Publications by authors named "Heera Moon"

Sensory abnormalities are observed in ~90% of individuals with autism spectrum disorders (ASD), but the underlying mechanisms are poorly understood. GluN2B, an NMDA receptor subunit that regulates long-term depression and circuit refinement during brain development, has been strongly implicated in ASD, but whether GRIN2B mutations lead to sensory abnormalities remains unclear. Here, we report that Grin2b-mutant mice show behavioral sensory hypersensitivity and brain hyperconnectivity associated with the anterior cingulate cortex (ACC).

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Article Synopsis
  • - ADNP syndrome is linked to developmental delays, intellectual disabilities, and autism spectrum disorders due to issues with the ADNP transcription factor in mice, particularly the Adnp-haploinsufficient (Adnp-HT) type.
  • - Adnp-HT mice exhibit cognitive inflexibility and synaptic plasticity deficits, indicated by hyperactivity of the protein CaMKIIα, affecting their learning and memory capabilities and causing social deficits.
  • - In adult Adnp-HT mice, the hippocampus shows elevated levels of phosphorylated CaMKIIα and prolonged long-term potentiation (LTP), which could be countered by inhibiting CaMKIIα, suggesting a link between ADNP deficiency and cognitive issues. *
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Apoptotic cells expressing phosphatidylserine (PS) on their cell surface are directly or indirectly recognized by phagocytes through PS-binding proteins. The PS-binding protein Tim-4 secures apoptotic cells to phagocytes to facilitate the engulfment of apoptotic cells. However, the molecular mechanism by which Tim-4 transduces signals to phagocytes during Tim-4-mediated efferocytosis is incompletely understood.

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