In this case we have two similarly structured proteins with different sequences that interact with the same region of a third part (ADIPOR1) by triggering the same cellular process.
Whatever their mechanism of action, both serve to illustrate that p38 or MK2 can be activated sufficiently to have an effect upon the cell cycle and cellular replicative capacity, but not sufficiently to make this activation readily detectable by immunoblot, and thus by extrapolation potentially not sufficiently to affect cellular morphology by triggering the expression of F-actin stress fibres.
This is achieved by using a homing endonuclease to introduce DNA double-stranded breaks (dsb) within the integrated proviral DNA, which is followed by triggering of the cellular DNA damage response and error-prone repair.
Studies have demonstrated that EBV is involved in direct carcinogenesis by triggering various cellular responses including the activation of inflammation [ 9, 10].
These respond by triggering further cellular changes, including an increase in calcium levels that makes the cell interior more alkaline and the addition of phosphate groups to the amino acid tyrosine in proteins.
The idea is also supported by the seminal research [20] suggesting that cellular cytoskeleton responds to gravity by triggering different cellular mechanisms.
In the light of these results, we conjecture that cell proliferation, in the presence of cell cell communication, could provide a mechanism for reliable decision making in the presence of noise, by triggering cellular transitions only when the whole cell population reaches a certain size.
By triggering a cellular energetic dysfunction, and by promoting proinflammatory gene expression, PARP activation significantly contributes to the pathogenesis of shock.
Cytokines can contribute to initiation and progression of atherosclerotic lesions by triggering multiple cellular functions such as leukocyte recruitment and synthesis/degradation of extracellular matrix.
For example, Eugenin et al. have elegantly demonstrated the role of astrocyte gap junctions in mediating blood brain barrier damage, possibly by triggering bystander cellular dysfunction and endothelial apoptosis.
