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As NF-κB can be activated through many different pathways, including phosphatidylinositol 3-kinase (PI3K) and its major downstream kinase, Akt [18], we hypothesize that PI3K/Akt contributes to myelin-induced NF-κB activation.
Flexible memory representations can be activated through many, even remotely related retrieval cues in situations that have little or no overlap with the encoding situation.
PI3K can be activated through many mechanisms other than mutations, and loss of negative feedback loops such as inactivation of PTEN (phosphatase and tensin homolog deleted on chromosome 10) can also activate this complex pathway [ 32].
Similar(57)
In mammals, CREB plays an important role in many biological processes [ 1] and can be activated through several signaling pathways (see reviews: [ 1, 3]).
The ad can also be activated through in-text ads.
Its protein product cannot be activated through Tyr phosphorylation.
Wnt signaling is activated through cytoplasmic β-catenin.
The substrate is activated through protonation by a conserved tyrosine.
Monocytes/macrophages were activated through the physiological CD23 pathway [ 22].
NFκB is activated through the upstream kinase TAK1.
The extrinsic pathway is activated through the death receptors (DRs).
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