Sentence examples for alternatively activation from inspiring English sources

Alternatively, activation of RSK may serve the only purpose of activating the PKN subunits of the YopM complex which subsequently phosphorylate physiological substrates.

Alternatively, activation may have occurred by antibody-independent mechanisms, either via the alternative pathway, or via a direct interaction of C1q with exposed cell constituents like perturbed cellular or mitochondrial membranes or chromatin.

Alternatively, activation of regulatory T cells that suppress the specific immunity may be too efficient.

Alternatively, activation is mediated by CoA ligases and the formed CoA derivatives are subject to oxygenations.

Alternatively, activation of the pathway can be triggered by Sterol Response Element Binding Proteins (SREBPs), as part of a compensatory feedback mechanism.

Alternatively, activation of α7 NNRs on glutamate afferents within the nucleus accumbens can, through spillover of glutamate, activate metabotropic glutamate receptors on dopamine terminals and depress dopamine release.

In contrast, macrophages can become alternatively activated (M2 activation) in response to anti-inflammatory molecules such as IL-4 (interleukin-4) and IL-10 and are the major wound-healing cells (Gordon, 2003; Biswas et al., 2008).

ILC2s are a critical innate source of type 2 cytokines, such as IL-4, IL-5, IL-9 and IL-13, which can induce eosinophilia, mastocytosis, activation of alternatively activated macrophages, goblet cell hyperplasia and muscle contractility, and tissue repair (Pulendran and Artis, 2012).

Mycobacterial antigens can signal macrophages via the Toll like receptors [40] and recently TLR9 has been implicated in the activation of alternatively activated macrophages (AAM φ) [41].

M1 is associated with classical TNF/IFNγ-mediated pro-inflammatory activation; whereas the alternatively activated M2 is subdivided into the M2a stage characterized by alternative activation-anti-inflammatory cytokines (IL-4 or IL-13) and the M2c stage as the deactivation-wound healing stage with cytokines that promote tissue repair [IL-10 and TGFβ (tumour growth factor β)].

We show that exposure to MMF switches the molecular and functional phenotype of activated microglia from classically activated, pro-inflammatory type to alternatively activated, neuroprotective one, through activation of the hydroxycarboxylic acid receptor 2 (HCAR2).