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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining
J Neurosci 2007, PMID: 18160642

FMRP phosphorylation reveals an immediate-early signaling pathway triggered by group I mGluR and mediated by PP2A.

Narayanan, Usha; Nalavadi, Vijayalaxmi; Nakamoto, Mika; Pallas, David C; Ceman, Stephanie; Bassell, Gary J; Warren, Stephen T

Fragile X syndrome is a common form of inherited mental retardation and is caused by loss of fragile X mental retardation protein (FMRP), a selective RNA-binding protein that influences the translation of target messages. Here, we identify protein phosphatase 2A (PP2A) as an FMRP phosphatase and report rapid FMRP dephosphorylation after immediate group I metabotropic glutamate receptor (mGluR) stimulation (<1 min) in neurons caused by enhanced PP2A enzymatic activity. In contrast, extended mGluR activation (1-5 min) resulted in mammalian target of rapamycin (mTOR)-mediated PP2A suppression and FMRP rephosphorylation. These activity-dependent changes in FMRP phosphorylation were also observed in dendrites and showed a temporal correlation with the translational profile of select FMRP target transcripts. Collectively, these data reveal an immediate-early signaling pathway linking group I mGluR activity to rapid FMRP phosphorylation dynamics mediated by mTOR and PP2A.

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Text Mining Data

PP2A ⊣ mammalian target of rapamycin (mTOR): " In contrast, extended mGluR activation ( 1-5 min ) resulted in mammalian target of rapamycin (mTOR) mediated PP2A suppression and FMRP rephosphorylation "

Manually curated Databases

No curated data.