ライフサイエンスコーパス: metarhodopsin

1 eated by binding of Arr2 to photo-isomerized metarhodopsin.

2 the dark-adapted state of 474 nm, while the metarhodopsin absorption maximum is 572 nm.

3 Upon illumination of metarhodopsin-containing membrane suspensions isolated f

4 en performed on the lumirhodopsin (Lumi) and metarhodopsin I (Meta I) photointermediates of rhodopsin

5 The pH dependence of the absorption of the metarhodopsin I (Meta I)-like photoproduct of E181Q is i

6 A was batho/bsi --> lumirhodopsin (lumi) --> metarhodopsin I (MI) --> metarhodopsin II (MII).

7 onsidered the issue of whether shifts in the metarhodopsin I (MI)-metarhodopsin II (MII) equilibrium

8 that the detergent strongly favors MII over metarhodopsin I (MI).

9 ular equilibrium between the two conformers, metarhodopsin I and II (MI and MII).

10 ce Raman (UVRR) spectra of rhodopsin and its metarhodopsin I and metarhodopsin II photointermediates

11 e equilibrium between the photointermediates metarhodopsin I and metarhodopsin II; increasing bilayer

12 structures of the ground state reveals that metarhodopsin I formation does not involve large rigid-b

13 BSI compared with that of lumirhodopsin and metarhodopsin I indicates weaker coupling between the 11

14 igated the structure of trans-retinal in the metarhodopsin I photointermediate (MI), where the retiny

15 n are accompanied by higher metarhodopsin II/metarhodopsin I ratios, faster rates of metarhodopsin II

16 facilitates the transition from an inactive metarhodopsin I to the active metarhodopsin II intermedi

17 Large increases were seen in the amount of metarhodopsin I which appeared after photolysis of 5-eth

18 irhodopsin, instead of deprotonating to form metarhodopsin I(380) on the submillisecond time scale as

19 wild type, the acidic form of E113Q produced metarhodopsin I(480), which decayed very slowly (exponen

20 In addition to forming more metarhodopsin I, the bicyclic analogue stabilized the me

21 f a photostationary state highly enriched in metarhodopsin I, to a resolution of 5.5 A in the membran

22 pled receptors, yet paradoxically shifts the metarhodopsin I-II (MI-MII) equilibrium (K(eq)) of light

23 psin I, the bicyclic analogue stabilized the metarhodopsin I-metarhodopsin II equilibrium similarly t

24 The equilibrium constant of metarhodopsin I-metarhodopsin II is 30-45% higher, and t

25 etarhodopsin II while oligomerization favors metarhodopsin I.

26 k-adapted rhodopsin, the photo-intermediates metarhodopsin I/II/III, and opsin.

27 The equilibria between metarhodopsins I and II (MI and MII) and the binding of

28 trongly suggest that the equilibrium between metarhodopsin-I and metarhodopsin-II is dependent upon t

29 od since approximately 44% conversion to the metarhodopsin-I component could be achieved, with only l

30 t the increased hydration is specific to the metarhodopsin-I intermediate.

31 st-occupied conformation of other GPCRs, and metarhodopsin-I may be similar to antagonist-occupied GP

32 The C8 resonance was not shifted in the metarhodopsin-I spectral component but was strongly broa

33 of metarhodopsin-II while it stabilizes the metarhodopsin-I state.

34 ope accessible in dark-adapted rhodopsin and metarhodopsin-I that is lost upon formation of metarhodo

35 he chromophore in the late photointermediate metarhodopsin-I, from observation of (13)C nuclei introd

36 hat, despite the chain being more relaxed in metarhodopsin-I, its average conformation with respect t

37 ng behavior, including an increased ratio of metarhodopsin-I-like species to metarhodopsin-II-like sp

38 izing and quantifying the photoconversion to metarhodopsin-I.

39 ct receptor states culminating in the active Metarhodopsin II (Meta II) state, which binds and activa

40 tional changes that lead to the active form, metarhodopsin II (META II), initiating a signaling casca

41 ational change upon light excitation to form metarhodopsin II (Meta II), which allows interaction and

42 6, and H7 leading to the active intermediate metarhodopsin II (Meta II).

43 The difference of rhodopsin and metarhodopsin II (MII) absorption spectra exhibits a cha

44 Metarhodopsin II (MII) and MII-G(t) complex formation ra

45 diesterase activity, and slower formation of metarhodopsin II (MII) and the MII-G(t) complex relative

46 The association constant (K(a)) for metarhodopsin II (MII) and transducin (G(t)) binding was

47 f whether shifts in the metarhodopsin I (MI)-metarhodopsin II (MII) equilibrium from lipid compositio

48 conditions to activation by flash-generated metarhodopsin II (MII) revealed that opsin- and R*-catal

49 1 micros), the mutant E113D lumi decayed to metarhodopsin II (MII), showing that the detergent stron

50 The equilibrium concentration of metarhodopsin II (MII), the conformation of photoactivat

51 f a series of n-alcohols on the formation of metarhodopsin II (MII), the photoactivated conformation

52 osmolytes on both the extent of formation of metarhodopsin II (MII), which binds and activates transd

53 hodopsin (lumi) --> metarhodopsin I (MI) --> metarhodopsin II (MII).

54 he lipid/protein film caused by formation of metarhodopsin II (MII).

55 tP with the light-activated signaling state, metarhodopsin II (MII).

56 bserved in rhodopsin is reduced in wild-type metarhodopsin II and in the E181Q mutant of rhodopsin.

57 le absorption spectra, (ii) the formation of metarhodopsin II and its rate of decay, and (iii) initia

58 proteoliposomes showed the rate of decay of metarhodopsin II and the initial rate of transducin acti

59 changes involved in converting rhodopsin to metarhodopsin II are not required for scrambling, and th

60 ormation of the active form of the receptor, metarhodopsin II b, which decays to opsin.

61 ted to a more active intermediate similar to metarhodopsin II b.

62 and isolation of a high affinity transducin-metarhodopsin II complex was demonstrated for a monodisp

63 hodopsin to achieve the enzymatically active metarhodopsin II conformation is exquisitely sensitive t

64 Additionally, the kinetics of metarhodopsin II decay is similar between rhodopsin in n

65 ark and after photobleaching and the rate of metarhodopsin II decay, (ii) initial rates of transducin

66 table and exhibited abnormal photobleaching, metarhodopsin II decay, and G protein activation.

67 clic analogue stabilized the metarhodopsin I-metarhodopsin II equilibrium similarly to what has been

68 VRR difference spectra between rhodopsin and metarhodopsin II exhibit significant differences for vib

69 monomeric rhodopsin and stabilize the active metarhodopsin II form.

70 role of this site in determining the rate of metarhodopsin II formation and decay in rod and cone pig

71 n II/metarhodopsin I ratios, faster rates of metarhodopsin II formation, an increase of tryptophan fl

72 rge conformational change known to accompany metarhodopsin II formation.

73 ating that the PWR spectral shifts monitored metarhodopsin II formation.

74 ore (lambda max 495 nm) in the dark, but the metarhodopsin II formed on illumination decayed about 6.

75 Since the timescale for the formation of the metarhodopsin II intermediate (>1 ms) is beyond that rea

76 vided by solid-state NMR measurements of the metarhodopsin II intermediate are combined with molecula

77 e NMR measurements on both rhodopsin and the metarhodopsin II intermediate show how retinal isomeriza

78 inal-protein contacts observed in the active metarhodopsin II intermediate suggest a general activati

79 inning NMR measurements of rhodopsin and the metarhodopsin II intermediate that support the proposal

80 ons of the retinal chromophore in the active metarhodopsin II intermediate.

81 ft of the Schiff base nitrogen in the active metarhodopsin II intermediate.

82 om an inactive metarhodopsin I to the active metarhodopsin II intermediate.

83 ces the ability of rhodopsin to form the key metarhodopsin II intermediate.

84 The equilibrium constant of metarhodopsin I-metarhodopsin II is 30-45% higher, and the apparent rate

85 he antibody correlated with formation of the metarhodopsin II photointermediate and was reduced signi

86 tra of rhodopsin and its metarhodopsin I and metarhodopsin II photointermediates have been obtained t

87 ly abnormal bleaching behavior with abnormal metarhodopsin II photointermediates.

88 f the retinylidene Schiff base in the active metarhodopsin II photoproduct.

89 mutants on illumination showed destabilized metarhodopsin II species and reduced transducin activati

90 Similarly, the metarhodopsin II spectrum obtained with a 500 micros del

91 0-350) to rhodopsin stabilizes the activated metarhodopsin II state (M II), consequently uncoupling t

92 re smaller than previously predicted for the metarhodopsin II state and include changes on the cytopl

93 Formation of metarhodopsin II was observed by the change in absorbanc

94 easing bilayer thickness favors formation of metarhodopsin II while oligomerization favors metarhodop

95 Comparison of the retinal chemical shifts in metarhodopsin II with those of retinal model compounds r

96 om the removal of metarhodopsin (most likely metarhodopsin II) from the outer segment.

97 re of the cytoplasmic face in the activated (metarhodopsin II) receptor.

98 nt in the dark-state of rhodopsin is lost in metarhodopsin II, and a new contact is formed with the C

99 t of nucleotide exchange rates, affinity for metarhodopsin II, and thermostability suggest that the K

100 een Trp265(6.48) and Gly121(3.36) is lost in metarhodopsin II, consistent with H6 motion away from H3

101 onal structure of ground state rhodopsin and metarhodopsin II, particularly in the cytoplasmic face o

102 .53) on H2 is observed in both rhodopsin and metarhodopsin II, suggesting that H3 does not change ori

103 e pigment has several structural features of metarhodopsin II, the active form of rhodopsin.

104 On decay of metarhodopsin II, the chemical shifts reverted largely t

105 On illumination to form metarhodopsin II, upfield changes in chemical shift were

106 nt in the Nanodisc was able to form a stable metarhodopsin II-G-protein complex.

107 In addition, the metarhodopsin II-like photoproducts of the mutant pigmen

108 The mutants formed metarhodopsin II-like photoproducts upon illumination bu

109 mational states of the protein (rhodopsin, a metarhodopsin II-mimic, and two forms of opsin) facilita

110 en upon formation of the active intermediate metarhodopsin II.

111 sequence in binding to and stabilization of metarhodopsin II.

112 r nanodiscs, as assessed by stabilization of metarhodopsin II.

113 ious work on the temperature-trapped form of metarhodopsin II.

114 etinal leading to the fully activated state, metarhodopsin II.

115 activation and formation of the active form, metarhodopsin II.

116 at the retinal translates 4-5 A toward H5 in metarhodopsin II.

117 helical conformation during interaction with metarhodopsin II.

118 miniscent of the G protein-activating state, metarhodopsin II.

119 weakly hydrogen bonded between rhodopsin and metarhodopsin II.

120 backbone carbonyl of His211 is disrupted in metarhodopsin II.

121 and becomes more strongly hydrogen bonded in metarhodopsin II.

122 h meta I380, a 380 nm absorbing precursor to metarhodopsin II.

123 in processes leading to the activated form, metarhodopsin II.

124 re for the activated state of this receptor, metarhodopsin II.

125 icity of rhodopsin are accompanied by higher metarhodopsin II/metarhodopsin I ratios, faster rates of

126 n the photointermediates metarhodopsin I and metarhodopsin II; increasing bilayer thickness favors fo

127 g pocket and resembles the G protein binding metarhodopsin-II conformation obtained by the natural ac

128 esolvable and the R(2) phase, which overlaps metarhodopsin-II formation, has a rapid risetime and com

129 the equilibrium between metarhodopsin-I and metarhodopsin-II is dependent upon the conformation of t

130 ctivation is of wide importance, because the metarhodopsin-II photoproduct is analogous to the agonis

131 K42-41L is shown to inhibit formation of metarhodopsin-II while it stabilizes the metarhodopsin-I

132 sed ratio of metarhodopsin-I-like species to metarhodopsin-II-like species and aberrant photoproduct

133 o be trapped in an open conformation that is metarhodopsin-II-like.

134 tarhodopsin-I that is lost upon formation of metarhodopsin-II.

135 mediate and was reduced significantly at the metarhodopsin III intermediate.

136 ther arrestin was also required to stabilize metarhodopsin in intact photoreceptor cells, metarhodops

137 f arrestin was observed upon illumination of metarhodopsin in lipid/detergent micellar extracts.

138 IP2 and by protecting the visual system from metarhodopsin-induced, low light degeneration.

139 trate that in disrupted photoreceptor cells, metarhodopsin is not stabilized unless arrestin is prese

140 ts because the light-activated conformation, metarhodopsin, is stable following exposure to light in

141 hereas Rh6 appears to be photoconverted to a metarhodopsin (lambda(max) = 468 nm) that is less therma

142 Rh5 is reversibly photoconverted to a stable metarhodopsin (lambda(max) = 494 nm), whereas Rh6 appear

143 ermined the lifetime of activated rhodopsin (metarhodopsin = M( *)) in whole-cell recordings from Dro

144 escues flies lacking PLC from light-induced, metarhodopsin-mediated degeneration and restores visual

145 odopsin and transducin was measured by extra-metarhodopsin (meta) II assay.

146 t this reduction results from the removal of metarhodopsin (most likely metarhodopsin II) from the ou

147 was used to hasten the decomposition of the metarhodopsin photoproducts.

148 the interaction of antibody K42-41L with the metarhodopsin photoproducts.

149 anes or micellar extracts, and the amount of metarhodopsin present was quantitated by spectroscopic m

150 iments in total head homogenates showed that metarhodopsin produced in the arr1(1), arr2(3) double mu

151 decrease was observed in the amounts of Rh1 metarhodopsin recovered from illuminated flies which wer

152 t in intact photoreceptor cells, significant metarhodopsin stabilization occurs even in the absence o

153 However, the metarhodopsin state is not stable as purified in dodecyl

154 ve protein states of the receptor (so-called metarhodopsin states) are regulated by the highly conser

155 The authors hypothesized that the decay of metarhodopsin to apo-opsin and free all-trans-retinaldeh

156 changes associated with the transition from metarhodopsin to rhodopsin were, however, similar in mem

157 nts for arrestin in the stabilization of Rh1 metarhodopsin under in vitro and in vivo conditions.

158 vidence that arrestin binding stabilizes Rh1 metarhodopsin under in vitro conditions.

159 metarhodopsin in intact photoreceptor cells, metarhodopsin was generated in arr1(1), arr2(3) double m

160 Compared to wild-type, approximately 64% Rh1 metarhodopsin was recovered in flies deficient in arrest

161 oproduct shows the formation of a protonated metarhodopsin with a maximum absorbance between 520 and