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Dissection of the ATP-binding domain of the chaperone hsc70 for interaction with the cofactor Hap46

G Petersen1, C Hahn, U Gehring

  • 1Institut für Molekulare Genetik, Im Neuenheimer Feld 230 and Biochemie-Zentrum Heidelberg, Biologische Chemie, Im Neuenheimer Feld 501, Universität Heidelberg, D-69120 Heidelberg, Germany. gabi@sirius.mgen.uni-heldelberg.de

Insights

Hap46 (BAG-1) interacts with the ATP-binding domain of heat shock protein 70 (hsp70) and hsc70, influencing their chaperone functions. This study identifies key contact sites on hsp70/hsc70 involved in this crucial molecular interaction.

Area of Science:

  • Molecular Biology
  • Protein Interactions
  • Chaperone Proteins

Background:

  • Mammalian hsp70 chaperone proteins are involved in various cellular processes.
  • Hap46 (BAG-1) is a protein that interacts with hsp70/hsc70 independently of the substrate-binding site.
  • This interaction affects the nucleotide-binding and protein-folding properties of hsp70/hsc70.

Purpose of the Study:

  • To identify the specific contact sites on hsp70/hsc70 involved in the interaction with Hap46.
  • To understand how Hap46 binding influences the conformation of the hsp70/hsc70 ATP-binding domain.

Main Methods:

  • Screening of membrane-bound peptide libraries based on the ATP-binding domain sequence of hsp70/hsc70.
  • Phage-display technique using random dodecapeptides to identify interaction regions.
  • Analysis of identified contact sites on a space-filling model of hsc70.

Main Results:

  • Both peptide library screening and phage display identified partially overlapping contact regions.
  • Two major contact areas for Hap46 were delineated on the hsc70 molecule.
  • These regions are located on either subdomain bordering the nucleotide-binding cleft.

Conclusions:

  • The interaction of Hap46 with hsp70/hsc70 involves specific contact sites on the ATP-binding domain.
  • These binding sites bridge the subdomains around the nucleotide-binding cleft.
  • This interaction likely alters the conformation of the ATP-binding domain, similar to GrpE's effect on DnaK.

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