ライフサイエンスコーパス: rhodopsin kinase

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

23 Our experiments indicate that rhodopsin kinase and recoverin, in addition to their wel

24 rminated when rhodopsin is phosphorylated by rhodopsin kinase and subsequently blocked by a protein c

25 Rhodopsin is first phosphorylated by rhodopsin kinase and subsequently deactivated by the bin

26 ed for their ability to be phosphorylated by rhodopsin kinase and to bind arrestin.

27 ing protein recoverin is thought to regulate rhodopsin kinase and to modulate the lifetime of the pho

28 ance of other prenylated proteins, including rhodopsin kinase and transducin, were unaffected.

29 the desensitizing substance is recognized by rhodopsin kinase and/or arrestin and, therefore, is prob

30 ylated by both a substrate-regulated kinase, rhodopsin kinase, and a second messenger-regulated kinas

31 Neither the activities of Abca4, rhodopsin kinase, and arrestin, nor the palmitylation of

32 with 11-cis-retinal, prephosphorylated with rhodopsin kinase, and examined for their ability to bind

33 ts and their constitutive phosphorylation by rhodopsin kinase, and it does so in the presence of cont

34 Examples include mutations in arrestin, rhodopsin kinase, and the cone-rod homeobox gene, CRX.

35 etinol formation depends on Abca4, arrestin, rhodopsin kinase, and the palmitylation of rhodopsin, al

36 ng assay involving purified bovine arrestin, rhodopsin kinase, and transducin.

37 n of the carboxyl-terminal opsin fragment by rhodopsin kinase, and/or phosphopeptide-stimulated arres

38 NMR resonance of rhodopsin phosphorylated by rhodopsin kinase at the C-terminal tail was observable w

39 ects of adenine nucleotides on the recoverin-rhodopsin kinase binding.

40 ators of protein kinase A, protein kinase G, rhodopsin kinase, CaM kinase II, casein kinase II, or cy

41 The results demonstrate that rhodopsin kinase can efficiently phosphorylate other ser

42 rived from the human RK locus using a bovine rhodopsin kinase cDNA fragment as a probe.

43 sv wild-type mice and Abca4-, arrestin-, and rhodopsin kinase-deficient mice and in genetically modif

44 threonine residues was not phosphorylated by rhodopsin kinase, demonstrating that phosphorylation is

45 interacts with the G-protein transducin and rhodopsin kinase during signal transduction.

46 on of photoactivated rhodopsin by the enzyme rhodopsin kinase followed by binding of the protein arre

47 Rh* is turned off by phosphorylation by rhodopsin kinase [G-protein-coupled receptor kinase 1 (G

48 results indicate that null mutations in the rhodopsin kinase gene are a cause of Oguchi disease and

49 ed, but all three cases had mutations in the rhodopsin kinase gene.

50 rt describes an analysis of the arrestin and rhodopsin kinase genes in three unrelated cases of Oguch

51 Immunocytochemistry showed that farnesylated rhodopsin kinase (GRK1) and prenylated rod PDE6 catalyti

52 bait that it can interact with farnesylated rhodopsin kinase (GRK1) and that prenylation is essentia

53 We determined how reduced concentrations of rhodopsin kinase (GRK1) and/or arrestin1 influenced the

54 omeric active rhodopsin is phosphorylated by rhodopsin kinase (GRK1) as efficiently as rhodopsin in t

55 hat includes calcium-dependent inhibition of rhodopsin kinase (GRK1) by recoverin.

56 G) gene mutations and type 2 associated with rhodopsin kinase (GRK1) gene mutations.

57 To determine the role of rhodopsin kinase (GRK1) in phosphorylating this opsin an

58 We show that overexpression of rhodopsin kinase (GRK1) increases phosphorylation of the

59 Here we report six crystal structures of rhodopsin kinase (GRK1), revealing not only three distin

60 of light-activated rhodopsin (Rho*) bound to rhodopsin kinase (GRK1), wherein the N terminus of GRK1

61 ions that lead to nonfunctional arrestin and rhodopsin kinase have Oguchi disease, a form of stationa

62 genicity of these mutations, wild-type human rhodopsin kinase (HRK) and mutant forms HRKV380D and HRK

63 , only Ser338 is a significant substrate for rhodopsin kinase in vitro.

64 s inhibitor had no effect on the activity of rhodopsin kinase in vitro.

65 responses in rods lacking both arrestin and rhodopsin kinase, indicating that p48 can also quench th

66 2+ is present and that a dependent recoverin/rhodopsin kinase interaction underlies the inhibitory ef

67 on, and adenine nucleotides on the recoverin-rhodopsin kinase interaction.

68 G-Protein receptor kinase 1 (GRK1) ("rhodopsin kinase") is necessary for the inactivation of

69 protein-coupled receptor kinase 1 (GRK1, or rhodopsin kinase) is critical for the deactivation of th

70 While GRK1 (rhodopsin kinase) is inhibited by the photoreceptor-spec

71 Among these enzymes, GRK1 (rhodopsin kinase) is involved in phototransduction and i

72 To the contrary, no translocation of rhodopsin kinase itself or either GCAP was identified.

73 signaling, which occurs in rod arrestin and rhodopsin kinase knock-out mice, caused a rapid and spec

74 of rhodopsin refers to a reaction in which a rhodopsin kinase molecule that has been activated by a l

75 decreases transducin binding and activation, rhodopsin kinase phosphorylation of rhodopsin significan

76 bated in the dark with SR(1-4/5-7), ATP, and rhodopsin kinase, phosphorylation of SR(1-4/5-7) would b

77 rt model showed that ciliary enrichment of a rhodopsin kinase probe occurs via recycling as it perpet

78 Murine whirlin cDNA driven by the human rhodopsin kinase promoter (hRK) was packaged as an AAV2/

79 uman AIPL1 coding sequence driven by a human rhodopsin kinase promoter region (rAAV8.hRKp.AIPL1).

80 osphorylation stoichiometry of >/=2 mol/mol, rhodopsin kinase promotes arrestin binding at a stoichio

81 bound to a functional N-terminal fragment of rhodopsin kinase (residues 1-25, called RK25).

82 lpha(12/13) KO cells) and used cells lacking rhodopsin kinase (RK cells) as a control.

83 Rhodopsin kinase (Rk or GRK1) is a photoreceptor-specifi

84 y, serves as a calcium sensor that regulates rhodopsin kinase (RK) activity in retinal rod cells.

85 aling, bypassing receptor phosphorylation by rhodopsin kinase (RK) and replacing this two-step mechan

86 cin (G(T)) activation and phosphorylation by rhodopsin kinase (RK) following illumination were studie

87 A suitable system for expression of the rhodopsin kinase (RK) gene and its mutants is needed for

88 velop short, active derivatives of the human rhodopsin kinase (RK) gene promoter for targeting transg

89 ansduction, the identity and function of the rhodopsin kinase (RK) have been elusive.

90 Rhodopsin kinase (RK) is a conserved component of the li

91 Phosphorylation of Rho* by rhodopsin kinase (RK) is necessary for the fast recovery

92 Addition of an inhibitory antibody against rhodopsin kinase (RK) lowered phosphorylation at Ser334,

93 In rod photoreceptors rhodopsin kinase (RK) mediates rapid desensitization of

94 e phosphorylation can be catalyzed either by rhodopsin kinase (RK) or by protein kinase C (PKC).

95 Two mAbs generated against rhodopsin kinase (RK) were characterized for their epito

96 Rhodopsin kinase (RK), a rod photoreceptor cytosolic enz

97 Rhodopsin kinase (RK), a specialized G-protein-coupled r

98 PL1 retinas, as were guanylate cyclase (GC), rhodopsin kinase (RK), and normalized phosphodiesterase

99 ted rhodopsin by the retina-specific enzyme, rhodopsin kinase (RK), is the primary event in the initi

100 Photoreceptor rhodopsin kinase (Rk, G protein-dependent receptor kinas

101 Structure-function studies of rhodopsin kinase (RK; EC 2.7.1.125) require a variety of

102 ducin [alpha-T], phosphodiesterase [PDE], or rhodopsin kinase [RK]).

103 ific AAV (adeno-associated virus)-hRK (human rhodopsin kinase)-sh_c-fos or a chemical inhibitor subst

104 problem, we have made mice that underexpress rhodopsin kinase so that Rh* turnoff is rate limiting fo

105 r kinase 2 (beta ark2), but not beta ark1 or rhodopsin kinase, specifically blocked receptor activati

106 Because GRK1 (rhodopsin kinase), the GRK that mediates rhodopsin desen

107 More importantly, the ratio of rhodopsin kinase to its modulator recoverin appears crit

108 the restriction of binding of transducin and rhodopsin kinase to rhodopsin.

109 ed for their ability to be phosphorylated by rhodopsin kinase, to bind arrestin, and to activate the

110 posed for high gain phosphorylation, whereby rhodopsin kinase, upon phosphorylating the activated rec

111 ivity, whereas phosphorylation of rho-GFP by rhodopsin kinase was 10% of wild-type levels.

112 lity of the mutants to act as substrates for rhodopsin kinase was analyzed.

113 Furthermore, photoreceptor-specific rhodopsin kinase was reduced.

114 ing, whereas the level of phosphorylation by rhodopsin kinase was similar to that of wild-type rhodop

115 ation, mutant mice deficient in arrestin and rhodopsin kinase were raised in the dark and then subjec

116 As rhodopsin kinase works with arrestin in shutting off rho