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Alternatively, JNK may be activated through other direct or indirect integrin signalling pathways.
However, besides IL6, STAT3 can be activated through other pathways, such as that of IGFIR signaling.
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ProSense 680 is preferentially hydrolyzed by cathepsin B, but it can be activated through proteolysis by other cathepsins and other related proteases [14].
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].
In addition, stabilization of β-catenin and amplification of its target gene, cyclin D1, is documented in > 50% of breast carcinomas [ 11, 12], suggesting that the downstream effectors of the Wnt cascade could also be activated through abnormalities in other signaling pathways.
Hence, in the context of a class C GPCR homodimer, G proteins might be activated through the ligand-bound subunit (cis-activation) and/or through the other subunit (trans-activation).
Thus, it seems that other immune mechanisms must be activated through exposure to high dose IFN-α that are important for virus clearance [ 50].
Lieblein, J. C. et al. STAT3 can be activated through paracrine signaling in breast epithelial cells.
Adsorbed CO2 can be activated through a plasmon-induced carrier-assisted mechanism.
The ad can also be activated through in-text ads.
Its protein product cannot be activated through Tyr phosphorylation.
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