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These mechanisms include activation of several downstream signal-transduction pathways, which regulate cell survival, proliferation and migration [18], [20], [21].
Proposed mechanisms include activation of kinases, overexpression of cytokines, dysregulation of cell surface receptors and activation of oncoproteins.
Other proposed mechanisms include activation of L-type Ca2+ channels, increase in the phospholipid turnover, activation of the adenylate cyclase/cAMP system (GLP-1) or blockage of ATP-dependent K+ channels [30].
The related mechanisms include activation of the sympathetic nervous system, release of catecholamines and other hormones, and inflammatory responses.
Other mechanisms include activation of neutrophils, monocytes and microvascular endothelial cells as well as activation of the complement, coagulation and fibrinolytic systems [ 4, 5].
Possible mechanisms include activation of Mps1 [ 26], promoting the interaction between Cdc20 and Mad2 [ 27], or aiding localization of the chromosomal passenger complex at kinetochores [ 3, 15].
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The proposed pathogenesis of burn- and smoke-induced myocardial dysfunction is based on inflammatory mechanisms, including activation of the p38-mitogen-activated protein kinase (p38-MAPK) pathway as well as production of tumor necrosis factor alpha (TNF-α) and nitric oxide (NO) [ 6- 8].
Both components lead to diabetic complications through several major mechanisms, including activation of oxidative stress and increased chronic inflammatory activity [ 3].
Through these receptors, PACAP leads to an increase in intracellular cAMP, which activates PKA and produces vasodilation by several mechanisms including activation of KATP channels (Fig. 4) [45].
CRL ligase activities are controlled by several complex regulation mechanisms, including activation by conjugation with the protein NEDD8 (neural precursor cell expressed, developmentally downregulated 8) and inhibition by binding of CAND1 (cullin-associated and neddylation-dissociated 1).
Although several mechanisms, including activation of the insulin-like growth factor receptor and mitogen-activated protein kinases, have been provided (Santen et al, 2005; Sabnis et al, 2007), some data indicate HER-2/neu may be important (Song et al, 2002; Martin et al, 2003, 2005).
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mechanisms include column
mechanisms include nanocrack
mechanisms include hypoxia
mechanisms include surface
mechanisms include thrombosis
mechanisms include promoter
mechanisms include ion
mechanisms include immunity
mechanisms include phagocytosis
mechanisms include endocytosis
mechanisms include glutathione
mechanisms include formation
mechanisms include anti-apoptosis
mechanisms include tissue
mechanisms include cell
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