Sentence examples for binding to an activating from inspiring English sources

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.

It does so by binding to an Upstream Activating Sequence (UAS) located in the promoters of target genes.

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].

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 was originally thought that ligands binding to a receptor would equally activate the G-protein pathway to produce a physiological response such as vasoconstriction (such as ET-1 acting on an ETA receptor) as well as activating the β-arrestin pathway, which eventually leads to desensitization, receptor internalization and 'silencing' of the pathway.

The well-investigated genomic anti-inflammatory effect of glucocorticoids is mediated by their binding to a cytoplasmic receptor which, when activated, migrates to the nucleus.

Moreover, several groups including ours have shown previously that several peptides that do not fit the consensus sequence for peptides binding to a given MHC molecule can activate T cells restricted to that MHC molecule very efficiently [ 33- 36].

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].

In addition to their activation via binding to cyclins, cyclin-dependent kinases (CDKs) can be activated via binding to a novel cell cycle regulator termed Speedy/Ringo, which shows no apparent similarity to cyclins.

Previous work in Andreasson's lab and other labs has shown that this molecule, a receptor protein called EP2, has a strong potential to cause inflammation when activated by binding to a substance called prostaglandin E2, or PGE2.