Identification of the critical features of a small peptide inhibitor of JNK activity

J Biol Chem. 2002 Mar 29;277(13):10987-97. doi: 10.1074/jbc.M107565200. Epub 2002 Jan 14.

Abstract

The c-Jun N-terminal kinases (JNKs) are a subfamily of the mitogen-activated protein kinases (MAPKs). Although progress in evaluating the functions of other MAPKs has been facilitated by the characterization of specific inhibitors, no JNK-directed inhibitor is commercially available. We have identified a 21-amino acid peptide inhibitor of activated JNKs, based on amino acids 143-163 of the JNK-binding domain (JBD) of the JNK scaffolding protein, JNK-interacting protein-1 (JIP-1). This peptide, I-JIP (Inhibitor of JNK-based on JIP-1), inhibited JNK activity in vitro toward recombinant c-Jun, Elk, and ATF2 up to 90%. A truncated I-JIP (TI-JIP), the C-terminal 11 amino acids of I-JIP, directly interacted with recombinant JNKs but not its substrates as shown by surface plasmon resonance analysis. Scanning alanine replacement within truncated I-JIP identified 4 residues (Arg-156, Pro-157, Leu-160, or Leu-162) as independently critical for inhibition. JBD peptide sequences from JIP-2 and JIP-3 shared these critical residues and accordingly were effective JNK inhibitors. In contrast, peptides based on the JBDs of ATF2 and c-Jun inhibited JNK activity by <40%, which agreed with their lack of homology to the critical Arg-156 and Pro-157. These studies thus define a small peptide inhibitor sequence of JNKs based on the JIP proteins.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Activating Transcription Factor 2
  • Amino Acid Sequence
  • Animals
  • COS Cells
  • Cyclic AMP Response Element-Binding Protein / metabolism
  • DNA-Binding Proteins*
  • Enzyme Inhibitors / pharmacology*
  • JNK Mitogen-Activated Protein Kinases
  • Kinetics
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors*
  • Mitogen-Activated Protein Kinases / metabolism
  • Molecular Sequence Data
  • Peptides / chemistry
  • Peptides / pharmacology*
  • Phosphorylation
  • Proto-Oncogene Proteins / metabolism
  • Recombinant Proteins / antagonists & inhibitors
  • Recombinant Proteins / metabolism
  • Sequence Homology, Amino Acid
  • Substrate Specificity
  • Surface Plasmon Resonance
  • Transcription Factors / metabolism
  • ets-Domain Protein Elk-1
  • p38 Mitogen-Activated Protein Kinases

Substances

  • Activating Transcription Factor 2
  • Cyclic AMP Response Element-Binding Protein
  • DNA-Binding Proteins
  • Enzyme Inhibitors
  • Peptides
  • Proto-Oncogene Proteins
  • Recombinant Proteins
  • Transcription Factors
  • ets-Domain Protein Elk-1
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases