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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining
Brain Res 2001, PMID: 11578622

PKC and CaMKII dependent synaptic potentiation in cultured cerebral neurons.

Kudoh, S N; Nagai, R; Kiyosue, K; Taguchi, T

We have reported that the long-lasting potentiation of spontaneous excitatory postsynaptic currents (SEPSCs) was induced by a Mg(2+)-free treatment in cultured chick cerebral neurons and a factor(s) extracellularly released during the treatment could induce the potentiation by itself. In this paper, protein kinase C (PKC) and calcium/calmodulin-dependent protein kinase type II (CaMKII) but not protein kinase A (PKA) were reported to contribute to the potentiation mechanism during a step between the activation of the N-methyl-D-aspartate receptors by the Mg(2+)-free treatment and the secretion of the protein factor(s).

Diseases/Pathways annotated by Medline MESH: Magnesium Deficiency, Synaptic Transmission
Document information provided by NCBI PubMed

Text Mining Data

protein kinase A (PKA) → calcium/calmodulin: " In this paper, protein kinase C ( PKC ) and calcium/calmodulin dependent protein kinase type II ( CaMKII ) but not protein kinase A (PKA) were reported to contribute to the potentiation mechanism during a step between the activation of the N-methyl-D-aspartate receptors by the Mg ( 2+ ) -free treatment and the secretion of the protein factor ( s ) "

Manually curated Databases

No curated data.