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MC1R variants are associated with sun-sensitive phenotypes but the association with melanoma appears to be mediated also through non-pigmentary pathways [ 12, 15].
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In this context, it is also interesting to note that although the effect of Rg1 could also be mediated through a MAPK pathway and there is evidence that ERK1/2 regulates HIF-1α function in certain cells [ 26], we ruled out this possibility in HUVEC, since treatment of cells with the ERK1/2 inhibitor PD98059 had no effect on Rg1-mediated activation of HIF-1α (Supplementary Fig. 1).
Suppression of COX2 expression may also be mediated through IFN-γ production with consequent effects upon prostanoid-mediated local inflammation.
We conclude that the antinociceptive activity of MEMC may also be mediated through inhibition of PKC pathway and bradykinin receptor as well as through the activation of K+ channels, adrenergic, serotonergic and adenosinergic receptor systems.
A potential effect of BPA on the hypothalamic pituitary gonadal hormone axis could, therefore, also be mediated through an antagonistic effect of BPA on the AR, likewise resulting in the same hormonal pattern.
The augmented glucose uptake observed in our study can also be mediated through AMPKα activation.
The experiment using anti-IFN-γ antibody revealed that the inhibitory role of IFN-β could also be mediated through enhancing the production of IFN-γ.
Alternatively, the association between telencephalon, cerebellum and habitat complexity could also be mediated through social factors, rather than purely ecological effects.
It has been proposed that the lipid tail of glycosphingolipids can interact with the inner membrane leaflet, and signaling may also be mediated through a membrane protein interacting with the Stx/Gb3-complex.
Whilst this observation suggests that the increased endocytic capacity of LMN and FN treated DC is due to a higher expression of MR and DC-SIGN, dextran uptake could also be mediated through macropinocytosis.
However, the excess mortality could also be mediated through shared susceptibility to some infectious pathogens or increased prevalence of HCV infection among siblings of HIV/HCV-co-infected individuals.
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