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IGF-2 can furthermore activate IR-A homodimer receptors.
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Furthermore, activated Chk2 can regulate not only p53-mediated apoptosis, but also p53-independent apoptosis [38].
Furthermore, activated NIK can cross-talk with the classical NF- κB pathway through the NIK-IKK complex.
Furthermore, activated Akt/PKB can induce serine phosphorylation of GSK3 (Ser21 for GSK3α; Ser9 for GSK3β) to inactivate the kinase activity, which subsequently lead to an activation of GS and then increased glycogen synthesis [ 34, 35].
Furthermore, activated mTOR/S6K pathway can cause insulin resistance (Khamzina et al., 2005; Krebs et al., 2007).
Furthermore, we can activate other essential activities of the AR learning system and examine them in conjunction with our approach in system design.
Interestingly, NK cells can furthermore function as "adaptive effectors" once activated by T cell-induced IFN-γ or when IgG eventually elicits antibody-dependent cell cytotoxicity [ 36– 36].
Furthermore, it can activate complement with similar activity to ficolin-A, and thus functionally more closely resembles its human, rather than mouse, counterpart.
Furthermore, ROS can activate apoptotic signaling via ASK1/JNK signASK1/JNK.
Furthermore, AKT2 can activate GYS1 by phosphorylating and inhibiting glycogen synthase kinase 3B (GSK-3B) which in turn phosphorylates and inactivates GYS163,64.
Furthermore, inflammation can activate autophagy [ 54].
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