Induction of hsp 72/73 by herbimycin A, an inhibitor of transformation by tyrosine kinase oncogenes

Exp Cell Res. 1991 Aug;195(2):338-44. doi: 10.1016/0014-4827(91)90382-5.

Abstract

Herbimycin A, which has been known to inactivate and degrade p60v-src tyrosine kinase, induced an elevated synthesis of a protein with a molecular size of 70 kDa in A431 human epidermoid carcinoma cells. This protein showed the same migration distance on SDS-polyacrylamide gel electrophoresis as that of the protein induced in the cells by heat shock treatment, and this 70-kDa protein was identified as a member of the heat shock protein 70 family (hsp70) through immunoprecipitation with anti-hsp72/73 antibody and partial digestion with V8 protease. The induced level of the 70-kDa protein was dependent on the length of period and the concentration of herbimycin A treatment. Cellular fractionation and indirect immunofluorescence analyses revealed that the 70-kDa protein induced by herbimycin A was localized in the cytoplasm, in contrast to the nuclear distribution of hsp70 induced by heat treatment. Induction of hsp70 by herbimycin A was also observed in several other cells, including HeLa S3 cells, chicken embryo fibroblasts, NIH3T3 cells, and Rous sarcoma virus-transformed NIH3T3 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antibiotics, Antineoplastic / pharmacology*
  • Benzoquinones
  • Cell Transformation, Neoplastic / drug effects
  • Heat-Shock Proteins / biosynthesis*
  • Heat-Shock Proteins / drug effects
  • Humans
  • Kinetics
  • Lactams, Macrocyclic
  • Oncogenes
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Quinones / pharmacology*
  • Rifabutin / analogs & derivatives
  • Tumor Cells, Cultured

Substances

  • Antibiotics, Antineoplastic
  • Benzoquinones
  • Heat-Shock Proteins
  • Lactams, Macrocyclic
  • Quinones
  • Rifabutin
  • herbimycin
  • Protein-Tyrosine Kinases