Example sentences for: grks

How can you use “grks” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • Furthermore, since some GPCRs can modulate MAP kinase activity, MAP kinase regulation of GPCR function may then serve as a form of negative feedback control in much the same way that protein kinase A, protein kinase C and the G protein-coupled receptor kinases (GRKs) regulate GPCRs.

  • Two molecular loci recently have been implicated as potential modulators of GnRH receptor signaling: one is the receptor itself [ 23 ] , and the other is the G protein that transduces the signal generated by binding of the receptor to its agonist [ 9 ] . With respect to the former locus, G protein coupled receptor kinases (GRKs) act in an agonist-specific manner to phosphorylate intracellular regions of the receptor thus permitting β arrestin binding that sterically inhibits G protein association with the receptor [ 1 45 ] . We have reported previously that experimental expression of GRKs in GnRH receptor-expressing heterologous cells (COS-1) suppressed GnRH-stimulated IP 3 production, and that co-expression of GRK2 and β-arrestin 2 suppressed GnRH receptor signaling more than that of either alone [ 23 ] . Stronger evidence that the GRK/β arrestin paradigm may play a role in regulating GnRH receptor signaling is our recent finding that adenovirus-mediated gene transfer of GRK2 into normal pituitary gonadotropes suppressed GnRH-stimulated LH secretion and IP 3 production [ 31 ] . However, no evidence has been presented for a direct interaction between β-arrestin and the GnRH receptor.

  • The function of GPCRs is tightly regulated by phosphorylation by second messenger activated kinases (protein kinase A and protein kinase C) and G protein-coupled receptor-specific kinases (GRKs).

  • Yet another typical feature of many of these receptors is the presence of multiple serine and threonine residues in their carboxyl termini and IC3 that serve as phosphorylation sites for G-protein-coupled receptor kinases (GRKs) as well as protein kinases C (PKC) and A (PKA), a mechanism involved in agonist-dependent desensitization of the receptors.


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