Sentence examples for mediators that act from inspiring English sources

Among a number of signaling mediators that act downstream of integrins, FAK, Akt, NFκB, and their regulators have been well-characterized as important players for cell survival13,14,16.

This can be exemplified by a number of proinflammatory molecular mediators that act as essential components of regeneration pathways within the cell.

EETs are lipid mediators that act as potent cellular signaling molecules regulating key cellular processes, such as limiting mitochondrial damage, inhibiting apoptosis and reducing inflammatory responses.

This biomolecule is the first in a line of highly pro-inflammatory mediators that act as potent chemoattractants and are implicated in a variety of diseases from asthma to cancer.

Activation of fibroblast-like synoviocytes (FLSs) leads to the release of a broad array of mediators that act on cells of the immune system as well as resident joint cells, exacerbating the inflammatory response and resulting in articular cartilage and bone damage [ 1].

Upon exposure of phagocytes to microbes or inflammatory mediators that act upon cell surface receptors, these components along with p40 phox assemble at the membrane, triggered in part by phosphorylation of p47 phox and GTP binding to Rac, resulting in activation of Nox2.

Lysophosphatidic acid (LPA) is a lipid mediator that acts through specific G protein-coupled receptors to stimulate the proliferation, migration and survival of many cell types.

Lysophosphatidic acid (LPA) is a potent lipid mediator that acts on a series of specific G protein-coupled receptors, leading to diverse biological actions.

It is now accepted that resolution of inflammation is an active process mediated by a group of mediators that can act in synchrony to switch the phenotype of cells, from a proinflammatory one to another that favors the return to homeostasis.

One likely mechanism whereby particulate debris may induce osteoclast generation and activation is an indirect one, mediated through the actions of proinflammatory mediators that can act on osteoclast precursors and, most importantly, modulate the RANKL/osteoprotegerin (OPG) ratio through actions on cells within the periprosthetic tissue.

In addition to these growth factors, chronically inflamed RA synovia contain a multitude of inflammatory mediators that may act in concert with each other.