DNA unzipping, the separation of its double helix into single strands, is crucial in modulating a host of genetic processes.
Upon exposure to exogenous alkylation damage, yeast respond by modulating a host of biological processes that includes, as expected, DNA repair and cell cycle checkpoint pathways, but also includes the following: (i) activation of protein degradation machinery, (ii) increased lipid metabolism, (iii) increased RNA processing and (iv) decreased protein synthesis (ribosomal biosynthesis) [1], [2].
By extension, the association of Clp protease domains with AAA+ mediated assemblies of protein complexes would allow them to modulate a host of cellular and physiological processes where AAA+ modules are required and would facilitate the availability of diverse substrates for degradation by Clp protease domain.
Some previous pre-clinical and clinical studies showed that both conventional Nonsteroidal anti-inflammatory drugs (NSAIDs) and those selective inhibitors of Cyclooxygenase-2 (COX-2) are able to modulate a host's immune-inflammatory reaction [ 10- 15].
Furthermore, since the primary functions of WAT are to store energy and act as an endocrine organ, stress-induced IL-1β signaling likely affects the metabolic and/or endocrine functions of WAT; however, because WAT also contains immune cells, mast cells, endothelial cells, preadipocytes and fibroblasts, IL-1β may also modulate a host of other functions.
It appears that coagulants, serine proteases, and matrix metalloproteases (MMPs) facilitate tumor cell metastasis by modulating a number of host vascular cell responses as well as by acting directly on tumor cells themselves.
In each case above, the function of the protein is to modulate a critical host defence molecule.
Additionally, it is capable of exchanging information with cells and thereby modulates a whole host of processes including development, cell migration, attachment, differentiation, and repair.
Our results suggest, however, a possible therapeutic approach in which A. fumigatus infection is treated by a combination of antifungals and MAPK inhibitors which can modulate an excessive host inflammatory response [37], [53].
Among the four proteins originating from the HBV genome, such as the polymerase, surface, core, and HBx proteins, hepatitis B virus X, a small 154-amino acid protein, is a multifunctional regulator which modulates a variety of host processes via interaction with virus and host factors [3], [4].
Rho GTPases modulate a variety of host cell processes in a GTP-dependent manner by activating a plethora of downstream effectors at specific host cell compartments (Stebbins and Galan, 2001).
