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Identification of an allosteric binding site on the transcription factor p53 using a phage-displayed peptide library

M W Ravera1, J Cárcamo, R Brissette

  • 1DGI BioTechnologies, Edison, New Jersey 08818, USA.

Oncogene
|May 20, 1998
PubMed

Insights

Monoclonal antibody PAb1620 inhibits the transcription factor p53

Area of Science:

  • Molecular Biology
  • Immunology
  • Cancer Research

Background:

  • The transcription factor p53 plays a critical role in cellular responses to stress.
  • Monoclonal antibody PAb1620 targets a specific epitope on p53.
  • Understanding antibody-protein interactions is key to developing targeted therapies.

Purpose of the Study:

  • To identify the precise binding site of monoclonal antibody PAb1620 on the p53 protein.
  • To elucidate the mechanism by which PAb1620 inhibits p53's DNA binding activity.

Main Methods:

  • Utilized a large phage-displayed peptide library (1.5 x 10^10 members) for screening.
  • Employed panning techniques to isolate peptides binding to PAb1620.
  • Analyzed sequence identities between selected peptides and p53 to map the epitope.

Main Results:

  • Identified three unique peptides with significant sequence homology to p53.
  • Localized the PAb1620 binding site to amino acids 106-113 and 146-156 of p53.
  • Proposed an allosteric inhibition mechanism involving indirect interaction with the p53 L1 loop.

Conclusions:

  • Monoclonal antibody PAb1620 binds to a conformational epitope on p53, encompassing residues 106-113 and 146-156.
  • PAb1620 allosterically inhibits p53 DNA binding through an indirect mechanism affecting the L1 loop.
  • These findings provide insights into p53 regulation and potential therapeutic strategies.

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