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Related Experiment Videos

E1A directly binds and regulates the P/CAF acetyltransferase

J L Reid1, A J Bannister, P Zegerman

  • 1Wellcome/CRC Institute, Department of Pathology, Cambridge University, UK.

The EMBO Journal
|August 4, 1998
PubMed
Summary

The P/CAF protein regulates transcription independently of CBP. Adenovirus E1A protein directly binds P/CAF, inhibiting its activity and highlighting P/CAF's role in cell differentiation.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Virology

Background:

  • P/CAF (p300/CBP-associated factor) is a protein with intrinsic histone acetyltransferase (HAT) activity.
  • P/CAF is known to bind the transcriptional co-activator CBP.

Purpose of the Study:

  • To investigate the transcriptional regulatory role of P/CAF.
  • To determine if P/CAF's transcriptional function is dependent on its interaction with CBP.
  • To examine the interaction between adenovirus E1A protein and P/CAF.

Main Methods:

  • Assessing the transcriptional activation potential of P/CAF's HAT domain in yeast.
  • Measuring P/CAF's ability to stimulate transcription of the RSV promoter in mammalian cells.
  • Investigating the direct binding of adenovirus E1A to P/CAF and its effect on P/CAF's activity.

Related Experiment Videos

  • Mapping the specific residues in E1A involved in P/CAF binding.
  • Main Results:

    • P/CAF regulates transcription independently of its binding to CBP.
    • The HAT domain of P/CAF possesses transcriptional activation potential.
    • Adenovirus E1A directly binds P/CAF, sequestering its transcriptional activity.
    • E1A binding to P/CAF requires specific residues in conserved region 1 and is independent of CBP.

    Conclusions:

    • P/CAF plays a significant role in transcriptional regulation through its HAT activity.
    • Adenovirus E1A directly inhibits P/CAF's transcriptional function, independent of CBP.
    • The direct interaction between E1A and P/CAF suggests a crucial role for P/CAF in cell differentiation processes disrupted by E1A.