ライフサイエンスコーパス: dent

1 nce identity range, the so-called 'BRaliBase Dent'.

2 te, and Kinepak using three tests: (1) plate dent, (2) reaction velocity and (3) air blast.

3 5-phosphatase OCRL1 causes Lowe syndrome and Dent-2 disease.

4 s the renal tubulopathy in Lowe syndrome and Dent-2 disease.

5 adjustment), 78.17% (contamination), 82.89% (dent), 80.17% (scratch), 96.66% (sealing components), 98

6 adjustment (90.52%), contamination (70.75%), dent (90.21%), scratch (90.34%), sealing components (90.

7 Dent and flint kernel architectures are important charac

8 ent of whole-grain-maize-based noodles using Dent and Flint maize genotypes.

9 predicted (AUC equals 0.59 and 0.67 for the Dent and Flint panels, respectively) and that the Chines

10 apping (NAM) populations from China, Europe (Dent and Flint) and the United States as well as in the

11 Plate dent and reaction velocity tests are suggested for asses

12 temporal endothelial cell density (DenC and DenT), and coefficient of variation in cell area (CVC an

13 Ga1-s can be transferred into dent corn but the effectiveness of the Ga1-s allele in p

14 While both popcorn and Ga1-s dent corn had significantly better pollen exclusion than

15 ctiveness of the Ga1-s allele in popcorn and dent corn has never been compared, which is important be

16 clusion of commercial popcorn hybrids, Ga1-s dent corn hybrids and normal dent corn hybrids for their

17 hybrids, Ga1-s dent corn hybrids and normal dent corn hybrids for their ability to exclude ga1 polle

18 popcorn was significantly better than Ga1-s dent corn on average.

19 mpatibility (UCI) occurs between popcorn and dent corn, and represents a critical step towards specia

20 ficantly better pollen exclusion than normal dent corn, popcorn was significantly better than Ga1-s d

21 Dent disease 1 (DD1) is caused by mutations in the CLCN5

22 Both this syndrome and Dent Disease 2 result from loss-of-function mutations in

23 hus, we created an animal model for OCRL and Dent Disease 2 tubulopathy by humanizing a modifier para

24 The dysfunction can be isolated (Dent disease 2) or associated with congenital cataracts,

25 Here, we investigate the role of OCRL in Dent disease 2/Lowe syndrome by using OcrlY/- mice, wher

26 The mechanistic understanding of Dent disease 2/Lowe syndrome remains scarce due to limit

27 bservation confirms genetic heterogeneity in Dent disease and demonstrates more-extensive phenotypic

28 The symptoms of Dent disease are replicated in Clcn5 knock-out mice.

29 Lowe syndrome and Dent disease are two conditions that result from mutatio

30 mal-tubular reabsorption and is decreased in Dent disease because of mutations of the chloride/proton

31 amilies, all of whom met strict criteria for Dent disease but lacked mutations in CLCN5.

32 les, phenocopying what has been reported for Dent disease caused by mutations in the gene encoding en

33 nction of the 2Cl - /H + antiporter ClC-5 in Dent disease causes an unknown impairment in endocytic t

34 s, our studies, which have established human Dent disease ciPTECs that will facilitate studies of mec

35 ected in Dent disease, but no other gene for Dent disease has been reported.

36 nction of the 2Cl - /H + antiporter ClC-5 in Dent disease impairs the uptake of filtered proteins by

37 n occur with the isolated renal phenotype of Dent disease in patients lacking the cataracts, renal tu

38 Dent disease is an X-linked renal proximal tubulopathy a

39 t with a scenario in which Lowe syndrome and Dent disease result from perturbations at multiple sites

40 ations are responsible for Lowe syndrome and Dent disease, and INPP5B are two similar proteins compri

41 Genetic heterogeneity has been suspected in Dent disease, but no other gene for Dent disease has bee

42 rders oculocerebrorenal syndrome of Lowe and Dent disease, two conditions giving rise to abnormal kid

43 isms in renal reabsorption, demonstrate that Dent disease-causing CLC-5 mutations have differing effe

44 erapeutic interventions in Lowe syndrome and Dent disease.

45 Mutations of the CLCN5 gene cause Dent disease.

46 ceptor expression and tubular proteinuria in Dent disease.

47 d Clcn5Y/- mice suggest shared mechanisms in Dent diseases 1 and 2.

48 We found mutation of ARFTF17 in a dent genetic background reduces IAA content in the seed

49 hree corn hybrids, including a novel flint x dent genotype.

50 The flint x dent hybrid showed higher carotenoid and lower mycotoxin

51 Some Ga1-s dent hybrids excluded as well or better than some popcor

52 t appears that the transient deformation (or dent) in the tube wall may provide a previously unknown

53 ion) into the background of N28 (a Corn Belt Dent inbred line).

54 ndoreduplication phenotype into a midwestern dent inbred line, a backcross population was generated f

55 Introgression of the ARFTF17 mutation into dent inbreds and hybrids improved their kernel texture,

56 In this article, we show this dent is owing to a bias in the composition of the BRaliB

57 idence of selection in the maize Krug Yellow Dent long-term divergent seed-size selection experiment.

58 arge and small seed size from Krug, a yellow dent maize cultivar.

59 genetic introgression from the high latitude Dent maize grown in Europe.

60 Dent maize noodles from traditional and ecological nixta

61 Dent maize noodles had undergone phenolics loss of 5-6%

62 Hybrid WF9 * 38MS, B73 * Missouri 17, Yellow Dent, Merit, and Great Lakes Hybrid 422) to reinvestigat

63 Studies in a Dent mouse model also revealed subsegment-specific diffe

64 The central dent of the prepore has a diameter of 3.2 +/- 0.2 nm.

65 rotenoid and lower mycotoxin levels than the dent one, thus supporting its potential for by-product r

66 The decreased IAA content of the dent pericarp appears to reduce cell division and expans

67 A score of 4 and above on Carlsson- Dent questionnaire was considered diagnostic of gastroes

68 Part B consisted of standard Carlsson-Dent questionnaire.

69 was observed for eight of nine families with Dent's disease (n = 10) and for the two families with Lo

70 ubules and thus decreased loss into urine in Dent's disease and Lowe's syndrome.

71 Their dysfunction causes Dent's disease and osteopetrosis, respectively.

72 uptake, based on evidence from patients with Dent's disease and studies in ClC-5 knockout mice.

73 us, CLC-5-deficient mice provide a model for Dent's disease and this will help in elucidating the fun

74 rome and low molecular weight proteinuria in Dent's disease can be explained by disruption of endosom

75 In patients with Dent's disease during chlorthalidone therapy, the supers

76 This suggests that hypercalciuria in Dent's disease is a direct consequence of CLC5 hypofunct

77 Dent's disease is an X-linked inherited disorder charact

78 Dent's disease is due to inactivating mutations of the r

79 A microdeletion in one Dent's disease kindred allowed the identification of a c

80 acilitate in vivo investigations of CLC-5 in Dent's disease we generated mice lacking CLC-5 by target

81 rine composition in eight male patients with Dent's disease, ages 6 to 49 yr, all of whom were hyperc

82 jor risk factor promoting stone formation in Dent's disease, also known as X-linked recessive nephrol

83 or are present in the urine of patients with Dent's disease, Lowe's syndrome, or autosomal dominant i

84 One such hypercalciuric disorder is Dent's disease, which is characterized by renal proximal

85 disorders of hypercalciuric nephrolithiasis (Dent's disease, X-linked recessive nephrolithiasis (XRN)

86 The common aetiology for Dent's disease, XRN and XLRH indicates that CLCN5 may be

87 l 5-phosphatase OCRL cause Lowe syndrome and Dent's disease.

88 of kidney stone recurrence in patients with Dent's disease.

89 DENT-seq produces a single deep sequence data set enrich

90 We apply DENT-seq to profile the off-target activity of the Nb.Bs

91 DENT-seq will be useful in exploring the activity of eng

92 Here, we developed a new method, DENT-seq, for efficient strand-specific profiling of nic

93 ssion (probands from the Depression Network [DeNT] study; N=332), and 3) a pharmacogenetic study (the

94 gastrointestinal digestion of 103 hybrids of dent type.

95 rix structure on carotenoid digestibility in dent-type maize hybrids.

96 ittle variation was found between midwestern dent types, and high levels of endoreduplication were ob

97 Tannerite and Rimfire did not produce dent values due to low brisance; with reaction velocity