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1 in is not a cone opsin but is likely to be a rod opsin.
2 oldfish ultraviolet cone opsin, and goldfish rod opsin.
3 bility and prevented the aggregation of P23H rod opsin.
4 were both required for these effects on P23H rod opsin.
5 that BiP (HSPA5) prevents the aggregation of rod opsin.
6 reduce the dominant negative effect of P23H rod opsin.
7 hort (S)-wavelength-sensitive cone opsin and rod opsin.
8 ow the skate opsin to be homologous to other rod opsins.
13 hromatin immunoprecipitation showed that the rod opsin and beta-PDE promoters are targets of both Sp4
17 ased the number of photoreceptors expressing rod opsin and red cone opsin, and decreased the number o
18 ion with cRNA probes generated from cDNA for rod opsin and red, green, blue, and ultraviolet cone ops
19 by visible flashes in cells expressing human rod opsin and regenerated with all-trans-retinal, compar
20 mation in cultured cells overexpressing P23H rod opsin, and increased rhodopsin aggregation in the P2
21 type-specific marker with respect to that of rod opsin, and then by killing the cells that generate r
22 abeling detected synaptic proteins, cone and rod opsins, and Muller glial processes separating the ph
23 ssess glutamate at residue 122, a feature of rod opsins, and the corresponding gene follows the typic
24 strated the preservation of PNA, S-cone, and rod opsin antibody labeling in the detachments maintaine
28 r of the proteostasis network that regulates rod opsin biogenesis and supports a role for disulphide
32 t be a factor that affects the biogenesis of rod opsin by studying wild-type (WT) or P23H rod opsin i
33 virally mediated ectopic expression of human rod opsin can restore vision under natural viewing condi
34 tions in the dim light photoreceptor protein rod opsin cause autosomal dominant retinitis pigmentosa.
38 re, we show that ectopically expressed human rod opsin, driven by either a non-selective or ON-bipola
39 -long wavelength-sensitive (M/L) cone opsin, rod opsin, excitatory amino acid transporter 1 (EAAT1),
44 ropose that in retinal disease, mislocalized rod opsin gains access to cAMP signaling, which leads to
45 pathophysiology of the E150K mutation in the rod opsin gene associated with autosomal recessive retin
48 scription from the rod-specific beta-PDE and rod opsin gene promoters and compared it to the ubiquito
53 We isolated a 20-kilobase (kbp) zebrafish rod opsin genomic clone, which consists of 18 kbp of 5'-
54 in the outer segments of rod photoreceptors, rod opsin immunolabeling was also observed in the inner
55 chemistry demonstrated a marked reduction in rod opsin immunostaining outer segments and relative pre
56 nd dominant negative properties of misfolded rod opsin in cells can be alleviated by drug treatments
57 rod opsin by studying wild-type (WT) or P23H rod opsin in combination with amino acid substitutions t
58 oning; phenotypes were assessed by assays of rod opsin in retinal extracts, and confocal microscopy o
60 on of BiP function results in aggregation of rod opsin in the ER, which suggests that BiP is importan
66 quality of vision restored, we suggest that rod opsin merits consideration as an optogenetic actuato
73 sidues near the C-terminus is deleted in the rod opsin of both marsupials and all eutherian mammals.
75 below that of the misfolding P23H mutant of rod opsin (P23H-GFP), which is retained in the ER and ca
76 sponding gene follows the typical vertebrate rod opsin pattern of five exons separated by four intron
77 in expression by labeling with antibodies to rod opsin, phosducin, synaptophysin, calbindin D, and gl
78 in the central fovea and found evidence that rod opsin positive cells were absent and violet-sensitiv
80 nd reduce the dominant negative effect on WT rod opsin processing, as well as reducing toxic gains of
82 s (rAAV) containing a proximal 472-bp murine rod opsin promoter (MOPS) to drive ribozyme synthesis.
83 DE promoters, whereas Sp1 activates only the rod opsin promoter and Sp3 activates neither promoter.
84 nriched Crx transcriptional regulator on the rod opsin promoter but not the beta-PDE promoter, althou
85 ression vector, the 4.4 kb Acc65I/Xhol mouse rod opsin promoter was ligated upstream to a 4.1 kb frag
87 rescent protein (EGFP) driven by the Xenopus rod opsin promoter was used to make Xenopus transgenic t
88 AAV) vectors incorporating a proximal bovine rod opsin promoter were used to transfer either hairpin
93 W opsin and the equivalent W161R mutation in rod opsin result in protein misfolding and retention in
96 munocytochemical staining with antibodies to rod opsin, S and M cone opsins, cytochrome oxidase, syna
97 ng using TUNEL, anti-M/L cone opsin and anti-rod opsin showed that hyperoxia had a remarkable effect
98 icing function in human cells using a bovine rod opsin splicing template did not detect any defect in
99 177R misfolding, unlike the P23H mutation in rod opsin that causes retinitis pigmentosa, is not rescu
102 ntibodies to anti-GFAP, -neurofilament, and -rod opsin to examine cellular changes after detachment.
104 DNA regulatory elements within 2.1 kb of the rod opsin upstream region were identified in fetal and a
106 ne opsins began approximately 10 hours after rod opsin was first expressed, and differentiation of co
107 r over the 6-month time course investigated, rod opsin was phosphorylated at a low level (approximate
108 tations, such as P23H, lead to misfolding of rod opsin with detrimental effects on photoreceptor func
109 tention and ubiquitylation of wild-type (WT) rod opsin (WT-green fluorescent protein [GFP]) at the ER
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