Structural basis for the autoinhibition of the C-terminal kinase domain of human RSK1

Acta Crystallogr D Biol Crystallogr. 2012 Jun;68(Pt 6):680-5. doi: 10.1107/S0907444912007457. Epub 2012 May 17.

Abstract

p90 ribosomal S6 kinases (RSKs) respond to various mitogen stimuli and comprise two distinct protein kinase domains. The C-terminal kinase domain (CTKD) receives signal from ERK1/2 and adopts an autoinhibitory mechanism. Here, the crystal structure of human RSK1 CTKD is reported at 2.7 Å resolution. The structure shows a standard kinase fold, with the catalytic residues in the ATP-binding cleft orientated in optimal conformations for phosphotransfer. The inactivation of the CTKD is conferred by an extra α-helix (αL), which occupies the substrate-binding groove. In combination with previous knowledge, this structure indicates that activation of RSK1 involves the removal of αL from the substrate-binding groove induced by ERK1/2 phosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Enzyme Activation
  • Humans
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3 / metabolism
  • Models, Molecular
  • Molecular Sequence Data
  • Phosphorylation
  • Protein Structure, Quaternary
  • Protein Structure, Tertiary
  • Ribosomal Protein S6 Kinases, 90-kDa / chemistry*
  • Ribosomal Protein S6 Kinases, 90-kDa / metabolism
  • Sequence Alignment
  • Substrate Specificity

Substances

  • Ribosomal Protein S6 Kinases, 90-kDa
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3