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Molecular targets of SIRT1 include LKB1 and peroxisome proliferator-activated receptor γ co-activator α (PGC1α), which is also activated through AMPK-mediated phosphorylation at Ser538 and Thr177 and cooperates with PPARα to induce mitochondrial biogenesis.
The proinflammatory pathway is also activated through nuclear factor-κB activation.
ERK1/2 is also activated through NMDA-dependent electrophysiological stimulating potentiation protocols [35], and by NMDA application upon hippocampal slices [20], [36].
In experimental stroke, the complement system is also activated through non classical pathways (either the alternative or the lectin pathways) [6], [7].
Caspase-8 is also activated through a virus-induced FADD-mediated apoptosis pathway.
p53 protein is also activated through a number of other post-translational modifications, including phosphorylations, acetylations and methylation (Toledo and Wahl, 2006).
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This whole neuronal network was also activated through chemosensory anxiety signals.
Many DREB/CBF-regulated genes are also activated through ABA-mediated pathway [ 5].
Other pathways are also activated through FGFRs, including STAT-dependent signalling.
Plant defense signaling pathways are also activated through WRKY transcription factors that bind to pathogen-response and wound-inducible promoter elements (W-boxes and GCC-like elements).
Besides being activated through H2, lactic acid production is also activated via osmolarity, which at high concentrations inhibits growth [ 23].
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