The elevation in TNF-α protein content observed in CR mice may elicit cell death through the activation of apoptotic proteins [62].
Therefore, algal extract may elicit cell cycle arrest responses.
Expression of particular embryonic mammary markers within tumor cells may reflect reactivation of genetic programs that influence the behavior of immature cell types present within the breast and may elicit cell behavior associated with embryonic cells, such as a less-differentiated, highly plastic state.
Some studies suggest that exogenous HA likely only transiently contacts and signals cells, and may elicit different cell responses when presented on a substrate (e.g., scaffold surface).
In parallel, we sought to determine whether co-treatment with I3C and bortezomib may elicit a cell cycle arrest at the G1-S boundary.
This suggests that the normal virulence mechanisms that may elicit host cell death are still functionally intact in the Δ ZtCBR1 strains but occur later, possibly as a consequence of the reduced hyphal growth rate.
To this end, these investigations provide insight into the conditions of the degenerate niche and indicate that further investigations to determine the effects this environment may elicit on cell behaviour are required.
We speculate that certain RGE or RGE-like motifs may elicit weak cell attachment, followed by apoptosis – a combination of properties, reminiscent of snake venom disintegrins [ 30, 31], that could have important functional implications in the context of the extensive tissue remodelling that occurs during placentation [ 32].
Primarily, the stimulation of P2X receptors causes Ca2+ influx and can stimulate distinct Ca2+-dependent signalling cascades, which may have particular propensity to elicit cell death [13] e.g., by ischemia-induced excitotoxic glutamate release [14], or the activation of extracellular signal-regulated protein kinase (ERK) by P2X2 receptors [15].
However, as nuclear localisation of GFPSmad2 is observed also in nonmotile cells, TGFβ signalling alone may not be sufficient to elicit cell motility in primary tumour cells.
Alternatively, plaque-associated activation of microglia may elicit T-cell-mediated neuroprotection and 'wound repair responses' that help maintain optimal CNS function during immune therapies with pro-inflammatory consequences (Fisher et al., 2010).
