ArticleMolecular brain2019
Inositol polyphosphate multikinase deficiency leads to aberrant induction of synaptotagmin-2 in the forebrain.
Article in Molecular brain, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 8 citations in OpenAlex.
- IPMK at the crossroads of cellular signaling in health and disease.FEBS letters · 2026Review
- IPPK-1 and IP6 contribute to ventral nerve cord assembly in C. elegans.Developmental biology · 2025Article
- Synaptotagmin 2 is ectopically overexpressed in excitatory presynapses of a widely used CaMKΙΙα-Cre mouse line.iScience · 2022Article
- Inositol hexakisphosphate kinase-1 is a key mediator of prepulse inhibition and short-term fear memory.Molecular brain · 2020Article
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3 authors at 1 institution in 1 country.
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Abstract
Inositol polyphosphate multikinase (IPMK), the key enzyme responsible for the synthesis of higher inositol polyphosphates and phosphatidylinositol 3, 4, 5-trisphosphate, is known to mediate various biological events, such as cellular growth and metabolism. Conditional deletion of IPMK in excitatory neurons of the mouse postnatal forebrain results in enhanced extinction of fear memory accompanied by activation of p85 S6 kinase 1 signaling in the amygdala; it also facilitates hippocampal long-term potentiation. However, the molecular changes triggered by IPMK deletion in the brain have not been fully elucidated. In the present study, we investigated gene expression changes in the hippocampal region of IPMK conditional knockout (cKO) mice by performing genome-wide transcriptome analyses. Here we show that expression of synaptotagmin 2 (Syt2), a synaptic vesicle protein essential for Ca
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