ArticleThe Journal of cell biology2018
The polarity protein Angiomotin p130 controls dendritic spine maturation.
Article in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Changes in AmotL2 Expression in Cells of the Human Enteral Nervous System in Oxaliplatin-Induced Enteric Neuropathy.Biomedicines · 2024Article
- Role of angiomotin family members in human diseases (Review).Experimental and therapeutic medicine · 2024Review
- WWC1/2 regulate spinogenesis and cognition in mice by stabilizing AMOT.Cell death & disease · 2023Article
- NCK1 Modulates Neuronal Actin Dynamics and Promotes Dendritic Spine, Synapse, and Memory Formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Depletion of endogenously biotinylated carboxylases enhances the sensitivity of TurboID-mediated proximity labeling in Caenorhabditis elegans.The Journal of biological chemistry · 2022Article
- Angiomotin Regulates YAP Localization during Neural Differentiation of Human Pluripotent Stem Cells.Stem cell reports · 2019Article
- Amot and Yap1 regulate neuronal dendritic tree complexity and locomotor coordination in mice.PLoS biology · 2019Article
- PAR3-PAR6-atypical PKC polarity complex proteins in neuronal polarization.Cellular and molecular life sciences : CMLS · 2018Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The actin cytoskeleton is essential for the structural changes in dendritic spines that lead to the formation of new synapses. Although the molecular mechanisms underlying spine formation are well characterized, the events that drive spine maturation during development are largely unknown. In this study, we demonstrate that Angiomotin (AMOT-130) is necessary for spine stabilization. AMOT-130 is enriched in mature dendritic spines and functions to stabilize the actin cytoskeleton by coupling F-actin to postsynaptic protein scaffolds. These functions of AMOT are transiently restricted during postnatal development by phosphorylation imposed by the kinase Lats1. Our study proposes that AMOT-130 is essential for normal spine morphogenesis and identifies Lats1 as an upstream regulator in this process. Moreover, our findings may link AMOT-130 loss and the related spine defects to neurological disorders.
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Registered trials
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