Literature DB >> 8001819

JNK2 contains a specificity-determining region responsible for efficient c-Jun binding and phosphorylation.

T Kallunki1, B Su, I Tsigelny, H K Sluss, B Dérijard, G Moore, R Davis, M Karin.   

Abstract

The transcriptional activity of c-Jun is augmented through phosphorylation at two sites by a c-Jun amino-terminal kinase (JNK). All cells express two distinct JNK activities, 46 and 55 kD in size. It is not clear which of them is the more important c-Jun kinase and how they specifically recognize c-Jun. The 46-kD form of JNK was identified as a new member of the MAP kinase group of signal-transducing enzymes, JNK1. Here, we report the molecular cloning of the 55-kD form of JNK, JNK2, which exhibits 83% identity and similar regulation to JNK1. Despite this close similarity, the two JNKs differ greatly in their ability to interact with c-Jun. JNK2 binds c-Jun approximately 25 times more efficiently than JNK1, and as a result has a lower Km toward c-Jun than JNK1. The structural basis for this difference was investigated and traced to a small beta-strand-like region near the catalytic pocket of the enzyme. Modeling suggests that this region is solvent exposed and therefore is likely to serve as a docking site that increases the effective concentration of c-Jun near JNK2. These results explain how two closely related MAP kinases can differ in their ability to recognize specific substrates and thereby elicit different biological responses.

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Year:  1994        PMID: 8001819     DOI: 10.1101/gad.8.24.2996

Source DB:  PubMed          Journal:  Genes Dev        ISSN: 0890-9369            Impact factor:   11.361


  168 in total

1.  Changes in protein conformational mobility upon activation of extracellular regulated protein kinase-2 as detected by hydrogen exchange.

Authors:  A N Hoofnagle; K A Resing; E J Goldsmith; N G Ahn
Journal:  Proc Natl Acad Sci U S A       Date:  2001-01-30       Impact factor: 11.205

2.  A conserved docking site in MEKs mediates high-affinity binding to MAP kinases and cooperates with a scaffold protein to enhance signal transmission.

Authors:  A J Bardwell; L J Flatauer; K Matsukuma; J Thorner; L Bardwell
Journal:  J Biol Chem       Date:  2000-12-28       Impact factor: 5.157

Review 3.  Mitogen-activated protein kinases: specific messages from ubiquitous messengers.

Authors:  H J Schaeffer; M J Weber
Journal:  Mol Cell Biol       Date:  1999-04       Impact factor: 4.272

4.  Characterization of Fus3 localization: active Fus3 localizes in complexes of varying size and specific activity.

Authors:  K Y Choi; J E Kranz; S K Mahanty; K S Park; E A Elion
Journal:  Mol Biol Cell       Date:  1999-05       Impact factor: 4.138

5.  Relative dependence of different outputs of the Saccharomyces cerevisiae pheromone response pathway on the MAP kinase Fus3p.

Authors:  F W Farley; B Satterberg; E J Goldsmith; E A Elion
Journal:  Genetics       Date:  1999-04       Impact factor: 4.562

6.  Cell stress-induced phosphorylation of ATF2 and c-Jun transcription factors in rat ventricular myocytes.

Authors:  A Clerk; P H Sugden
Journal:  Biochem J       Date:  1997-08-01       Impact factor: 3.857

7.  ets-2 is a target for an akt (Protein kinase B)/jun N-terminal kinase signaling pathway in macrophages of motheaten-viable mutant mice.

Authors:  J L Smith; A E Schaffner; J K Hofmeister; M Hartman; G Wei; D Forsthoefel; D A Hume; M C Ostrowski
Journal:  Mol Cell Biol       Date:  2000-11       Impact factor: 4.272

8.  Distinct roles of c-Jun N-terminal kinase isoforms in neurite initiation and elongation during axonal regeneration.

Authors:  Monia Barnat; Hervé Enslen; Friedrich Propst; Roger J Davis; Sylvia Soares; Fatiha Nothias
Journal:  J Neurosci       Date:  2010-06-09       Impact factor: 6.167

Review 9.  Molecular mechanisms of nitrogen dioxide induced epithelial injury in the lung.

Authors:  Rebecca L Persinger; Matthew E Poynter; Karna Ckless; Yvonne M W Janssen-Heininger
Journal:  Mol Cell Biochem       Date:  2002 May-Jun       Impact factor: 3.396

10.  c-Jun N-terminal protein kinase 1 (JNK1), but not JNK2, is essential for tumor necrosis factor alpha-induced c-Jun kinase activation and apoptosis.

Authors:  Jing Liu; Yuzuru Minemoto; Anning Lin
Journal:  Mol Cell Biol       Date:  2004-12       Impact factor: 4.272

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