Inhibition of the c-Jun N-terminal kinase/AP-1 and NF-kappaB pathways by PICOT, a novel protein kinase C-interacting protein with a thioredoxin homology domain

J Biol Chem. 2000 Jan 21;275(3):1902-9. doi: 10.1074/jbc.275.3.1902.

Abstract

Protein kinase C-theta (PKCtheta) is a Ca(2+)-independent PKC isoform that is selectively expressed in T lymphocytes (and muscle), and is thought to play an important role in T cell receptor-induced activation. To gain a better understanding of the function and regulation of PKCtheta, we have employed the yeast two-hybrid system to identify PKCtheta-interacting proteins. We report the isolation and characterization of a cDNA encoding a novel 335-amino acid (37. 5-kDa) PKCtheta-interacting protein termed PICOT (for PKC-interacting cousin of thioredoxin). PICOT is expressed in various tissues, including in T cells, where it colocalizes with PKCtheta. PICOT displays an N-terminal thioredoxin homology domain, which is required for the interaction with PKC. Comparison of the unique C-terminal region of PICOT with expressed sequence tag data bases revealed two tandem repeats of a novel domain that is highly conserved from plants to mammals. Transient overexpression of full-length PICOT (but not its N- or C-terminal fragments) in T cells inhibited the activation of c-Jun N-terminal kinase (but not extracellular signal-regulated kinase), and the transcription factors AP-1 or NF-kappaB. These findings suggest that PICOT and its evolutionary conserved homologues may interact with PKC-related kinases in multiple organisms and, second, that it plays a role in regulating the function of the thioredoxin system.

Publication types

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

MeSH terms

  • Amino Acid Sequence
  • Carrier Proteins / chemistry*
  • Carrier Proteins / pharmacology
  • Carrier Proteins / physiology*
  • Glutathione Transferase / metabolism
  • Humans
  • JNK Mitogen-Activated Protein Kinases
  • Jurkat Cells
  • Lymphocyte Activation / physiology
  • MAP Kinase Signaling System / drug effects
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors*
  • Molecular Sequence Data
  • NF-kappa B / antagonists & inhibitors*
  • Plasmids
  • Protein Binding
  • Protein Kinase C / metabolism*
  • Recombinant Fusion Proteins / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sequence Homology, Amino Acid
  • T-Lymphocytes / drug effects
  • Thioredoxins / metabolism*
  • Transcription Factor AP-1 / antagonists & inhibitors*
  • Transfection
  • Two-Hybrid System Techniques

Substances

  • Carrier Proteins
  • GLRX3 protein, human
  • NF-kappa B
  • Recombinant Fusion Proteins
  • Transcription Factor AP-1
  • Thioredoxins
  • Glutathione Transferase
  • Protein Kinase C
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases