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Previous studies showed that activin A is increased in the CSF of patients suffering from BM. Furthermore, activin A may decrease the secretion of NO and pro-inflammatory mediators by activated microglia, and enhances microglial proliferation, suggesting that activin A may counteract the activation of microglial cells in BM [ 25].
These findings show that URB937 may counteract the activation of nuclei involved in migraine attacks probably via the increase of anandamide levels at the meningeal level, within the trigeminovascular system, or on extracerebral vessels.
183, 208, 239 Furthermore, PUFAs counteract the activation of SREBP-1c by increasing SREBP-1c proteolytic cleavage and decreasing its mRNA abundance (Table 2).
Indeed, unlike diuretics, which appear to activate neurohormonal systems, such as the renin-angiotensin-aldosterone system (RAAS) [ 50– 52], serelaxin appears to counteract the activation of neurohormonal systems.
One possible explanation for these results is that the upregulation of CD109 in SSc fibroblasts is not sufficient to completely counteract the activation of TGF-β or other profibrotic pathways in SSc.
DUSPS counteract the activation of MAP kinase pathways, known regulators of chondrocyte differentiation [ 85], and are thought to mediate DEX's anti-inflammatory functions and to influence hepatic gluconeogenesis [ 83, 86, 87].
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One example is the docking of Ras-GAP to the activated PDGFRβ; this counteracts the activation of Ras which occurs by the simultaneous docking of the Grb2-SOS1 complex [ 17].
Takada, S. & Goto, K. Terminal flower2, an Arabidopsis homolog of heterochromatin protein1, counteracts the activation of FLOWERING LOCUS T by constans in the vascular tissues of leaves to regulate flowering time.
Takada, S. & Goto, K. TERMINAL FLOWER2, an Arabidopsis homolog of HETEROCHROMATIN PROTEIN1, counteracts the activation of FLOWERING LOCUS T by CONSTANS in the vascular tissues of leaves to regulate flowering time.
These results show that this protein counteracts the activation of the yp genes by the endogenous Drosophila DsxF protein.
The tumour-suppressor phosphatase and tensin homology (PTEN) mediates the conversion of PIP3 to PIP2, counteracting the activation of AKT.
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