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1 by the increased phosphorylation of opsin by rhodopsin kinase.
2 % identical in amino acid sequence to bovine rhodopsin kinase.
3 ding protein kinase A, protein kinase C, and rhodopsin kinase.
4 on, and (iii) the rate of phosphorylation by rhodopsin kinase.
5 naling after the third phosphate is added by rhodopsin kinase.
6 dues in the cytoplasmic tail of rhodopsin by rhodopsin kinase.
7 tential binding site for the target protein, rhodopsin kinase.
8 at it was not due to effects of delta-GST on rhodopsin kinase.
9 to the effects of delta-GST on transducin or rhodopsin kinase.
10 are the main targets for phosphorylation by rhodopsin kinase.
11 stoylated Ca2+-binding protein that inhibits rhodopsin kinase.
12 Oguchi disease might be caused by defects in rhodopsin kinase.
13 ains thought to interact with transducin and rhodopsin kinase.
14 time of photoexcited rhodopsin by inhibiting rhodopsin kinase.
15 rrestin in the absence of phosphorylation by rhodopsin kinase.
16 reported to be the preferred substrates for rhodopsin kinase.
17 Synthesis and transport of transducin, and rhodopsin kinase 1 (GRK1), also prenylated substrates of
18 ronal calcium sensing (NCS) family, inhibits rhodopsin kinase, a Ser/Thr kinase responsible for termi
19 ly, depending on whether protein kinase C or rhodopsin kinase activity dominates, and that, under the
20 e in photoreceptor-specific markers (RET-P1, rhodopsin kinase), an increase in the cell death marker
21 ibitory constraint that recoverin imposes on rhodopsin kinase, an enzyme responsible for quenching th
22 al of the mutants could be phosphorylated by rhodopsin kinase and could bind arrestin in the absence
24 rminated when rhodopsin is phosphorylated by rhodopsin kinase and subsequently blocked by a protein c
27 ing protein recoverin is thought to regulate rhodopsin kinase and to modulate the lifetime of the pho
28 the desensitizing substance is recognized by rhodopsin kinase and/or arrestin and, therefore, is prob
29 ylated by both a substrate-regulated kinase, rhodopsin kinase, and a second messenger-regulated kinas
31 with 11-cis-retinal, prephosphorylated with rhodopsin kinase, and examined for their ability to bind
32 ts and their constitutive phosphorylation by rhodopsin kinase, and it does so in the presence of cont
34 etinol formation depends on Abca4, arrestin, rhodopsin kinase, and the palmitylation of rhodopsin, al
36 n of the carboxyl-terminal opsin fragment by rhodopsin kinase, and/or phosphopeptide-stimulated arres
37 NMR resonance of rhodopsin phosphorylated by rhodopsin kinase at the C-terminal tail was observable w
39 ators of protein kinase A, protein kinase G, rhodopsin kinase, CaM kinase II, casein kinase II, or cy
42 sv wild-type mice and Abca4-, arrestin-, and rhodopsin kinase-deficient mice and in genetically modif
43 threonine residues was not phosphorylated by rhodopsin kinase, demonstrating that phosphorylation is
45 on of photoactivated rhodopsin by the enzyme rhodopsin kinase followed by binding of the protein arre
47 results indicate that null mutations in the rhodopsin kinase gene are a cause of Oguchi disease and
49 rt describes an analysis of the arrestin and rhodopsin kinase genes in three unrelated cases of Oguch
50 Immunocytochemistry showed that farnesylated rhodopsin kinase (GRK1) and prenylated rod PDE6 catalyti
51 bait that it can interact with farnesylated rhodopsin kinase (GRK1) and that prenylation is essentia
52 We determined how reduced concentrations of rhodopsin kinase (GRK1) and/or arrestin1 influenced the
53 omeric active rhodopsin is phosphorylated by rhodopsin kinase (GRK1) as efficiently as rhodopsin in t
57 Here we report six crystal structures of rhodopsin kinase (GRK1), revealing not only three distin
58 ions that lead to nonfunctional arrestin and rhodopsin kinase have Oguchi disease, a form of stationa
59 genicity of these mutations, wild-type human rhodopsin kinase (HRK) and mutant forms HRKV380D and HRK
62 responses in rods lacking both arrestin and rhodopsin kinase, indicating that p48 can also quench th
63 2+ is present and that a dependent recoverin/rhodopsin kinase interaction underlies the inhibitory ef
66 protein-coupled receptor kinase 1 (GRK1, or rhodopsin kinase) is critical for the deactivation of th
70 signaling, which occurs in rod arrestin and rhodopsin kinase knock-out mice, caused a rapid and spec
71 of rhodopsin refers to a reaction in which a rhodopsin kinase molecule that has been activated by a l
72 decreases transducin binding and activation, rhodopsin kinase phosphorylation of rhodopsin significan
73 bated in the dark with SR(1-4/5-7), ATP, and rhodopsin kinase, phosphorylation of SR(1-4/5-7) would b
75 osphorylation stoichiometry of >/=2 mol/mol, rhodopsin kinase promotes arrestin binding at a stoichio
79 y, serves as a calcium sensor that regulates rhodopsin kinase (RK) activity in retinal rod cells.
80 aling, bypassing receptor phosphorylation by rhodopsin kinase (RK) and replacing this two-step mechan
81 cin (G(T)) activation and phosphorylation by rhodopsin kinase (RK) following illumination were studie
83 velop short, active derivatives of the human rhodopsin kinase (RK) gene promoter for targeting transg
87 Addition of an inhibitory antibody against rhodopsin kinase (RK) lowered phosphorylation at Ser334,
93 PL1 retinas, as were guanylate cyclase (GC), rhodopsin kinase (RK), and normalized phosphodiesterase
94 ted rhodopsin by the retina-specific enzyme, rhodopsin kinase (RK), is the primary event in the initi
98 ific AAV (adeno-associated virus)-hRK (human rhodopsin kinase)-sh_c-fos or a chemical inhibitor subst
99 problem, we have made mice that underexpress rhodopsin kinase so that Rh* turnoff is rate limiting fo
100 r kinase 2 (beta ark2), but not beta ark1 or rhodopsin kinase, specifically blocked receptor activati
104 ed for their ability to be phosphorylated by rhodopsin kinase, to bind arrestin, and to activate the
105 posed for high gain phosphorylation, whereby rhodopsin kinase, upon phosphorylating the activated rec
109 ing, whereas the level of phosphorylation by rhodopsin kinase was similar to that of wild-type rhodop
110 ation, mutant mice deficient in arrestin and rhodopsin kinase were raised in the dark and then subjec
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