Main Results:

    • E1A mutants unable to bind p300 or pRb showed severe defects in c-myc and S-phase induction.
    • Impaired binding of E1A to p400 moderately affected c-myc and S-phase induction.
    • Analysis suggested PCAF also plays a role in c-myc repression, potentially independent of p300.

    Conclusions:

    • E1A deregulates c-myc expression through interactions with chromatin-associated proteins like p300 and pRb.
    • These interactions are crucial for E1A-mediated cell cycle deregulation.
    • E1A's disruption of host protein interactions may contribute to viral-induced cell transformation.