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Sunoh Kim

Researcher at Korea University

Publications -  28
Citations -  986

Sunoh Kim is an academic researcher from Korea University. The author has contributed to research in topics: Receptor & NMDA receptor. The author has an hindex of 13, co-authored 25 publications receiving 921 citations. Previous affiliations of Sunoh Kim include Natural Resources Research Institute & Chonbuk National University.

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The Novel Cellular Mechanism of Human 5-HT6 Receptor through an Interaction with Fyn

TL;DR: It is demonstrated that the activation of 5-HT6R activated the extracellular signal-regulated kinase1/2 via an Fyn-dependent pathway, suggesting that Fyn may play an important role in 5- HT6R- mediated signaling pathways in the central nervous system.
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Inhibitory effect of ginsenosides on NMDA receptor-mediated signals in rat hippocampal neurons.

TL;DR: Examination of the direct modulation of ginseng on the activation of glutamate, especially NMDA, receptors in cultured hippocampal neurons suggests that the inhibition of NMDA receptors by gINSeng, in particular by ginsenoside Rg3, could be one of the mechanisms for ginsENG-mediated neuroprotective actions.
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Activation of NMDA receptors increases proliferation and differentiation of hippocampal neural progenitor cells.

TL;DR: The results are the first to show that stimulation of NPCs may lead to either proliferation or neuronal differentiation, depending on the level of NMDA receptor activation, and suggest that neurogenesis in the developing brain is likely to be both directly and indirectly regulated by complex interactions between Ca2+ influx and excitation-releasable cytokines, even at mild levels of excitation.
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Functional interaction of neuronal Cav1.3 L-type calcium channel with ryanodine receptor type 2 in the rat hippocampus.

TL;DR: It is found that the N terminus of the rat Cav1.3 α1 subunit interacts with a partial N-terminal amino acid sequence of ryanodine receptor type 2 (RyR2) and that RyR2 mRNA itself is increased by long term treatment of high-K via activation of L-type Ca2+ channels.