ArticleCell death & disease2023
WWC1/2 regulate spinogenesis and cognition in mice by stabilizing AMOT.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Reducing CETP activity prevents memory decline in an Alzheimer's disease mouse model.EMBO molecular medicine · 2026Article
- From Synapses to Circuits, the Role of KIBRA and the WWC Family in Adaptive Brain Function.Journal of neurochemistry · 2026Review
- Patient-derived AMOTL1 mutations lead to defective cell migration and tissue development.Bioscience reports · 2026Article
- Acetate enhances long-term memory in female mice by sex-, context-, and brain region-specific epigenetic and transcriptional remodeling.Science signaling · 2026Article
- Long-read whole-genome sequencing of SHR rat substrains with distinct substance use phenotypes.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- High Levels of Endogenous Omega-3 Fatty Acids Promote Dendritic Cell Antigen Presentation and Improve Dendritic Cell-Based Cancer Vaccine Efficacy in Mice.Cancer immunology research · 2025Article
- PICK1 links KIBRA and AMPA receptor subunit GluA2 in coiled-coil-driven supramolecular complexes.The Journal of biological chemistry · 2025Article
- WWC proteins-mediated compensatory mechanism restricts schwannomatosis driven byScience advances · 2025Article
- Genome-wide DNA methylation analysis of hippocampal tissue in a murine model of attention deficit-hyperactivity disorder.PloS one · 2025Article
- Role of angiomotin family members in human diseases (Review).Experimental and therapeutic medicine · 2024Review
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
WWC1 regulates episodic learning and memory, and genetic nucleotide polymorphism of WWC1 is associated with neurodegenerative diseases such as Alzheimer's disease. However, the molecular mechanism through which WWC1 regulates neuronal function has not been fully elucidated. Here, we show that WWC1 and its paralogs (WWC2/3) bind directly to angiomotin (AMOT) family proteins (Motins), and recruit USP9X to deubiquitinate and stabilize Motins. Deletion of WWC genes in different cell types leads to reduced protein levels of Motins. In mice, neuron-specific deletion of Wwc1 and Wwc2 results in reduced expression of Motins and lower density of dendritic spines in the cortex and hippocampus, in association with impaired cognitive functions such as memory and learning. Interestingly, ectopic expression of AMOT partially rescues the neuronal phenotypes associated with Wwc1/2 deletion. Thus, WWC proteins modulate spinogenesis and cognition, at least in part, by regulating the protein stability of Motins.
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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 Socratic graph.