ArticleCell structure and function2020
Prickle2 and Igsf9b Coordinately Regulate the Cytoarchitecture of the Axon Initial Segment.
Article in Cell structure and function, 2020. 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, 11 citations in OpenAlex.
- Secondary analysis of GenRED data (Genetics of Recurrent Early-Onset major Depression) using MERLIN.European archives of psychiatry and clinical neuroscience · 2026Article
- Strained actin binding by the Prickle2 LIM domains and their regulation in the full-length protein.Molecular biology of the cell · 2026Article
- Neuroanatomical characterization of the cell adhesion molecule IgSF9b reveals localization to inhibitory and excitatory synapses in the mouse limbic system.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Identification of a 13-Gene Immune Signature in Liver Fibrosis Reveals GABRE as a Novel Candidate Biomarker.International journal of molecular sciences · 2025Article
- Evolving Insights into Prickle2 in Neurodevelopment and Neurological Disorders.Molecular neurobiology · 2025Review
- Transcriptional Regulators YAP and TAZ Have Distinct Abilities to Compensate for One Another in Podocytes.Journal of the American Society of Nephrology : JASN · 2025Article
- Decoding Epilepsy: Prickle2 and Multifaceted Molecular Pathway Connections.Current pharmaceutical design · 2025Review
- The role of cell adhesion molecule IgSF9b at the inhibitory synapse and psychiatric disease.Neuroscience and biobehavioral reviews · 2024Review
- The core PCP protein Prickle2 regulates axon number and AIS maturation by binding to AnkG and modulating microtubule bundling.Science advances · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prickle2 has been identified in genetic studies of subjects with autism spectrum disorder (ASD) and epilepsy, but the pathological mechanism of Prickle2 remains to be fully understood. Proteomic analysis of Prickle2 with mass spectrometry revealed twenty-eight Prickle2 interactors, including immunoglobulin superfamily member 9b (Igsf9b), in the brain. Here, because Igsf9 family proteins are associated with psychiatric diseases and seizures, we studied the physiological interaction between Prickle2 and Igsf9b. Prickle2 colocalized with Igsf9b in cultured hippocampal neurons. Knockdown of Prickle2 affected the subcellular localization of Igsf9b. Interestingly, Igsf9b localized along axonal processes in a pattern opposite to the ASD-related molecule ANK3/AnkG. AnkG is a major component of the axon initial segment (AIS), where a variety of ASD and epilepsy susceptibility proteins accumulate. Igsf9b-knockdown neurons displayed altered AnkG localization. Prickle2 depletion caused defects in AnkG and voltage-gated Na+ channel localization, resulting in altered network activity. These results support the idea that Prickle2 regulates AnkG distribution by controlling the proper localization of Igsf9b. The novel function of Prickle2 in AIS cytoarchitecture provides new insights into the shared pathology of ASD and epilepsy.Key words: Prickle2, Igsf9b, axon initial segment, neuronal excitability, ASD.
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