ArticleMolecular and cellular biology2007
Noncanonical function of MEKK2 and MEK5 PB1 domains for coordinated extracellular signal-regulated kinase 5 and c-Jun N-terminal kinase signaling.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- The MEK5/ERK5 Pathway in Health and Disease.International journal of molecular sciences · 2021Review
- Discovery of a Gatekeeper Residue in the C-Terminal Tail of the Extracellular Signal-Regulated Protein Kinase 5 (ERK5).International journal of molecular sciences · 2020Article
- Silencing of the MEKK2/MEKK3 Pathway Protects against Spinal Cord Injury via the Hedgehog Pathway and the JNK Pathway.Molecular therapy. Nucleic acids · 2019Article
- Oncogenic signaling of MEK5-ERK5.Cancer letters · 2017Review
- Cell Signaling and Stress Responses.Cold Spring Harbor perspectives in biology · 2016Review
- Structure and dynamics of the MKK7-JNK signaling complex.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Ubiquitin-dependent regulation of MEKK2/3-MEK5-ERK5 signaling module by XIAP and cIAP1.The EMBO journal · 2014Article
- Structural mechanism for the specific assembly and activation of the extracellular signal regulated kinase 5 (ERK5) module.The Journal of biological chemistry · 2013Article
- MEK5/ERK5 pathway: the first fifteen years.Biochimica et biophysica acta · 2012Review
- CHIP-dependent termination of MEKK2 regulates temporal ERK activation required for proper hyperosmotic response.The EMBO journal · 2010Article
- PB1 domain interaction of p62/sequestosome 1 and MEKK3 regulates NF-kappaB activation.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
MEKK2 and MEK5 encode Phox/Bem1p (PB1) domains that heterodimerize with one another. MEKK2, MEK5, and extracellular signal-related kinase 5 (ERK5) form a ternary complex through interactions involving the MEKK2 and MEK5 PB1 domains and a 34-amino-acid C-terminal extension of the MEK5 PB1 domain. This C-terminal extension encodes an ERK5 docking site required for MEK5 activation of ERK5. The PB1 domains bind in a front-to-back arrangement, with a cluster of basic amino acids in the front of the MEKK2 PB1 domain binding to the back-end acidic clusters of the MEK5 PB1 domain. The C-terminal moiety, including the acidic cluster of the MEKK2 PB1 domain, is not required for MEK5 binding and binds MKK7. Quiescent MEKK2 preferentially binds MEK5, and MEKK2 activation results in ERK5 activation. Activated MEKK2 binds and activates MKK7, leading to JNK activation. The findings define how the MEKK2 and MEK5 PB1 domains are uniquely used for differential binding of two mitogen-activated protein kinase kinases, MEK5 and MKK7, for the coordinated control of ERK5 and c-Jun N-terminal kinase activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.