Sentence examples for activation rage from inspiring English sources

In addition to triggering NF-κB activation, RAGE engagement by its myriad ligands is linked to an array of signaling pathways, including MAPK family members, such as Jun-N-terminal kinase (JNK), p38 and extracellular signal-regulated kinase (ERK), PI3K/Akt, Rho GTPases, Jak/STAT and Src family kinases [ 7].

It is, however, noted that attenuation of kainate-induced gamma oscillations in S100B KO [18] has recently been demonstrated to be dependent on activation of RAGE [13], suggesting a role of RAGE in hyperactive brain states.

The initial accumulation of AGEs in the vascular tissue could exacerbate local inflammation and lead to downstream cellular activities that favor cell-mediated vascular calcification by activation of RAGE [ 3, 4].

The activation of RAGE results in activation of an inflammatory signaling cascade, and up-regulation of RAGE is associated with sustained cellular perturbation and tissue injury [ 5].

As activation of RAGE accelerates pathological progression of diabetes or Alzheimer's disease, therapeutic treatments to attenuate activation of RAGE have been suggested [24] and experimented in animal disease or inflammation models [8], [25], [26], [27].

Besides, activation of RAGE induces generation of oxygen radicals by a yet unknown mechanism [ 28, 46].

Activation of RAGE results in sustained activation of NF-κB, thereby converting transient proinflammatory responses into lasting cellular dysfunction [ 19].

The activation of RAGE stimulates critical signaling pathways linked to inflammation, resulting in the activation of various inflammatory genes [ 55].

Activation of RAGE induces and supports inflammatory responses, mainly by NF-κB and mitogen-activated protein kinase (MAPK) activation.

One of the earliest events following activation of RAGE is phosphorylation of the extracellular signal-regulated kinase (ERK) (19).

Activation of RAGE results in sustained activation of nuclear factor-kappa B (NF-κB), thereby converting transient pro-inflammatory responses into lasting cellular dysfunction [ 4].