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Immunotherapy strengthens the immune system by supporting activation of the body's cancer-fighting T-cells.
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Phosphorylation of AKT, ERK/MAPK, and S6 were also induced by HRG, further supporting activation of GF signaling in response to stimulation by HRG.
Increased expression of Srebf2, Cebpd, and Scap was identified by quantitative PCR (Fig. 6d), supporting activation of UPR pathway components associated with lipid biosynthesis following birth.
These observations, along with recent findings supporting activation of MAPKs by 15d-PGJ2 in a number of cells (Wilmer et al, 2001; Lennon et al, 2002), provide another possible explanation for 15d-PGJ2 effects on Stat3 signalling.
Activation of ERBB2 by EGF or HRG could be found in Jones et al. (1999) (EGF/HRG → ERBB2/3), which also supported activation of PKCα by HRG through the cascade HRG → ERBB2 → PKCα, since crosstalk between ERBB2 and PKCα in ERBB2 overexpressing breast cancer cells was reported by Magnifico et al. (2007).
Moreover, it has been repeatedly shown that inflammatory cells can influence fibrogenesis by supporting the activation of human pancreatic stellate cells (hPSCs), which consequently release ECM proteins leading to fibrosis [ 4, 5].
Thus, formation of the bulgy morph may also require and be supported by activation of innate immune systems.
As proposed by Panksepp, a variety of stressors may induce perturbed neural circuits, and changes towards an opposite preferred endorphin state can be described, supported by activation of the mesolimbic dopaminergic pathways, creating reward when approaching the desired state.
Thus, formation of the bulgy morph to reduce predation risk involves a clear remodeling of the connective tissues and physiological control of bodily fluids, and may also be supported by activation of innate immune systems.
Thus, our data suggest that inflammation and/or pathogens in the brain cause hBMVEC to modulate their own basolateral iron efflux by supporting a cytokine-mediated activation of sCp expression in neighboring astrocytes.
These responses were completely and reversibly blocked by 20 nM MLA supporting the activation of α7* nAChRs (Figure 4E F).
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