p(HGNC:S100B) increases act(p(HGNC:AGER))

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PubMed:18494933

Utilizing Western blot, electrophoretic mobility shift assay, supershift and reverse transcriptase-polymerase chain reaction techniques, it has been demonstrated that micromolar S100B concentrations stimulate c-Jun N-terminal kinase (JNK) phosphorylation through the receptor for advanced glycation ending products, and subsequently activate nuclear AP-1/cJun transcription, in cultured human neural stem cells. In addition, as revealed by Western blot, small interfering RNA and immunofluorescence analysis, S100B-induced JNK activation increased expression of Dickopff-1 that, in turn, promoted glycogen synthase kinase 3β phosphorylation and β-catenin degradation, causing canonical Wnt pathway disruption and tau protein hyperphosphorylation. These findings propose a previously unrecognized link between S100B and tau hyperphosphorylation, suggesting S100B can contribute to NFT formation in AD and in all other conditions in which neuroinflammation may have a crucial role.

Related Edges 4

• p(HGNC:S100B) increases p(FPLX:JNK)
• p(FPLX:JNK) positiveCorrelation act(p(HGNC:AGER))
• p(FPLX:JNK) increases p(HGNC:DKK1)
• act(p(HGNC:AGER)) positiveCorrelation p(FPLX:JNK)

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