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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 nges, we measured reversible shifting of the metarhodopsin equilibrium due to osmotic stress using an
5 en performed on the lumirhodopsin (Lumi) and metarhodopsin I (Meta I) photointermediates of rhodopsin
6   The pH dependence of the absorption of the metarhodopsin I (Meta I)-like photoproduct of E181Q is i
7 A was batho/bsi --> lumirhodopsin (lumi) --> metarhodopsin I (MI) --> metarhodopsin II (MII).
8 onsidered the issue of whether shifts in the metarhodopsin I (MI)-metarhodopsin II (MII) equilibrium
9  that the detergent strongly favors MII over metarhodopsin I (MI).
10 ular equilibrium between the two conformers, metarhodopsin I and II (MI and MII).
11 ce Raman (UVRR) spectra of rhodopsin and its metarhodopsin I and metarhodopsin II photointermediates
12 e equilibrium between the photointermediates metarhodopsin I and metarhodopsin II; increasing bilayer
13  structures of the ground state reveals that metarhodopsin I formation does not involve large rigid-b
14  BSI compared with that of lumirhodopsin and metarhodopsin I indicates weaker coupling between the 11
15 igated the structure of trans-retinal in the metarhodopsin I photointermediate (MI), where the retiny
16 n are accompanied by higher metarhodopsin II/metarhodopsin I ratios, faster rates of metarhodopsin II
17  facilitates the transition from an inactive metarhodopsin I to the active metarhodopsin II intermedi
18   Large increases were seen in the amount of metarhodopsin I which appeared after photolysis of 5-eth
19 irhodopsin, instead of deprotonating to form metarhodopsin I(380) on the submillisecond time scale as
20 wild type, the acidic form of E113Q produced metarhodopsin I(480), which decayed very slowly (exponen
21                  In addition to forming more metarhodopsin I, the bicyclic analogue stabilized the me
22 f a photostationary state highly enriched in metarhodopsin I, to a resolution of 5.5 A in the membran
23 pled receptors, yet paradoxically shifts the metarhodopsin I-II (MI-MII) equilibrium (K(eq)) of light
24 psin I, the bicyclic analogue stabilized the metarhodopsin I-metarhodopsin II equilibrium similarly t
25                  The equilibrium constant of metarhodopsin I-metarhodopsin II is 30-45% higher, and t
26 etarhodopsin II while oligomerization favors metarhodopsin I.
27 k-adapted rhodopsin, the photo-intermediates metarhodopsin I/II/III, and opsin.
28                       The equilibria between metarhodopsins I and II (MI and MII) and the binding of
29 trongly suggest that the equilibrium between metarhodopsin-I and metarhodopsin-II is dependent upon t
30 od since approximately 44% conversion to the metarhodopsin-I component could be achieved, with only l
31 t the increased hydration is specific to the metarhodopsin-I intermediate.
32 st-occupied conformation of other GPCRs, and metarhodopsin-I may be similar to antagonist-occupied GP
33      The C8 resonance was not shifted in the metarhodopsin-I spectral component but was strongly broa
34  of metarhodopsin-II while it stabilizes the metarhodopsin-I state.
35 ope accessible in dark-adapted rhodopsin and metarhodopsin-I that is lost upon formation of metarhodo
36 he chromophore in the late photointermediate metarhodopsin-I, from observation of (13)C nuclei introd
37 hat, despite the chain being more relaxed in metarhodopsin-I, its average conformation with respect t
38 ng behavior, including an increased ratio of metarhodopsin-I-like species to metarhodopsin-II-like sp
39 izing and quantifying the photoconversion to metarhodopsin-I.
40 ct receptor states culminating in the active Metarhodopsin II (Meta II) state, which binds and activa
41 tional changes that lead to the active form, metarhodopsin II (META II), initiating a signaling casca
42 ational change upon light excitation to form metarhodopsin II (Meta II), which allows interaction and
43 6, and H7 leading to the active intermediate metarhodopsin II (Meta II).
44              The difference of rhodopsin and metarhodopsin II (MII) absorption spectra exhibits a cha
45                                              Metarhodopsin II (MII) and MII-G(t) complex formation ra
46 diesterase activity, and slower formation of metarhodopsin II (MII) and the MII-G(t) complex relative
47          The association constant (K(a)) for metarhodopsin II (MII) and transducin (G(t)) binding was
48 f whether shifts in the metarhodopsin I (MI)-metarhodopsin II (MII) equilibrium from lipid compositio
49  conditions to activation by flash-generated metarhodopsin II (MII) revealed that opsin- and R*-catal
50  1 micros), the mutant E113D lumi decayed to metarhodopsin II (MII), showing that the detergent stron
51             The equilibrium concentration of metarhodopsin II (MII), the conformation of photoactivat
52 f a series of n-alcohols on the formation of metarhodopsin II (MII), the photoactivated conformation
53 osmolytes on both the extent of formation of metarhodopsin II (MII), which binds and activates transd
54 hodopsin (lumi) --> metarhodopsin I (MI) --> metarhodopsin II (MII).
55 he lipid/protein film caused by formation of metarhodopsin II (MII).
56 tP with the light-activated signaling state, metarhodopsin II (MII).
57 bserved in rhodopsin is reduced in wild-type metarhodopsin II and in the E181Q mutant of rhodopsin.
58 le absorption spectra, (ii) the formation of metarhodopsin II and its rate of decay, and (iii) initia
59  proteoliposomes showed the rate of decay of metarhodopsin II and the initial rate of transducin acti
60  changes involved in converting rhodopsin to metarhodopsin II are not required for scrambling, and th
61 ormation of the active form of the receptor, metarhodopsin II b, which decays to opsin.
62 ted to a more active intermediate similar to metarhodopsin II b.
63  and isolation of a high affinity transducin-metarhodopsin II complex was demonstrated for a monodisp
64 hodopsin to achieve the enzymatically active metarhodopsin II conformation is exquisitely sensitive t
65                Additionally, the kinetics of metarhodopsin II decay is similar between rhodopsin in n
66 ark and after photobleaching and the rate of metarhodopsin II decay, (ii) initial rates of transducin
67 table and exhibited abnormal photobleaching, metarhodopsin II decay, and G protein activation.
68 clic analogue stabilized the metarhodopsin I-metarhodopsin II equilibrium similarly to what has been
69 VRR difference spectra between rhodopsin and metarhodopsin II exhibit significant differences for vib
70 monomeric rhodopsin and stabilize the active metarhodopsin II form.
71 role of this site in determining the rate of metarhodopsin II formation and decay in rod and cone pig
72 n II/metarhodopsin I ratios, faster rates of metarhodopsin II formation, an increase of tryptophan fl
73 rge conformational change known to accompany metarhodopsin II formation.
74 ating that the PWR spectral shifts monitored metarhodopsin II formation.
75 ore (lambda max 495 nm) in the dark, but the metarhodopsin II formed on illumination decayed about 6.
76 Since the timescale for the formation of the metarhodopsin II intermediate (>1 ms) is beyond that rea
77 vided by solid-state NMR measurements of the metarhodopsin II intermediate are combined with molecula
78 e NMR measurements on both rhodopsin and the metarhodopsin II intermediate show how retinal isomeriza
79 inal-protein contacts observed in the active metarhodopsin II intermediate suggest a general activati
80 inning NMR measurements of rhodopsin and the metarhodopsin II intermediate that support the proposal
81 ons of the retinal chromophore in the active metarhodopsin II intermediate.
82 ft of the Schiff base nitrogen in the active metarhodopsin II intermediate.
83 om an inactive metarhodopsin I to the active metarhodopsin II intermediate.
84 ces the ability of rhodopsin to form the key metarhodopsin II intermediate.
85  The equilibrium constant of metarhodopsin I-metarhodopsin II is 30-45% higher, and the apparent rate
86 he antibody correlated with formation of the metarhodopsin II photointermediate and was reduced signi
87 tra of rhodopsin and its metarhodopsin I and metarhodopsin II photointermediates have been obtained t
88 ly abnormal bleaching behavior with abnormal metarhodopsin II photointermediates.
89 f the retinylidene Schiff base in the active metarhodopsin II photoproduct.
90  mutants on illumination showed destabilized metarhodopsin II species and reduced transducin activati
91                               Similarly, the metarhodopsin II spectrum obtained with a 500 micros del
92 0-350) to rhodopsin stabilizes the activated metarhodopsin II state (M II), consequently uncoupling t
93 re smaller than previously predicted for the metarhodopsin II state and include changes on the cytopl
94                                 Formation of metarhodopsin II was observed by the change in absorbanc
95 easing bilayer thickness favors formation of metarhodopsin II while oligomerization favors metarhodop
96 Comparison of the retinal chemical shifts in metarhodopsin II with those of retinal model compounds r
97 om the removal of metarhodopsin (most likely metarhodopsin II) from the outer segment.
98 re of the cytoplasmic face in the activated (metarhodopsin II) receptor.
99 nt in the dark-state of rhodopsin is lost in metarhodopsin II, and a new contact is formed with the C
100 t of nucleotide exchange rates, affinity for metarhodopsin II, and thermostability suggest that the K
101 een Trp265(6.48) and Gly121(3.36) is lost in metarhodopsin II, consistent with H6 motion away from H3
102 onal structure of ground state rhodopsin and metarhodopsin II, particularly in the cytoplasmic face o
103 .53) on H2 is observed in both rhodopsin and metarhodopsin II, suggesting that H3 does not change ori
104 e pigment has several structural features of metarhodopsin II, the active form of rhodopsin.
105                                  On decay of metarhodopsin II, the chemical shifts reverted largely t
106     Our data support the interpretation that metarhodopsin II, the signaling state of rhodopsin, is t
107                      On illumination to form metarhodopsin II, upfield changes in chemical shift were
108 nt in the Nanodisc was able to form a stable metarhodopsin II-G-protein complex.
109                             In addition, the metarhodopsin II-like photoproducts of the mutant pigmen
110                           The mutants formed metarhodopsin II-like photoproducts upon illumination bu
111 mational states of the protein (rhodopsin, a metarhodopsin II-mimic, and two forms of opsin) facilita
112 en upon formation of the active intermediate metarhodopsin II.
113  sequence in binding to and stabilization of metarhodopsin II.
114 r nanodiscs, as assessed by stabilization of metarhodopsin II.
115 ious work on the temperature-trapped form of metarhodopsin II.
116 etinal leading to the fully activated state, metarhodopsin II.
117 activation and formation of the active form, metarhodopsin II.
118 at the retinal translates 4-5 A toward H5 in metarhodopsin II.
119 helical conformation during interaction with metarhodopsin II.
120 miniscent of the G protein-activating state, metarhodopsin II.
121 weakly hydrogen bonded between rhodopsin and metarhodopsin II.
122  backbone carbonyl of His211 is disrupted in metarhodopsin II.
123 and becomes more strongly hydrogen bonded in metarhodopsin II.
124 h meta I380, a 380 nm absorbing precursor to metarhodopsin II.
125  in processes leading to the activated form, metarhodopsin II.
126 re for the activated state of this receptor, metarhodopsin II.
127 icity of rhodopsin are accompanied by higher metarhodopsin II/metarhodopsin I ratios, faster rates of
128 n the photointermediates metarhodopsin I and metarhodopsin II; increasing bilayer thickness favors fo
129 g pocket and resembles the G protein binding metarhodopsin-II conformation obtained by the natural ac
130 esolvable and the R(2) phase, which overlaps metarhodopsin-II formation, has a rapid risetime and com
131  the equilibrium between metarhodopsin-I and metarhodopsin-II is dependent upon the conformation of t
132 ctivation is of wide importance, because the metarhodopsin-II photoproduct is analogous to the agonis
133 ogether with greater hydration in the active metarhodopsin-II state.
134     K42-41L is shown to inhibit formation of metarhodopsin-II while it stabilizes the metarhodopsin-I
135 sed ratio of metarhodopsin-I-like species to metarhodopsin-II-like species and aberrant photoproduct
136 o be trapped in an open conformation that is metarhodopsin-II-like.
137 tarhodopsin-I that is lost upon formation of metarhodopsin-II.
138 mediate and was reduced significantly at the metarhodopsin III intermediate.
139 ther arrestin was also required to stabilize metarhodopsin in intact photoreceptor cells, metarhodops
140 f arrestin was observed upon illumination of metarhodopsin in lipid/detergent micellar extracts.
141 IP2 and by protecting the visual system from metarhodopsin-induced, low light degeneration.
142 trate that in disrupted photoreceptor cells, metarhodopsin is not stabilized unless arrestin is prese
143 ts because the light-activated conformation, metarhodopsin, is stable following exposure to light in
144 hereas Rh6 appears to be photoconverted to a metarhodopsin (lambda(max) = 468 nm) that is less therma
145 Rh5 is reversibly photoconverted to a stable metarhodopsin (lambda(max) = 494 nm), whereas Rh6 appear
146 ermined the lifetime of activated rhodopsin (metarhodopsin = M( *)) in whole-cell recordings from Dro
147 escues flies lacking PLC from light-induced, metarhodopsin-mediated degeneration and restores visual
148 odopsin and transducin was measured by extra-metarhodopsin (meta) II assay.
149 t this reduction results from the removal of metarhodopsin (most likely metarhodopsin II) from the ou
150  was used to hasten the decomposition of the metarhodopsin photoproducts.
151 the interaction of antibody K42-41L with the metarhodopsin photoproducts.
152 anes or micellar extracts, and the amount of metarhodopsin present was quantitated by spectroscopic m
153 iments in total head homogenates showed that metarhodopsin produced in the arr1(1), arr2(3) double mu
154  decrease was observed in the amounts of Rh1 metarhodopsin recovered from illuminated flies which wer
155 t in intact photoreceptor cells, significant metarhodopsin stabilization occurs even in the absence o
156                                 However, the metarhodopsin state is not stable as purified in dodecyl
157 ve protein states of the receptor (so-called metarhodopsin states) are regulated by the highly conser
158   The authors hypothesized that the decay of metarhodopsin to apo-opsin and free all-trans-retinaldeh
159  changes associated with the transition from metarhodopsin to rhodopsin were, however, similar in mem
160 nts for arrestin in the stabilization of Rh1 metarhodopsin under in vitro and in vivo conditions.
161 vidence that arrestin binding stabilizes Rh1 metarhodopsin under in vitro conditions.
162 metarhodopsin in intact photoreceptor cells, metarhodopsin was generated in arr1(1), arr2(3) double m
163 Compared to wild-type, approximately 64% Rh1 metarhodopsin was recovered in flies deficient in arrest
164 oproduct shows the formation of a protonated metarhodopsin with a maximum absorbance between 520 and

 
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