Extracellular processing of amphoterin generates a peptide active on erythroleukaemia cell differentiation

Biochem J. 2001 Jul 15;357(Pt 2):569-74. doi: 10.1042/0264-6021:3570569.

Abstract

The release of amphoterin by murine erythroleukaemia cells exposed to the chemical inducer hexamethylenebisacetamide represents an essential step for the process of their terminal differentiation. Once exported in the culture medium, amphoterin undergoes limited proteolysis, catalysed by a serine proteinase also secreted by stimulated cells. The isolated proteinase is responsible for degradation of amphoterin, with the production of a 10-amino-acid-residue fragment, specifically retaining the cell-differentiation-stimulating activity of the native protein molecule. This peptide does not express other properties of amphoterin, such as protein kinase C-stimulating activity or systemic toxicity. These findings define a selective mechanism accounting for extracellular amphoterin functional maturation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomarkers, Tumor / metabolism
  • Carrier Proteins / metabolism*
  • Cations, Divalent / pharmacology
  • Cell Differentiation / drug effects*
  • HMGB1 Protein
  • High Mobility Group Proteins / metabolism*
  • Kinetics
  • Leukemia, Erythroblastic, Acute
  • Metals / pharmacology
  • Mice
  • Peptide Fragments / metabolism*
  • Peptide Fragments / pharmacology*
  • Protease Inhibitors / pharmacology
  • Protein Kinase C / metabolism
  • Recombinant Proteins / metabolism
  • Tumor Cells, Cultured

Substances

  • Biomarkers, Tumor
  • Carrier Proteins
  • Cations, Divalent
  • HMGB1 Protein
  • High Mobility Group Proteins
  • Metals
  • Peptide Fragments
  • Protease Inhibitors
  • Recombinant Proteins
  • Protein Kinase C