IndraLab

Statements


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"The specific effect of lithium on T91 and T93 phosphorylation, together with the evidence that the c-JunD95 mutant resumes GCG apoptosis in presence of lithium, is consistent with a model whereby lithium blocks c-Jun pro apoptotic activity by targeting the priming T95 phosphorylation event for T91 and T93 phosphorylation."

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"Yet, the mechanism by which lithium inhibits c-Jun activity remains to be elucidated."

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"Here we show that lithium blocks the canonical c-Jun apoptotic pathway in cerebellar granule neurons deprived of trophic support."

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"Lithium blocks the c-Jun stress response and protects neurons via its action on glycogen synthase kinase 3."

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"In these same neurodegenerative disorders as well as in stroke, TBI and SCI, retinal degeneration, MS, and HIV, lithium inhibits glutamate induced excitotoxicity mediated by NMDA receptors, specifically attenuating the NR2B subunit constitutive tyrosine phosphorylation, and subsequent calcium influx, thus suppressing excitotoxicity induced p38 and c-Jun N-terminal kinase (JNK), and subsequent transcription factor activator protein-1 (AP-1) activation to block neuronal apoptosis."

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"A further question addressed by our study is the mechanism through which lithium blocks c-Jun pro apoptotic function without inhibiting JNK activity."