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1                                              ORD inhibition of 3,3'-T2 formation from rT3 was also ob
2 port (MDW) and O'Hare International Airport (ORD).
3                                      ECD and ORD spectra are used to investigate the complementarity
4 ed by the chromosome axis proteins C(2)M and ORD.
5 use C(2)M encodes a Kleisin-like protein and ORD is required for sister-chromatid cohesion, we tested
6 on meiosis-specific proteins SOLO, SUNN, and ORD is required for sister-chromatid cohesion, localizes
7 ion between cone photoreceptor terminals and ORDs suggests a novel photoreceptor to ganglion cell con
8                        Second, we calculated ORD and CD spectra of the structural models and compared
9 ole for biplexiform melanopsin ganglion cell ORDs.
10                          After condensation, ORD remains bound at the centromeres of wild-type sperma
11                     Outer Retinal Dendrites (ORDs) either ramify within the outer plexiform layer (OP
12 oximately 40% decrease in the time-dependent ORD signal at 230 nm that is best fit to a single-expone
13 nd experimental optical rotatory dispersion (ORD) data provides the most straightforward way to assig
14 oism (ECD), and optical rotatory dispersion (ORD) spectroscopy.
15 ination of NMR, optical rotatory dispersion (ORD), and circular dichroism (CD) spectroscopy together
16 ectroscopy, and optical rotatory dispersion (ORD).
17 d time-resolved optical rotatory dispersion (ORD).
18 tem to study the oligopeptide repeat domain (ORD) expansions of the prion protein, PrP, and their eff
19                  Their OSBP-related domains (ORDs) harbored either PI4P or phosphatidylserine (PS) an
20 Sup35p with that from wild type and expanded ORDs of PrP and compared their biochemical properties in
21 normal meiotic chromosome segregation, extra ORD+ protein in mei-S332 mutant males enhances nondisjun
22 rotein-protein interactions are critical for ORD function.
23                       Additionally, we found ORDs asymmetrically distributed to the dorsal retina.
24                                           If ORD activity is more severely disrupted, achiasmate chro
25  the morphology of melanopsin-immunopositive ORDs in the OPL at different developmental time points i
26                                            L-ORD shows striking phenotypic similarities to age-relate
27 ved serine to arginine (Ser163Arg) in 7/14 L-ORD families and 0/1000 control individuals.
28 rotein 5 (C1QTNF5) has been shown to cause L-ORD in a subset of affected families.
29           Late-onset retinal degeneration (L-ORD) is a rare autosomal dominant retinal dystrophy, cha
30           Late-onset retinal degeneration (L-ORD) is an autosomal dominant disorder with striking cli
31   Late-onset retinal macular degeneration (L-ORD) is an autosomal dominant inherited disorder caused
32  dominant late-onset retinal degeneration (L-ORD), a retinopathy that becomes symptomatic after age 5
33 (LAZ) and late-onset retinal degeneration (L-ORD).
34 uggests that the heterozygous mutations in L-ORD show a dominant negative, rather than a haploinsuffi
35 ls (ages 35-60) at a 50:50 risk to inherit L-ORD were also studied with dark adaptometry.
36 rotein may underlie the pathophysiology of L-ORD and LAZ.
37  precede symptoms and funduscopic signs of L-ORD by at least a decade.
38 new insight into the pathogenetic basis of L-ORD has implications for future therapeutic strategies s
39               Early phenotypic features of L-ORD include: dark adaptation abnormalities, nyctalopia,
40                          Here we show that L-ORD is genetically heterogeneous and that a proposed fou
41 dditional power for genetic mapping of the L-ORD locus.
42                        Three families with L-ORD were included; two families had postmortem eye donor
43 germ-line mitotic divisions in flies lacking ORD activity.
44 esion is severely disrupted in flies lacking ORD protein.
45 on directly, we confirm that oocytes lacking ORD activity exhibit cohesion defects, consistent with p
46      Our results suggest that association of ORD with meiotic chromosomes during mid to late G2 is re
47 ions demonstrate that the C-terminal half of ORD is essential for sister chromatid cohesion and sugge
48                The analytical performance of ORD, LCOR, and their coupling resulted from the CSI simu
49  prophase condensation and that retention of ORD at the centromeres after condensation ensures the ma
50         While it is known that the number of ORDs in the retina is developmentally regulated, little
51 he mouse retina and identified five types of ORDs originating from either M1 or M1d cells.
52 mers with very similar mass spectra based on ORD, LCOR, and their coupling were much more efficient,
53 eport here a new strategy based on ordering (ORD), linear correlation (LCOR) algorithms, and their co
54 eak mutation in the meiotic cohesion protein ORD coupled with a reduction in centromere-proximal hete
55 tiation sites depend on the cohesion protein ORD.
56                Brain deiodinase activity (T4-ORD) was reduced by approximately 65% at both doses.
57 T3), and hepatic outer ring deiodination (T4-ORD).
58 T3 and TT4, thyroid histology and hepatic T4-ORD were determined at the final 18 day exposure.
59  no effect on plasma FT3, TT3, or hepatic T4-ORD.
60 nerally longer and more highly branched than ORDs from conventional M1 cells.
61                             We conclude that ORD activity suppresses sister chromatid exchange and st
62                     We provide evidence that ORD is concentrated within the extrachromosomal domains
63 observed for ord null flies, indicating that ORD function is not essential for cohesion during somati
64                                 We show that ORD protein localizes along oocyte chromosomes during th
65 analysis of weaker ord alleles suggests that ORD is required for proper centromeric cohesion after ar
66 e severity with respect to the length of the ORD in humans.
67 On the other hand, TDDFT calculations of the ORD of (1R,5S,8S,9S,10S)-1 and -2 over the range of 365-
68 lish a system to study the properties of the ORD of PrP both in vivo and in vitro.
69                              We replaced the ORD of the yeast prion protein Sup35p with that from wil
70                                   Therefore, ORD activity appears to promote centromeric cohesion dur
71     However, a pattern emerges within these: ORDs from M1d cells are generally longer and more highly
72 ocytes shortly after the time when wild-type ORD associates with the chromosomes.
73                   The simulation of CSI with ORD, LCOR, and their coupling of six TeCBs (IUPAC no.

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