Since Akt strongly activates TORC1 activity and induces tissue growth, this suggests other targets of Akt must be responsible for these effects.
As expected, addition of POLβ strongly activates FEN1 exonuclease activity on both αdAT and THFT substrates, suggesting that the strand-displacement synthesis is necessary for FEN1 nuclease function.
Upon hyperphosphorylation in the hop Tum-l mutant, STAT92E becomes transcriptionally active and strongly activates GFP expression.
Importantly, phosphorylation does not always predict cotransport activity and ouabain strongly activates both NKCC1 and NKCC2.
We speculate that the activation of PL excitatory neurons strongly activates the descending inhibitory pathway, which thus increases the pain threshold.
Inhibition of HMGCR strongly activates LATS1/2 and reduces the transcriptional activity of TAZ, hence exhibiting anti-proliferation and apoptotic effects on breast cancer (Sorrentino et al., 2014).
The mutant receptor strongly activates Stat3 and induces the feedback inhibitor SOCS3, however, it only causes partial activation of the JAK/Erk cascade.
Especially HI briefly but strongly activates the innate immune system.
Chronic nicotine exposure strongly activates Stat3, leading to cyclin D1 overexpression, cell cycle perturbations, and chemoresistance.
Conversely, membrane targeting of Flt3-ITD strongly activates the MAPK and PI3K pathways, with diminished phosphorylation of STAT5.
Conversely, exercise that strongly activates JNK (e.g., weight lifting; Fig. 7) will result in inhibition of myostatin and a shift toward a hypertrophic adaptive program.
