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It was further shown that Id proteins also inhibit ETS transcription factors (Yates et al, 1999) which are able to influence p16 expression by binding to and activate its promoter (Ohtani et al, 2001).
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For instance, the phytoestrogen genistein and the xenoestrogen bisphenol A, which exert estrogen-like activities binding to and activating ERα [ 9, 59], displayed the ability to bind to and activate GPER signaling [ 9, 27, 60].
These proteins act in the neutrophil cytosol, binding to and activating host caspase 1, the activation of which leads to host cell apoptosis.
However, not only may aromatase inhibitors increase circulating endogenous androgen concentrations, but some possess intrinsic androgenic activity by binding to and activating the AR [ 78, 87] – highlighting the limitations of pharmacological blockade of steroidal mechanisms, where blockers or their metabolites may have off-target effects.
These include inhibition of other kinases, tyrosine kinases such as Syk and JAK1, the serine/threonine kinase IκB, and the lipid kinase PI3K, as well as nonkinase activity such as binding to and activating estrogen receptors.
HIF-1 α inhibits c-Myc activity by promoting its degradation via the proteasome and by binding to and activating Mxi-1, which represses c-Myc transcriptional activity (Zhang et al, 2007a).
This demonstrates that Chi3l1 controls pyroptosis, apoptosis, inflammasome activation, and antipneumococcal responses by binding to and activating IL-13Rα2.
Hormones act on their target tissues by binding to and activating specific molecules called receptors.
It acts by binding to and activating a receptor in the cytoplasm of renal tubular cells.
VEGF-C mediates its signals by binding to and activating the vascular endothelial growth factor receptors VEGFR-3 and VEGFR-24.
The ELR+ CXC chemokine system includes many small and structurally similar chemoattractant ligands capable of binding to and activating the related CXCR1 and CXCR2 G protein-coupled receptors (GCPR) expressed on the surface of neutrophils4.
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