ArticleNature genetics2017
Divergent effects of intrinsically active MEK variants on developmental Ras signaling.
Article in Nature genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 61 citations in OpenAlex.
- ERK inhibits Capicua repressor function via multisite phosphorylation.Journal of cell science · 2026Article
- Disrupted developmental signaling induces novel transcriptional states.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- ERK synchronizes embryonic cleavages in Drosophila.Developmental cell · 2024Article
- Hyperactivation of MEK1 in cortical glutamatergic neurons results in projection axon deficits and aberrant motor learning.Disease models & mechanisms · 2024Article
- Non-Mammalian Models for Understanding Neurological Defects in RASopathies.Biomedicines · 2024Review
- Gene model for the ortholog ofmicroPublication biology · 2024Article
- A guide to ERK dynamics, part 2: downstream decoding.The Biochemical journal · 2023Article
- Evolutionary history of MEK1 illuminates the nature of deleterious mutations.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Abrogation of MAP4K4 protein function causes congenital anomalies in humans and zebrafish.Science advances · 2023Article
- Stochastic phenotypes in RAS-dependent developmental diseases.Current biology : CB · 2023Article
- New prospectives on treatment opportunities in RASopathies.American journal of medical genetics. Part C, Seminars in medical genetics · 2022Review
- ERK1/2-RSK2 Signaling in Regulation of ERα-Mediated Responses.Endocrinology · 2022Review
- Qualitative differences in disease-associated MEK mutants reveal molecular signatures and aberrant signaling-crosstalk in cancer.Nature communications · 2022Article
- Review
- ERK signaling dissolves ERF repression condensates in living embryos.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Altered canonical and striatal-frontal resting state functional connectivity in children with pathogenic variants in the Ras/mitogen-activated protein kinase pathway.Molecular psychiatry · 2022Article
- How can same-gene mutations promote both cancer and developmental disorders?Science advances · 2022Article
- Preformation and epigenesis converge to specify primordial germ cell fate in the early Drosophila embryo.PLoS genetics · 2022Article
- Zebrafish disease models in drug discovery: from preclinical modelling to clinical trials.Nature reviews. Drug discovery · 2021Review
- Temporal integration of inductive cues on the way to gastrulation.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Germline mutations in Ras pathway components are associated with a large class of human developmental abnormalities, known as RASopathies, that are characterized by a range of structural and functional phenotypes, including cardiac defects and neurocognitive delays. Although it is generally believed that RASopathies are caused by altered levels of pathway activation, the signaling changes in developing tissues remain largely unknown. We used assays with spatiotemporal resolution in Drosophila melanogaster (fruit fly) and Danio rerio (zebrafish) to quantify signaling changes caused by mutations in MAP2K1 (encoding MEK), a core component of the Ras pathway that is mutated in both RASopathies and cancers in humans. Surprisingly, we discovered that intrinsically active MEK variants can both increase and reduce the levels of pathway activation in vivo. The sign of the effect depends on cellular context, implying that some of the emerging phenotypes in RASopathies may be caused by increased, as well as attenuated, levels of Ras signaling.
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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.