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PMID: 9915826 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Identification of an extracellular signal-regulated kinase (ERK) docking site in ribosomal S6 kinase, a sequence critical for activation by ERK in vivo.

The Journal of biological chemistry ·Vol. 274 ·No. 5 ·1999-01-29 ·Pages 2893-8

Smith JA, Poteet-Smith CE, Malarkey K, Sturgill TW

Abstract

Glutathione S-transferase (GST)-fusion proteins containing the carboxyl-terminal tails of three p90 ribosomal S6 kinase (RSK) isozymes (RSK1, RSK2, and RSK3) interacted with extracellular signal-regulated kinase (ERK) but not c-Jun-NH2-kinase (JNK) or p38 mitogen-activated protein kinase (MAPK). Within the carboxyl-terminal residues of the RSK isozymes is a region of high conservation corresponding to residues 722LAQRRVRKLPSTTL735 in RSK1. Truncation of the carboxyl-terminal 9 residues, 727VRKLPSTTL735, completely eliminated the interaction of the GST-RSK1 fusion protein with purified recombinant ERK2, whereas the truncation of residues 731PSTTL735 had no effect on the interaction with purified ERK2. ERK1 and ERK2 co-immunoprecipitated with hemagglutinin-tagged wild type RSK2 (HA-RSK2) in BHK cell cytosol. However, ERK did not co-immunoprecipitate with HA-RSK2((1-729)), a mutant missing the carboxyl-terminal 11 amino acids, similar to the minimal truncation that eliminated in vitro interaction of ERK with the GST-RSK1 fusion protein. Kinase activity of HA-RSK2 increased 6-fold in response to insulin. HA-RSK2((1-729)) had a similar basal kinase activity to that of HA-RSK2 but was not affected by insulin treatment. Immunoprecipitated HA-RSK2 and HA-RSK2((1-729)) could be activated to the same extent in vitro by active ERK2, demonstrating that HA-RSK2((1-729)) was properly folded. These data suggest that the conserved region of the RSK isozymes (722LAQRRVRKL730 of RSK1) provides for a specific ERK docking site approximately 150 amino acids carboxyl-terminal to the nearest identified ERK phosphorylation site (Thr573). Complex formation between RSK and ERK is essential for the activation of RSK by ERK in vivo. Comparison of the docking site of RSK with the carboxyl-terminal tails of other MAPK-activated kinases reveals putative docking sites within each of these MAPK-targeted kinases. The number and placement of lysine and arginine residues within the conserved region correlate with specificity for activation by ERK and p38 MAPKs in vivo.

MeSH Terms
Amino Acid Sequence Animals Binding Sites COS Cells Calcium-Calmodulin-Dependent Protein Kinases/chemistry,metabolism Cells, Cultured Conserved Sequence Cricetinae Enzyme Activation Isoenzymes/chemistry,metabolism Mice Molecular Sequence Data Protein Serine-Threonine Kinases/chemistry,metabolism Ribosomal Protein S6 Kinases/chemistry,metabolism Sequence Alignment Sequence Homology, Amino Acid Structure-Activity Relationship
Chemicals
Isoenzymes Mknk1 protein, mouse Mknk2 protein, mouse Protein Serine-Threonine Kinases Ribosomal Protein S6 Kinases Calcium-Calmodulin-Dependent Protein Kinases
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Smith J A
Howard Hughes Medical Institute and the Markey Center for Cell Signaling, Department of Medicine and Pharmacology, University of Virginia, Charlottesville, Virginia 22908, USA.
Poteet-Smith C E
Malarkey K
Sturgill T W
Article Info
Journal
The Journal of biological chemistry
Abbr.
J Biol Chem
ISSN
0021-9258
Published
1999-01-29
Pages
2893-8
Language
English
Region
United States
NLM ID
2985121R
Subset
IM
Grants
NIDDK NIH HHS · DK41077 · United States
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