Casein kinase II activity is required for transferrin receptor endocytosis

J Biol Chem. 1999 Oct 22;274(43):30550-6. doi: 10.1074/jbc.274.43.30550.

Abstract

The effect of protein kinase inhibitors on transferrin receptor (TR) internalization was examined in HeLa, A431, 3T3-L1 cells, and primary chicken embryo fibroblasts. We show that TR endocytosis is not affected by tyrosine kinase or protein kinase C inhibitors, but is inhibited by one serine/threonine kinase inhibitor, H-89. Inhibition occurred within 15 min, was completely reversible after H-89 withdrawal, and was specific for endocytosis rather than pinocytosis since a TR mutant lacking an internalization signal was not affected. Interestingly, H-89 also inhibited the internalization of a TR chimera containing the major histocompatibility complex class II invariant chain cytoplasmic tail, indicating that the effect was not specific for the TR. Since H-89 inhibits a number of kinases, we employed a permeabilized cell endocytosis assay to further characterize the kinase. In permeabilized 3T3-L1 cells, addition of pseudosubstrate inhibitor peptides of casein kinase II (CKII) blocked TR internalization by more than 50%, whereas pseudosubstrates of cyclic AMP-dependent kinase A, protein kinase C, and casein kinase I had no effect. Furthermore, addition of purified CKII to the cell-free reactions containing CKII pseudosubstrates reversed the endocytosis block, suggesting that CKII or a CKII-like activity is required for constitutive endocytosis.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 3T3 Cells
  • Amino Acid Sequence
  • Amino Acid Substitution
  • Animals
  • Casein Kinase II
  • Chick Embryo
  • Consensus Sequence
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Endocytosis / drug effects
  • Endocytosis / physiology*
  • Enzyme Inhibitors / pharmacology*
  • Fibroblasts / metabolism
  • HeLa Cells
  • Histocompatibility Antigens Class II / metabolism
  • Humans
  • Kinetics
  • Mice
  • Molecular Sequence Data
  • Mutagenesis, Site-Directed
  • Peptides / chemical synthesis
  • Peptides / metabolism
  • Phosphorylation
  • Protein Kinase C / metabolism
  • Protein Serine-Threonine Kinases / metabolism*
  • Receptors, Transferrin / chemistry
  • Receptors, Transferrin / metabolism*
  • Recombinant Proteins / metabolism
  • Substrate Specificity

Substances

  • Enzyme Inhibitors
  • Histocompatibility Antigens Class II
  • Peptides
  • Receptors, Transferrin
  • Recombinant Proteins
  • Casein Kinase II
  • Protein Serine-Threonine Kinases
  • Cyclic AMP-Dependent Protein Kinases
  • Protein Kinase C