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The activation of the first kinase, MAPKKK, is initiated by it binding to an activated Ras or Rho family protein.
Furthermore, E/S/L has the ability to promote platelet binding to an activated endothelium and therefore concentrate this inhibitor at susceptible sites; i.e., tumor-adjacent vasculature.
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The five hnwd genes encode for proteins of the STAND class thought to act as molecular switches with a closed inactive form and an open active form adopted upon binding to an activating molecule [ 26, 27].
After binding to an activating ligand, such as corticosteroid, the glucocorticoid receptor (GR) performs an impressive array of functions ranging from nuclear translocation, oligomerization, cofactor⧸kinase⧸transcription factor association, and DNA binding.
These results suggested ATP binding to a P2YR activating an inositol 1,4,5-trisphosphate (IP3 -mediated IP3 -mediated release of Ca2+ and a subsequent entry of dintracellularhreleaseof [ 21, 22].
It does so by binding to an Upstream Activating Sequence (UAS) located in the promoters of target genes.
Glucocorticoids exert their effects by binding to and activating an intracellular glucocorticoid receptor (GR) protein (Fig. 1), as well as a mineralocorticoid receptor protein [ 18, 19].
Such a hypothetical nucleator would function analogously to the actin nucleating complex Arp2/3, which becomes activated on binding to an existing actin filament [6].
It acts by binding to and activating a receptor in the cytoplasm of renal tubular cells.
PGCs regulate the muscle metabolic phenotype by binding to and activating a variety of nuclear receptors and additional transcription factors.
ATP mediates its diverse effects by binding to and activating a broad range of cell surface P2Y and P2X receptors [ 45].
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