Translocation of the alpha- and beta-isoforms of protein kinase C following activation of human T-lymphocytes

FEBS Lett. 1991 Jun 3;283(2):321-4. doi: 10.1016/0014-5793(91)80618-d.

Abstract

We have analyzed how activation of human Jurkat T-cells by the mitogenic lectin, concanavalin A (Con A), may affect the cellular distribution of the alpha- and beta-isoforms of protein kinase C (PKC) in T-cells. In non-stimulated cells almost all of the alpha- and beta-PKC was localized to the cytoplasmic compartment. Stimulation with Con A caused a transient translocation of both alpha- and beta-PKC from the cytoplasm to the cell membrane. The alpha-isoform appeared to be translocated to a somewhat greater extent and for a longer period of time than the beta-form. Translocation was maximal between 1 and 5 min for both of the isoforms. 30 min after stimulation, beta-PKC had returned to basal levels, whereas a substantial amount of alpha-PKC remained associated with the particulate fraction. We conclude that activation of human T-cells causes the translocation of at least two different isoforms of PKC, alpha-PKC and beta-PKC.

MeSH terms

  • Amino Acid Sequence
  • Cell Line
  • Cell Membrane / enzymology
  • Concanavalin A / pharmacology
  • Cytosol / enzymology
  • Humans
  • Immune Sera
  • Immunoassay
  • Isoenzymes / isolation & purification
  • Isoenzymes / metabolism*
  • Kinetics
  • Lymphocyte Activation*
  • Molecular Sequence Data
  • Molecular Weight
  • Peptides / chemical synthesis
  • Protein Kinase C / isolation & purification
  • Protein Kinase C / metabolism*
  • T-Lymphocytes / enzymology
  • T-Lymphocytes / immunology*
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Immune Sera
  • Isoenzymes
  • Peptides
  • Concanavalin A
  • Protein Kinase C
  • Tetradecanoylphorbol Acetate