ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Loss of Ahi1 affects early development by impairing BM88/Cend1-mediated neuronal differentiation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Mitochondrial membrane junction-mediated ATP channeling drives activity-dependent glucose metabolism.bioRxiv : the preprint server for biology · 2025Article
- Neuronal differentiation regulator CEND1 coordinately suppresses tumor growth and energetics via AMPK signaling in brain glioma.Cell & bioscience · 2025Article
- Unraveling neuroprotection with Kv1.3 potassium channel blockade by a scorpion venom peptide.Scientific reports · 2024Article
- GR/Ahi1 regulates WDR68-DYRK1A binding and mediates cognitive impairment in prenatally stressed offspring.Cellular and molecular life sciences : CMLS · 2024Article
- Depression compromises antiviral innate immunity via the AVP-AHI1-Tyk2 axis.Cell research · 2022Article
- Ahi1 regulates serotonin production by the GR/ERβ/TPH2 pathway involving sexual differences in depressive behaviors.Cell communication and signaling : CCS · 2022Article
- Cell cycle exit and neuronal differentiation 1-engineered embryonic neural stem cells enhance neuronal differentiation and neurobehavioral recovery after experimental traumatic brain injury.Neural regeneration research · 2022Article
- Ahi1 regulates the nuclear translocation of glucocorticoid receptor to modulate stress response.Translational psychiatry · 2021Article
- WD40-Repeat Proteins in Ciliopathies and Congenital Disorders of Endocrine System.Endocrinology and metabolism (Seoul, Korea) · 2020Review
- Alzheimer's Disease and Diabetes: Insulin Signaling as the Bridge Linking Two Pathologies.Molecular neurobiology · 2020Review
- Expression of Mammalian BM88/CEND1 in Drosophila Affects Nervous System Development by Interfering with Precursor Cell Formation.Neuroscience bulletin · 2019Article
- Expression of AHI1 Rescues Amyloidogenic Pathology in Alzheimer's Disease Model Cells.Molecular neurobiology · 2019Article
- Loss of the neurodevelopmental Joubert syndrome causing protein, Ahi1, causes motor and muscle development delays independent of central nervous system involvement.Developmental biology · 2019Article
- Cend1, a Story with Many Tales: From Regulation of Cell Cycle Progression/Exit of Neural Stem Cells to Brain Structure and Function.Stem cells international · 2019Review
- Mutant Ahi1 Affects Retinal Axon Projection in ZebrafishFrontiers in cellular neuroscience · 2019Article
- Tyrosine hydroxylase down-regulation after loss of Abelson helper integration site 1 (AHI1) promotes depression via the circadian clock pathway in mice.The Journal of biological chemistry · 2018Article
- Alterations in the expression of a neurodevelopmental gene exert long-lasting effects on cognitive-emotional phenotypes and functional brain networks: translational evidence from the stress-resilient Ahi1 knockout mouse.Molecular psychiatry · 2017Article
- Cytoplasmic mislocalization of RNA splicing factors and aberrant neuronal gene splicing in TDP-43 transgenic pig brain.Molecular neurodegeneration · 2015Article
- Response to Heller and Bolz.Genetics in medicine : official journal of the American College of Medical Genetics · 2015Article
- The influence of AHI1 variants on the diagnosis and treatment outcome in schizophrenia.International journal of molecular sciences · 2015Article
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Authors and funding
14 authors at 6 institutions in 4 countries.
Funding
Abstract
Mutations in the Abelson helper integration site-1 (AHI1) gene result in N-terminal Ahi1 fragments and cause Joubert syndrome, an autosomal recessive brain malformation disorder associated with delayed development. How AHI1 mutations lead to delayed development remains unclear. Here we report that full-length, but not N-terminal, Ahi1 binds Hap1, a huntingtin-associated protein that is essential for the postnatal survival of mice and that this binding is regulated during neuronal differentiation by nerve growth factor. Nerve growth factor induces dephosphorylation of Hap1A and decreases its association with Ahi1, correlating with increased Hap1A distribution in neurite tips. Consistently, Ahi1 associates with phosphorylated Hap1A in cytosolic, but not in synaptosomal, fractions isolated from mouse brain, suggesting that Ahi1 functions mainly in the soma of neurons. Mass spectrometry analysis of cytosolic Ahi1 immunoprecipitates reveals that Ahi1 also binds Cend1 (cell cycle exit and neuronal differentiation protein 1)/BM88, a neuronal protein that mediates neuronal differentiation and is highly expressed in postnatal mouse brain. Loss of Ahi1 reduces the levels of Cend1 in the hypothalamus of Ahi1 KO mice, which show retarded growth during postnatal days. Overexpressed Ahi1 can stabilize Cend1 in cultured cells. Furthermore, overexpression of Cend1 can rescue the neurite extension defects of hypothalamic neurons from Ahi1 KO mice. Our findings suggest that Cend1 is involved in Ahi1-associated hypothalamic neuronal differentiation in early development, giving us fresh insight into the mechanism behind the delayed development in Joubert syndrome.
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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 OpenQuestion graph.