ArticleGenetics2015
Neuronal development in Caenorhabditis elegans is regulated by inhibition of an MLK MAP kinase pathway.
Article in Genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Molecular regulation of axon termination in mechanosensory neurons.Development (Cambridge, England) · 2024Review
- Multiple p38/JNK mitogen-activated protein kinase (MAPK) signaling pathways mediate salt chemotaxis learning in C. elegans.G3 (Bethesda, Md.) · 2023Article
- Ubiquitin ligase activity inhibits Cdk5 to control axon termination.PLoS genetics · 2022Article
- Historical perspective and progress on protein ubiquitination at glutamatergic synapses.Neuropharmacology · 2021Review
- Timing of neuronal plasticity in development and aging.Wiley interdisciplinary reviews. Developmental biology · 2018Review
- RPM-1 regulates axon termination by affecting growth cone collapse and microtubule stability.Development (Cambridge, England) · 2017Article
- A MIG-15/JNK-1 MAP kinase cascade opposes RPM-1 signaling in synapse formation and learning.PLoS genetics · 2017Article
- Defining Minimal Binding Regions in Regulator of Presynaptic Morphology 1 (RPM-1) UsingThe Journal of biological chemistry · 2017Article
- The PHR proteins: intracellular signaling hubs in neuronal development and axon degeneration.Neural development · 2016Review
- Developmental Function of the PHR Protein RPM-1 Is Required for Learning in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
We show that loss-of-function mutations in kinases of the MLK-1 pathway (mlk-1, mek-1, and kgb-1/jnk) function cell-autonomously in neurons to suppress defects in synapse formation and axon termination caused by rpm-1 loss of function. Our genetic analysis also suggests that the phosphatase PPM-1, like RPM-1, is a potential inhibitor of kinases in the MLK-1 pathway.
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What OpenQuestion holds
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.