Possibly activation of TFT by thymidine kinase (TK) is very efficient, preventing inactivation by TP.
Possibly, activation of murine T cells improves the accessibility of the target mRNA and/or structure as well as transfection efficiency.
Possibly, activation of the innate immune response following radiation exposure confers a selective advantage by somehow enabling organisms to survive the immediate consequence of this exposure.
Possibly, activation of bone-seeking pathways in primary BCa cells, such as Src1 [ 8, 9], results in the stimulation of SNAI2 and other Runx2-regulated genes despite high levels of ERα.
Furthermore, since the NE and clonidine-mediated activation of PI3Kγ, PKCζ and of the SMD was prevented by yohimbine, our results demonstrate that activation of α2-adrenoceptors is required for activation of PI3Kγ and PKCζ, and possibly for activation of membrane Cl- and/or NCSS channels and SMD in canine mesenteric vein.
Combined activation of JNK and p38 appears to promote the transcriptional induction and possibly also activation of the BH3-only proteins Bim and Puma.
Together with its ability to induce cell surface expression of RANKL by osteoblasts and possibly induce activation of B cells into plasma cells we postulate that TWEAK in this context would be pro-osteoclastogenic and would thus contribute to the bone loss associated with this chronic inflammatory disease.
In summary, we have shown that intracellular levels of NF- κB-p65 and IKK α are increased in malignant colorectal epithelial cells, compatible with the hypothesis that NF- κB is involved in COX-2 induction in these tumours, and possibly the activation of other antiapoptotic genes that influence the development of colorectal carcinogenesis.
P. acnes has adapted to this environment and evolved strategies to survive in such a niche; such strategies include (among others) a strong lipolytic activity, pH regulatory mechanisms [ 61], biofilm formation [ 30], and possibly the activation of a dormant state and the escape into host cells [ 29].
It was postulated early that the contribution of malaria to BL pathogenesis involves its immunostimulatory effects on B cells [80] and possibly selective activation of the memory B-cell compartment [81], [82].
