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The results show that osteoblasts-derived SDF-1 activates CXCR4 receptor and results in the activation of extracellular signal-regulated kinase (ERK /IκB kinase αβ (IKKαβ) and nuclear factor-kappa B (NF-κB), leading to upregulation of IL-6 expression and promoting osteoclastogenesis.
IL-22 signals through the Janus kinase/signal transducer and activator of transcription (STAT) signal pathway, and results in the activation of STAT3 through tyrosine phosphorylation.
It is possible that disassembly of focal adhesion molecules during mitosis releases the protein complexes and results in the activation of Aurora-A [38].
In subsets of VHL mutations, the lack of functional pVHL leads to accumulation of HIF, and results in the activation of HIFα target genes even in the presence of oxygen [12].
This pathway is initiated by p53 in response to cellular stress such as growth factor deprivation, hypoxia, cell detachment, or DNA damage [83] and results in the activation of the Bcl-2 family of proapoptotic genes.
Binding of the LPS/MD-2 complex to TLR4 causes TLR4 dimerization, and results in the activation of NF-κB leading to acute and severe inflammation and sepsis [7] [9], [19].
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These activation degrees are then summed up and result in the activation degree of the particular neuro-symbol.
In parallel, gp130 activation results in the activation of Raf/Ras/MEK cascade, and finally in phosphorylation and subsequent activation of p42 and p44 [11].
This results in the activation of HIF1 and NF- κB.
Activation of RIG-I leads to a signaling results in the activation of IRF-3 and IRF-7 [56] [58].
In turn, this results in the activation of RhoA, JNK, and transcriptional activation of ALDH1 through Jun-responsive promoter elements.
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