ArticleScientific reports2018
Intrinsically active MEK variants are differentially regulated by proteinases and phosphatases.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Molecular basis of mitogen-activated protein kinase ERK2 activation by its upstream kinase MEK1.bioRxiv : the preprint server for biology · 2026Article
- Kinase Inhibitors in Genetic Diseases.International journal of molecular sciences · 2023Review
- Article
- Fibroblasts from Patients with Melorheostosis Promote Angiogenesis in Healthy Endothelial Cells through Secreted Factors.The Journal of investigative dermatology · 2022Article
- Qualitative differences in disease-associated MEK mutants reveal molecular signatures and aberrant signaling-crosstalk in cancer.Nature communications · 2022Article
- The RASopathies: from pathogenetics to therapeutics.Disease models & mechanisms · 2022Review
- Drosophila RASopathy models identify disease subtype differences and biomarkers of drug efficacy.iScience · 2021Article
- Molecular mechanisms underlying cellular effects of human MEK1 mutations.Molecular biology of the cell · 2021Article
- Article
- Small noncoding vault RNA modulates synapse formation by amplifying MAPK signaling.The Journal of cell biology · 2021Article
- Novel Molecular Basis for Synapse Formation: Small Non-coding Vault RNA Functions as a Riboregulator of MEK1 to Modulate Synaptogenesis.Frontiers in molecular neuroscience · 2021Article
- Inference of Multisite Phosphorylation Rate Constants and Their Modulation by Pathogenic Mutations.Current biology : CB · 2020Article
- An ultrasensitive fiveplex activity assay for cellular kinases.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
MAPK/ERK kinase (MEK) 1/2 are central signaling proteins that serve as specificity determinants of the MAPK/ERK cascade. More than twenty activating mutations have been reported for MEK1/2, and many of them are known to cause diseases such as cancers, arteriovenous malformation and RASopathies. Changes in their intrinsic activity do not seem to correlate with the severity of the diseases. Here we studied four MEK1/2 mutations using biochemical and molecular dynamic methods. Although the studied mutants elevated the activating phosphorylation of MEK they had no effect on the stimulated ERK1/2 phosphorylation. Studying the regulatory mechanism that may explain this lack of effect, we found that one type of mutation affects MEK stability and two types of mutations demonstrate a reduced sensitivity to PP2A. Together, our results indicate that some MEK mutations exert their function not only by their elevated intrinsic activity, but also by modulation of regulatory elements such as protein stability or dephosphorylation.
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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.