It can activate mitogen-activated protein kinase (MAPK) cascades and negatively regulates MAPK activity.
But the DNA damage induced by VP16 has been shown that it can activate the activity of p53 [11] 11].
Together with its transcriptional co-activator, YAP65, it can activate the expression of genes that serve different functions during cell differentiation and development.
When a GPCR is active, it can activate the G protein, which can then interact with several other signal proteins to amplify the signal from the GPCR.
Once awake, it can activate its instruments and prepare for the rendezvous.
As discussed before, HSP60 may be able to do this on its own, as it can activate both the innate and adaptive immune systems.
Thus ADAM17 has an essential role in the epithelial-stromal cross-talk that regulates mammary development by liberating an essential ligand (amphiregulin) that is expressed only on epithelial cells so it can activate its receptor (EGFR) on stromal cells.
Furthermore, it can activate complement with similar activity to ficolin-A, and thus functionally more closely resembles its human, rather than mouse, counterpart.
In Fadd−/− MEFs, ligation of TNFR1 can activate RIPK3 when its levels are elevated, and it can activate the necroptotic pathway but not the caspase 8-dependent cell death pathway (panel 4).
Since auto-activated EGFR is maintained at the PM, it can activate Akt via PIP3 production by PI3K at the PM (Cantley, 2002), resulting in survival signaling.
It can activate NF-κB and all three classes of mitogen-activated protein (MAP) kinases including extracellular signal-related kinase (ERK 1 and ERK2, c-Jun N-terminal kinase (JNK), and p38 [ 13- 15].
