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1 psins in vertebrates (two cone opsins and 38 rod opsins).
2 in is not a cone opsin but is likely to be a rod opsin.
3 oldfish ultraviolet cone opsin, and goldfish rod opsin.
4 le pharmacological properties that stabilize rod opsin.
5 bility and prevented the aggregation of P23H rod opsin.
6 were both required for these effects on P23H rod opsin.
7 that BiP (HSPA5) prevents the aggregation of rod opsin.
8  reduce the dominant negative effect of P23H rod opsin.
9 hort (S)-wavelength-sensitive cone opsin and rod opsin.
10 ow the skate opsin to be homologous to other rod opsins.
11 vates the expressed salamander and human red rod opsins, acting as an agonist.
12 nals in cells stably expressing normal human rod opsin after regeneration with 11-cis-retinal.
13                                         P23H rod opsin aggregation, inclusion formation with associat
14 3H-GFP, suggesting that it can reduce mutant rod opsin aggregation.
15 hromatin immunoprecipitation showed that the rod opsin and beta-PDE promoters are targets of both Sp4
16                       Sp4 activates both the rod opsin and beta-PDE promoters, whereas Sp1 activates
17                  The goldfish opsins include rod opsin and four different cone opsins: red, green, bl
18 lecules that bind to the orthosteric site of rod opsin and improve its folding and trafficking.
19                               Misfolded P23H rod opsin and other mutations in the intradiscal domain
20 ased the number of photoreceptors expressing rod opsin and red cone opsin, and decreased the number o
21 ion with cRNA probes generated from cDNA for rod opsin and red, green, blue, and ultraviolet cone ops
22 by visible flashes in cells expressing human rod opsin and regenerated with all-trans-retinal, compar
23 mation in cultured cells overexpressing P23H rod opsin, and increased rhodopsin aggregation in the P2
24 type-specific marker with respect to that of rod opsin, and then by killing the cells that generate r
25 abeling detected synaptic proteins, cone and rod opsins, and Muller glial processes separating the ph
26 ssess glutamate at residue 122, a feature of rod opsins, and the corresponding gene follows the typic
27 strated the preservation of PNA, S-cone, and rod opsin antibody labeling in the detachments maintaine
28 trans-retinal can form a visual pigment with rod opsin apoprotein.
29 tained markers of early rod differentiation: rod opsin, arrestin, and recoverin.
30 ence for the recurrent evolution of multiple rod opsin-based vision in vertebrates.
31 e for disulphide bond formation/reduction in rod opsin biogenesis and disease.
32 r of the proteostasis network that regulates rod opsin biogenesis and supports a role for disulphide
33 f disulphide bond formation/reduction during rod opsin biogenesis.
34 acted as dominant negatives that affected WT rod opsin biogenesis.
35 derstand the role of molecular chaperones in rod opsin biogenesis.
36 t be a factor that affects the biogenesis of rod opsin by studying wild-type (WT) or P23H rod opsin i
37 virally mediated ectopic expression of human rod opsin can restore vision under natural viewing condi
38 tions in the dim light photoreceptor protein rod opsin cause autosomal dominant retinitis pigmentosa.
39 es have class-specific sites compared to the rod opsin class.
40 em, we have reduced or eliminated endogenous rod opsin content by targeted gene disruption.
41             ERdj5 reduction by shRNA delayed rod opsin degradation and promoted aggregation.
42 re, we show that ectopically expressed human rod opsin, driven by either a non-selective or ON-bipola
43 hese compounds reversibly bind to unliganded rod opsin, each with a Kd comparable to 9-cis-retinal an
44  flavonoids also bind directly to unliganded rod opsin, enhancing its folding, stability, and regener
45 -long wavelength-sensitive (M/L) cone opsin, rod opsin, excitatory amino acid transporter 1 (EAAT1),
46                                    Mice with rod opsin expression driven by the ON-bipolar specific p
47                         In contrast, reduced rod opsin expression provided enhanced rod and cone phot
48 for any other cone opsins or pigments, rods, rod opsin expression, or rod visual pigment.
49 ssion, and (3) the relative time of cone and rod opsin expression.
50 ropose that in retinal disease, mislocalized rod opsin gains access to cAMP signaling, which leads to
51 pathophysiology of the E150K mutation in the rod opsin gene associated with autosomal recessive retin
52 important in the developmental regulation of rod opsin gene expression.
53 rn blotting, and DNA sequencing revealed the rod opsin gene lacks introns.
54 scription from the rod-specific beta-PDE and rod opsin gene promoters and compared it to the ubiquito
55  a single nucleotide change in exon 2 of the rod opsin gene resulting in the E150K mutation.
56                          Rh1, the intronless rod opsin gene, first emerged in ancestral Actinopterygi
57                                   The Exorh (rod opsin) gene has been retained in 56 genomes.
58 he cloned opsin sequences are orthologues of rod opsin genes from other vertebrate species.
59    We isolated a 20-kilobase (kbp) zebrafish rod opsin genomic clone, which consists of 18 kbp of 5'-
60 in the outer segments of rod photoreceptors, rod opsin immunolabeling was also observed in the inner
61 chemistry demonstrated a marked reduction in rod opsin immunostaining outer segments and relative pre
62 nd dominant negative properties of misfolded rod opsin in cells can be alleviated by drug treatments
63 rod opsin by studying wild-type (WT) or P23H rod opsin in combination with amino acid substitutions t
64 oning; phenotypes were assessed by assays of rod opsin in retinal extracts, and confocal microscopy o
65 tive (M&L) opsin appears in foveal cones and rod opsin in rods around the fovea at Fd 100.
66 on of BiP function results in aggregation of rod opsin in the ER, which suggests that BiP is importan
67  important for maintaining the solubility of rod opsin in the ER.
68               Here, we expressed P23H bovine rod opsin in the nervous system of Caenorhabditis elegan
69  degeneration suggests that nonpalmitoylated rod opsin is unstable.
70                                  Regenerable rod opsin levels were similar over the 6-month time cour
71 ernal protein structure network (PSN), these rod opsin ligands also enhanced the plasma membrane expr
72 edium/long wavelength sensitive (M/LWS), and rod opsin like 1 and 2 (RH1, RH2).
73  quality of vision restored, we suggest that rod opsin merits consideration as an optogenetic actuato
74 rs in a retinitis pigmentosa mouse model for rod opsin misfolding.
75 ved a similar AAV2/5 vector carrying a mouse rod opsin (mOps) promoter-controlled GFP reporter.
76                       Some of these dominant rod opsin mutant proteins, which desensitize transgenic
77             For example, the common class II rod opsin mutation P23H misfolds and is retained in the
78                                         Many rod opsin mutations lead to protein misfolding, and ther
79                                 A variety of rod opsin mutations result in autosomal dominant retinit
80                                         Many rod opsin mutations, such as P23H, lead to misfolding of
81 sidues near the C-terminus is deleted in the rod opsin of both marsupials and all eutherian mammals.
82                         The P23H mutation of rod opsin (P23H opsin) is the most common cause of human
83  below that of the misfolding P23H mutant of rod opsin (P23H-GFP), which is retained in the ER and ca
84 sponding gene follows the typical vertebrate rod opsin pattern of five exons separated by four intron
85 in expression by labeling with antibodies to rod opsin, phosducin, synaptophysin, calbindin D, and gl
86 in the central fovea and found evidence that rod opsin positive cells were absent and violet-sensitiv
87 ession was identical to that of the goldfish rod opsin probe.
88 nd reduce the dominant negative effect on WT rod opsin processing, as well as reducing toxic gains of
89                      Using a proximal murine rod opsin promoter (+86 to -385) to drive expression, re
90 s (rAAV) containing a proximal 472-bp murine rod opsin promoter (MOPS) to drive ribozyme synthesis.
91 DE promoters, whereas Sp1 activates only the rod opsin promoter and Sp3 activates neither promoter.
92 nriched Crx transcriptional regulator on the rod opsin promoter but not the beta-PDE promoter, althou
93 lowed PDE5r expressed under control of mouse rod opsin promoter to accumulate in rod outer segments.
94 ression vector, the 4.4 kb Acc65I/Xhol mouse rod opsin promoter was ligated upstream to a 4.1 kb frag
95                                    The mouse rod opsin promoter was used to drive expression of mouse
96 rescent protein (EGFP) driven by the Xenopus rod opsin promoter was used to make Xenopus transgenic t
97 AAV) vectors incorporating a proximal bovine rod opsin promoter were used to transfer either hairpin
98 deno-associated virus (rAAV) incorporating a rod opsin promoter.
99                                     However, rod opsin protein appears in and around the fovea at fet
100 s encodes constitutively active forms of the rod opsin protein.
101 ilar developmental expression profile as the rod opsin protein.
102 W opsin and the equivalent W161R mutation in rod opsin result in protein misfolding and retention in
103                               In contrast, a rod opsin (RH1) and three cone opsins (SWS2, RH2, and LW
104                                    In bovine rod opsin (RH1), two critical amino acids form a salt br
105 lly distinct visual pigments and opsins: one rod opsin, RH1 (498 nm), and five cone opsins, SWS1 (370
106 ight, vertebrates generally rely on a single rod opsin [rhodopsin 1 (RH1)] for obtaining visual infor
107 munocytochemical staining with antibodies to rod opsin, S and M cone opsins, cytochrome oxidase, syna
108 ng using TUNEL, anti-M/L cone opsin and anti-rod opsin showed that hyperoxia had a remarkable effect
109 icing function in human cells using a bovine rod opsin splicing template did not detect any defect in
110 ms quercetin-3-rhamnoside and myricetrin) on rod opsin stability, function, and membrane organization
111 177R misfolding, unlike the P23H mutation in rod opsin that causes retinitis pigmentosa, is not rescu
112                                 Mutations in rod opsin, the visual pigment protein of rod photorecept
113                                 Mutations in rod opsin-the light-sensitive protein of rod cells-cause
114 ntibodies to anti-GFAP, -neurofilament, and -rod opsin to examine cellular changes after detachment.
115                                 In contrast, rod opsin traffics normally in mutant rods.
116 DNA regulatory elements within 2.1 kb of the rod opsin upstream region were identified in fetal and a
117  membrane trafficking of multiple RP-related rod opsin variants in vitro.
118            Importantly, this novel ligand of rod opsin was effective in vivo in murine models, protec
119                               In the retina, rod opsin was expressed first, and it was restricted to
120 ne opsins began approximately 10 hours after rod opsin was first expressed, and differentiation of co
121 r over the 6-month time course investigated, rod opsin was phosphorylated at a low level (approximate
122        They bind to and stabilize unliganded rod opsin, which in excess accelerates degenerative proc
123 mpound reversibly binds to unliganded bovine rod opsin with an EC50 value comparable to the 9-cis-ret
124 tations, such as P23H, lead to misfolding of rod opsin with detrimental effects on photoreceptor func
125 tention and ubiquitylation of wild-type (WT) rod opsin (WT-green fluorescent protein [GFP]) at the ER

 
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