Identification of tyrosine 187 as a protein kinase C-delta phosphorylation site

J Biol Chem. 1996 Oct 18;271(42):26404-9. doi: 10.1074/jbc.271.42.26404.

Abstract

Protein kinase C-delta (PKC-delta) has been demonstrated to be phosphorylated on tyrosine residue(s) in many different biological systems (Li, W., Yu, J.-C., Michieli, P., Beeler, J. F., Ellmore, N., Heidaran, M. A., and Pierce, J. H. (1994) Mol. Cell. Biol. 14, 6727-6735; Li, W., Mischak, H., Yu, J.-C., Wang, L.-M., Mushinski, J. F., Heidaran, M. A., and Pierce, J. H. (1994) J. Biol. Chem. 269, 2349-2352; Denning, M. F., Dlugosz, A. A., Howett, M. A., and Yuspa, S. H. (1993) J. Biol. Chem. 268, 26079-26081). Tyrosine phosphorylation of PKC-delta has also been shown to occur in vitro when purified PKC-delta is coincubated with different tyrosine kinase sources. However, the tyrosine phosphorylation site(s) is currently unknown and the exact effect of this phosphorylation on its serine/threonine kinase activity and biological functions is still controversial. To directly investigate the potential role of PKC-delta tyrosine phosphorylation, tyrosine 187 was converted to phenylalanine (PKC-deltaY187F) by site-directed mutagenesis, and expression vectors containing PKC-deltaY187F cDNAs were transfected into both 32D myeloid progenitor cells and NIH 3T3 fibroblasts. The results showed that tyrosine 187 of PKC-delta became phosphorylated in vivo in response to 12-O-tetradecanoylphorbol-13-acetate stimulation or platelet-derived growth factor receptor activation. In vivo labeling and subsequent two-dimensional phosphopeptide analysis demonstrated that one phosphopeptide was absent in PKC-deltaY187F when compared to wild type PKC-delta, further substantiating that tyrosine 187 of PKC-delta is phosphorylated in vivo. Although the phosphotyrosine content of PKC-deltaY187F was reduced compared with PKC-deltaWT, the kinase activity of PKC-deltaY187F toward a PKC-delta substrate was not altered. Moreover, 12-O-tetradecanoylphorbol-13-acetate-mediated monocytic differentiation of 32D cells was not affected by expression of the PKC-deltaY187F mutant. Taken together, these results suggest that tyrosine phosphorylation of PKC-delta on 187 may not influence PKC-delta activation and known functions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Animals
  • DNA, Complementary / chemistry
  • Electrophoresis, Gel, Two-Dimensional
  • Isoenzymes / genetics
  • Isoenzymes / metabolism*
  • Mice
  • Mutagenesis, Site-Directed
  • Phenylalanine / metabolism
  • Phosphorylation
  • Platelet-Derived Growth Factor / pharmacology
  • Protein Kinase C / genetics
  • Protein Kinase C / metabolism*
  • Protein Kinase C-delta
  • Substrate Specificity
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transfection
  • Tyrosine / metabolism*

Substances

  • DNA, Complementary
  • Isoenzymes
  • Platelet-Derived Growth Factor
  • Tyrosine
  • Phenylalanine
  • Prkcd protein, mouse
  • Protein Kinase C
  • Protein Kinase C-delta
  • Tetradecanoylphorbol Acetate