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Example sentences for: grk
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Similarly, mutation of only two serine residues in the human alpha-2A receptor resulted in a loss of desensitization [ 12 ] . Because the EESSSSE motif in the human alpha-2A receptor is a known GRK substrate, and because eliminating two potential phosphorylation sites prevents down-reguation, phosphorylation of the opossum alpha-2C receptor may be important in the mechanism of down-regulation of this receptor.
The opossum alpha-2C adrenergic receptor has a EESSTSE acidic serine/threonine motif in the third intracellular loop (Figures 1and 2), which could be a substrate for GRK based on the EESSSSD motif of the alpha-2A subtype.
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 expressed 5-HT 2C receptor exhibits homologous and heterologous desensitization in oocytes [ 32 ] mediated by protein kinase C [ 33 34 35 ] . A calmodulin-dependent kinase may also be involved in homologous desensitization [ 36 ] . In contrast, a recent study indicates that neither PKC nor calmodulin-dependent protein kinase II are involved, instead desensitization of the 5-HT 2C receptor is dependent on GRK activity [ 37 ] . Interestingly, tyrosine kinase involvement in the agonist-mediated phosphorylation of the rat 5-HT 2C receptor has also been reported [ 38 ] , although as yet no report has shown that the 5-HT 2C receptor directly activates tyrosine kinases.
One of these is Grk2 , a member of the family of ionotropic glutamate receptor genes that is thought to play a role in modulating Huntington disease [ 44].
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