Selectivity of docking sites in MAPK kinases

J Biol Chem. 2009 May 8;284(19):13165-73. doi: 10.1074/jbc.M900080200. Epub 2009 Feb 5.

Abstract

Protein kinases often recognize their substrates and regulators through docking interactions that occur outside of the active site; these interactions can help us to understand kinase networks, and to target kinases with drugs. During mitogen-activated protein kinase (MAPK) signaling, the ability of MAPK kinases (MKKs, or MEKs) to recognize their cognate MAPKs is facilitated by a short docking motif (the D-site) in the MKK N terminus, which binds to a complementary region on the MAPK. MAPKs then recognize many of their targets using the same strategy, because many MAPK substrates also contain D-sites. The extent to which docking contributes to the specificity of MAPK transactions is incompletely understood. Here we characterize the selectivity of the interaction between MKK-derived D-sites and MAPKs by measuring the ability of D-site peptides to inhibit MAPK-mediated phosphorylation of D-site-containing substrates. We find that all MKK D-sites bind better to their cognate MAPKs than they do to non-cognate MAPKs. For instance, the MKK3 D-site peptide, which is a remarkably potent inhibitor of p38alpha (IC(50) < 10 nm), does not inhibit JNK1 or JNK2. Likewise, MAPKs generally bind as well or better to cognate D-sites than to non-cognate D-sites. For instance, JNK1 and JNK2 do not appreciably bind to any D-sites other than their cognate D-sites from MKK4 and MKK7. In general, cognate, within-pathway interactions are preferred about an order of magnitude over non-cognate interactions. However, the selectivity of MAPKs and their cognate MKK-derived D-sites for each other is limited in some cases; in particular, ERK2 is not very selective. We conclude that MAPK-docking sites in MAPK kinases bind selectively to their cognate MAPKs.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Activating Transcription Factor 2 / metabolism
  • Animals
  • Binding Sites*
  • Binding, Competitive
  • Humans
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • MADS Domain Proteins / metabolism
  • MAP Kinase Kinase 3 / metabolism
  • MAP Kinase Kinase 6 / metabolism
  • MEF2 Transcription Factors
  • Mice
  • Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 8 / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase 8 / metabolism
  • Mitogen-Activated Protein Kinase 9 / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase 9 / metabolism
  • Mitogen-Activated Protein Kinase Kinases / chemistry*
  • Mitogen-Activated Protein Kinase Kinases / metabolism*
  • Myogenic Regulatory Factors / metabolism
  • Phosphorylation
  • Protein Binding
  • Substrate Specificity
  • ets-Domain Protein Elk-1 / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • ATF2 protein, human
  • Activating Transcription Factor 2
  • MADS Domain Proteins
  • MEF2 Transcription Factors
  • MEF2A protein, human
  • Myogenic Regulatory Factors
  • ets-Domain Protein Elk-1
  • Mitogen-Activated Protein Kinase 9
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 8
  • p38 Mitogen-Activated Protein Kinases
  • MAP Kinase Kinase 3
  • MAP Kinase Kinase 6
  • MAP2K3 protein, human
  • MAP2K6 protein, human
  • Mitogen-Activated Protein Kinase Kinases