Protein disulfide isomerase mutant lacking its isomerase activity accelerates protein folding in the cell

FEBS Lett. 1995 Dec 27;377(3):505-11. doi: 10.1016/0014-5793(95)01410-1.

Abstract

We investigated the effect of protein disulfide isomerase (PDI) on in vivo protein folding of human lysozyme (h-LZM) in a specially constructed yeast coexpression system. Coexpression with PDI increased the amounts of intracellular h-LZM with the native conformation, leading to an increase in h-LZM secretion. The results indicated that PDI is a real catalyst of protein folding in the cell. The secretion of h-LZM increased even when both active sites of PDI were disrupted, suggesting that the effect of PDI resulted from a function other than the formation of disulfide bonds. This is the first finding that PDI without isomerase activity accelerates protein folding in vivo.

MeSH terms

  • Base Sequence
  • Cloning, Molecular
  • Gene Amplification
  • Genetic Vectors
  • Humans
  • Isomerases / genetics
  • Isomerases / metabolism*
  • Molecular Chaperones / genetics
  • Molecular Chaperones / metabolism*
  • Molecular Sequence Data
  • Muramidase / genetics
  • Muramidase / metabolism*
  • Mutagenesis, Site-Directed
  • Polymerase Chain Reaction
  • Protein Disulfide-Isomerases
  • Protein Folding*
  • Recombinant Proteins / metabolism
  • Saccharomyces cerevisiae / genetics
  • Saccharomyces cerevisiae / metabolism

Substances

  • Molecular Chaperones
  • Recombinant Proteins
  • Muramidase
  • Isomerases
  • Protein Disulfide-Isomerases