Here, the authors aimed to explore the part played by TDNs in proliferation and osteo/odontogenic differentiation of DPSCs, and attempted to investigate if these cellular responses could be driven by activating the canonical Notch signaling pathway.
Moreover, this hypothesis is strongly supported by our result that ATP oscillations depend on VDCC and SOC because Ca2+ oscillations are known to be driven by activating periodically VDCC through the repetitive membrane depolarizations or modulating release and uptake of Ca2+ at intracellular Ca2+ stores.
The majority of GISTs are driven by activating mutations in the receptor tyrosine kinases KIT or PDGFR-α, whose aberrant signaling induces uncontrolled proliferation and decreased apoptosis.
For instance, KIT overexpression in GISTs is driven by activating KIT mutations (Gomes et al, 2008), whereas HER2 overexpression in breast cancer is driven by HER2 gene amplification (Arriola et al, 2008).
In the clinical setting, it will be important to define tumours whose growth is dependent on the EGFR and which are being driven by activating ligands such as TGFα and EGF.
However, a growing body of evidence reveals that the pathological process of IPF may be driven by aberrantly activated AECs [ 1].
Although dichotomizing complex diseases such as RA in terms of Th1 or Th2 patterns may be an over-simplification, evidence is accumulating that suggests that human autoimmune diseases, such as RA, might also be driven by preferentially activated Th1 cells without sufficient Th2 cell development to downregulate inflammation.
Hence, although it is not proved that MT/V5 and V6 projections originate from the same neurons of layer IVB (see Vogt-Weisenhorn et al. 1995), one might have expected that human area V6 would be driven by stimuli activating human MT+.
The activation, however, appears to be driven by word, rather than sentence, processing because both single words and sentences activate the region to the same extent [39, 40].
Both peroxymonosulfate and peroxydisulfate can be driven by visible light for photochemical oxidation [21], while H2O2 can hardly be activated [22].
