ArticleNature communications2024
Membrane remodeling by FAM92A1 during brain development regulates neuronal morphology, synaptic function, and cognition.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Neutrophil-mediated BDNF delivery for the treatment of moderate to severe Alzheimer's disease.Acta pharmaceutica Sinica. B · 2026Article
- The planar cell polarity protein Vangl2 interacts with the PDZ-domains of Scribble but not with a unique PDZ-like domain in Inturned.FEBS letters · 2026Article
- YTHDC1 functions as a molecular chaperone to suppress ALS-linked hnRNPA1 mutants from aggregation.Nature communications · 2026Article
- Mitochondrial Dynamics and SLC25 Transporters in Neurodegeneration: From Mechanisms to Therapeutic Opportunities.Biomolecules · 2026Review
- Morphology-coupled formation and reversible gating of membrane channels in synthetic cells using reconfigurable DNA nanorafts.Nature protocols · 2026Review
- Long-chain polyphosphates induce glomerular microthrombi and exacerbate LPS-induced acute kidney injury in mouse.Disease models & mechanisms · 2026Article
- Leveraging Fiber Photometry to Decipher Neural Circuits Underlying Anxiety in Mice.Fundamental & clinical pharmacology · 2025Review
- Mechanistic adaptation of the metazoan RabGEFs Mon1-Ccz1 and Fuzzy-Inturned.Science advances · 2025Article
- Genetic evidence for the liver-brain axis: lipid metabolism and neurodegenerative disease risk.Lipids in health and disease · 2025Article
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Authors and funding
24 authors.
Funding
Abstract
The Bin/Amphiphysin/Rvs (BAR) domain protein FAM92A1 is a multifunctional protein engaged in regulating mitochondrial ultrastructure and ciliogenesis, but its physiological role in the brain remains unclear. Here, we show that FAM92A1 is expressed in neurons starting from embryonic development. FAM92A1 knockout in mice results in altered brain morphology and age-associated cognitive deficits, potentially due to neuronal degeneration and disrupted synaptic plasticity. Specifically, FAM92A1 deficiency impairs diverse neuronal membrane morphology, including the mitochondrial inner membrane, myelin sheath, and synapses, indicating its roles in membrane remodeling and maintenance. By determining the crystal structure of the FAM92A1 BAR domain, combined with atomistic molecular dynamics simulations, we uncover that FAM92A1 interacts with phosphoinositide- and cardiolipin-containing membranes to induce lipid-clustering and membrane curvature. Altogether, these findings reveal the physiological role of FAM92A1 in the brain, highlighting its impact on synaptic plasticity and neural function through the regulation of membrane remodeling and endocytic processes.
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