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PMID: 8910287 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

The dual specificity phosphatases M3/6 and MKP-3 are highly selective for inactivation of distinct mitogen-activated protein kinases.

The Journal of biological chemistry ·Vol. 271 ·No. 44 ·1996-11-01 ·Pages 27205-8

Muda M, Theodosiou A, Rodrigues N, Boschert U, Camps M, Gillieron C, Davies K, Ashworth A, Arkinstall S

Abstract

The mitogen-activated protein (MAP) kinase family includes extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase/stress-activated protein kinase (JNK/SAPK) and p38/RK/CSBP (p38) as structurally and functionally distinct enzyme classes. Here we describe two new dual specificity phosphatases of the CL100/MKP-1 family that are selective for inactivating ERK or JNK/SAPK and p38 MAP kinases when expressed in COS-7 cells. M3/6 is the first phosphatase of this family to display highly specific inactivation of JNK/SAPK and p38 MAP kinases. Although stress-induced activation of p54 SAPKbeta, p46 SAPKgamma (JNK1) or p38 MAP kinases is abolished upon co-transfection with increasing amounts of M3/6 plasmid, epidermal growth factor-stimulated ERK1 is remarkably insensitive even to the highest levels of M3/6 expression obtained. In contrast to M3/6, the dual specificity phosphatase MKP-3 is selective for inactivation of ERK family MAP kinases. Low level expression of MKP-3 blocks totally epidermal growth factor-stimulated ERK1, whereas stress-induced activation of p54 SAPKbeta and p38 MAP kinases is inhibited only partially under identical conditions. Selective regulation by M3/6 and MKP-3 was also observed upon chronic MAP kinase activation by constitutive p21(ras) GTPases. Hence, although M3/6 expression effectively blocked p54 SAPKbeta activation by p21(rac) (G12V), ERK1 activated by p21(ras) (G12V) was insensitive to this phosphatase. ERK1 activation by oncogenic p21(ras) was, however, blocked totally by co-expression of MKP-3. This is the first report demonstrating reciprocally selective inhibition of different MAP kinases by two distinct dual specificity phosphatases.

MeSH Terms
Amino Acid Sequence Animals Binding Sites COS Cells Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors,metabolism Cloning, Molecular Dual Specificity Phosphatase 6 Enzyme Activation Epidermal Growth Factor/pharmacology GTP-Binding Proteins/metabolism Mice Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases Molecular Sequence Data Peptide Fragments/chemistry Phosphoprotein Phosphatases/chemistry,metabolism Protein Tyrosine Phosphatases/chemistry,metabolism Proto-Oncogene Proteins p21(ras)/metabolism Recombinant Proteins/chemistry,metabolism Substrate Specificity Transfection rac GTP-Binding Proteins
Chemicals
Peptide Fragments Recombinant Proteins Epidermal Growth Factor Calcium-Calmodulin-Dependent Protein Kinases Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases Phosphoprotein Phosphatases Dual Specificity Phosphatase 6 Dusp6 protein, mouse Protein Tyrosine Phosphatases GTP-Binding Proteins Proto-Oncogene Proteins p21(ras) rac GTP-Binding Proteins
Authors & Affiliations
9 authors, click to expand affiliations / ORCID
Muda M
Geneva Biomedical Research Institute, Glaxo Wellcome Research and Development S. A., CH-1228 Plan-les-Ouates, Geneva, Switzerland. SA7182@GGR.CO.UK
Theodosiou A
Rodrigues N
Boschert U
Camps M
Gillieron C
Davies K
Ashworth A
Arkinstall S
Article Info
Journal
The Journal of biological chemistry
Abbr.
J Biol Chem
ISSN
0021-9258
Published
1996-11-01
Pages
27205-8
Language
English
Region
United States
NLM ID
2985121R
Subset
IM
Grants
Wellcome Trust · United Kingdom
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