ライフサイエンスコーパス: amelogenesis

1 eater than optimal levels of fluoride during amelogenesis.

2 modification of gene expression important to amelogenesis.

3 le for nascent amelogenin polypeptide during amelogenesis.

4 TP) effectors during events related to early amelogenesis.

5 bility and organization of amelogenin during amelogenesis.

6 oblasts during the early maturation stage of amelogenesis.

7 expressed throughout the secretory stage of amelogenesis.

8 namel proteins during the secretory phase of amelogenesis.

9 in reduced ameloblasts at the conclusion of amelogenesis.

10 ccurs in the developing enamel matrix during amelogenesis.

11 f GPR68 in the enamel organ at all stages of amelogenesis.

12 ence for the crucial function of ACPT during amelogenesis.

13 onal role in subsequent tooth patterning and amelogenesis.

14 material formed by the intricate process of amelogenesis.

15 eral formation during the secretory stage of amelogenesis.

16 ndant enamel matrix protein expressed during amelogenesis.

17 enamel defects reflecting failure of normal amelogenesis.

18 uring the secretory and maturation stages of amelogenesis.

19 in endosome/lysosome-related pathways during amelogenesis.

20 s led us to investigate the effect of BPA on amelogenesis.

21 n ameloblasts during the maturation stage of amelogenesis.

22 efect in tooth enamel that reflects impaired amelogenesis.

23 e clarified due to a lack of knowledge about amelogenesis.

24 f these genes during the maturation stage of amelogenesis.

25 ble function in enamel mineralization during amelogenesis.

26 enamel extracellular matrix proteins during amelogenesis.

27 ing a possible signal for the termination of amelogenesis.

28 enamel matrix during the secretory stage of amelogenesis.

29 t that AE2 and NBCe1 play important roles in amelogenesis.

30 ys regulate dental epithelial stem cells and amelogenesis.

31 and for the robust nature of the process of amelogenesis.

32 ibute to its physiological regulation during amelogenesis.

33 ssion throughout the developmental stages of amelogenesis.

34 hat accumulate during the secretory stage of amelogenesis?

35 Although amelogenesis and dentinogenesis initiate in the molar to

36 of enamel with the developmental process of amelogenesis and structural development, since they are

37 periodontal ligament is required for normal amelogenesis and that periostin is critically required f

38 tor (CSF-1) is a key regulatory cytokine for amelogenesis, and ameloblasts synthesize CSF-1.

39 hoprotein contributes to the early events of amelogenesis, and in particular to those events that res

40 in is a cell adhesion molecule essential for amelogenesis, and it plays a role in maintaining the dif

41 s ameloblastin during the secretory stage of amelogenesis, and we present a hypothesis about the sequ

42 d a rapid rate of tooth enamel elongation or amelogenesis at 0.24 mm/day with dental tissues common t

43 Starting with the onset of amelogenesis beneath the future cusp tips, the shape of

44 Data suggest that BPA exerts its effects on amelogenesis by disrupting normal protein removal from t

45 nclusion, miR-153 regulates maturation-stage amelogenesis by targeting key genes involved in the endo

46 Our findings demonstrate that early and late amelogenesis depend upon cell-matrix interactions.

47 he OMIM database was searched with the terms amelogenesis, enamel, dental, and tooth, and all results

48 These data suggest rapid amelogenesis evolved among non-hadrosauriform iguanodont

49 and growth of hydroxyapatite crystals during amelogenesis generate a large number of protons that mus

50 The pivotal role of AMBN in amelogenesis has been confirmed experimentally using mou

51 Among ornithopods, high rates of amelogenesis have been previously observed in hadrosauri

52 Recent studies on rodent amelogenesis have identified a multitude of gene product

53 in SLC24A4 in a family with hypomineralized amelogenesis imperfect a (AI), a condition in which toot

54 ciated with autosomal-dominant hypocalcified amelogenesis imperfecta (ADHCAI), which is typically cha

55 q24.3 cause autosomal-dominant hypocalcified amelogenesis imperfecta (ADHCAI).

56 The Amelogenesis Imperfecta (AI) are a group of clinically a

57 Amelogenesis Imperfecta (AI) can be caused by the defici

58 Amelogenesis imperfecta (AI) describes a broad group of

59 Amelogenesis imperfecta (AI) describes a clinically and

60 Amelogenesis imperfecta (AI) describes a heterogeneous g

61 Patients with amelogenesis imperfecta (AI) have defective enamel; ther

62 ge would lead to an enamel defect similar to amelogenesis imperfecta (AI) in humans, we generated tra

63 generalized hypoplastic autosomal-recessive amelogenesis imperfecta (AI) in individuals from six app

64 Amelogenesis imperfecta (AI) is a broad group of heredit

65 Non-syndromic amelogenesis imperfecta (AI) is a collection of isolated

66 Amelogenesis imperfecta (AI) is a collective term for fa

67 Amelogenesis imperfecta (AI) is a group of inherited con

68 Amelogenesis imperfecta (AI) is a group of inherited def

69 Amelogenesis imperfecta (AI) is a heterogeneous group of

70 Amelogenesis imperfecta (AI) is a heterogeneous group of

71 Amelogenesis imperfecta (AI) is a heterogeneous group of

72 Amelogenesis imperfecta (AI) is group of inherited disor

73 s the first gene involved in the etiology of amelogenesis imperfecta (AI) that does not encode a secr

74 ively inherited cone-rod dystrophy (CRD) and amelogenesis imperfecta (AI) was first reported by Jalil

75 ort stature with brachyolmia and hypoplastic amelogenesis imperfecta (AI) with almost absent enamel.

76 genes, FAM20A mutations are associated with Amelogenesis Imperfecta (AI) with gingival hyperplasia a

77 ied a family in which pitted hypomineralized amelogenesis imperfecta (AI) with premature enamel failu

78 f26, as a cause of recessive hypomineralized amelogenesis imperfecta (AI), a disease in which the for

79 in gene a prime candidate in the etiology of amelogenesis imperfecta (AI), a genetic disease in which

80 d displayed severe enamel defects that mimic amelogenesis imperfecta (AI), with a rough, irregular en

81 AM gene have been found to cause hypoplastic amelogenesis imperfecta (AI), with phenotypes ranging fr

82 usly linked to an autosomal-dominant form of amelogenesis imperfecta (AI).

83 el phenotypes that are collectively known as amelogenesis imperfecta (AI).

84 spanic families with generalized hypoplastic amelogenesis imperfecta (AI).

85 alformed tooth enamel that phenocopies human amelogenesis imperfecta (AI).

86 altered conditions is collectively known as amelogenesis imperfecta (AI).

87 Defects in the enamelin gene (ENAM) cause amelogenesis imperfecta (AI).

88 sulting in an inherited tooth enamel defect, amelogenesis imperfecta (AI).

89 d improve the clinical diagnosis of X-linked amelogenesis imperfecta (AI).

90 ysin (MMP20) genes cause autosomal-recessive amelogenesis imperfecta (ARAI).

91 X-linked amelogenesis imperfecta (MIM 301200), a phenotypically d

92 features and inheritance pattern of X-linked amelogenesis imperfecta (XAI).

93 mutated amelogenin (TgP70T), which leads to amelogenesis imperfecta in humans, have heterogeneous en

94 hreonine, as in some cases of human X-linked amelogenesis imperfecta or when tyrosyl residues were su

95 hreonine, as in some cases of human X-linked amelogenesis imperfecta or when tyrosyl residues were su

96 c regions similar to those in enamel of male amelogenesis imperfecta patients with an identical mutat

97 in X-linked forms of the human enamel defect amelogenesis imperfecta resulting from amelogenin gene m

98 ions in amelogenin observed in patients with amelogenesis imperfecta who demonstrate defects in ename

99 'Amelogenesis imperfecta' (AI) describes a group of inher

100 ous variants in GPR68 in three families with amelogenesis imperfecta, a genetically and phenotypicall

101 e non-syndromic enamel malformations, termed amelogenesis imperfecta, and ablation of Mmp20 in mice r

102 erized by sensorineural hearing loss (SNHL), amelogenesis imperfecta, nail abnormalities, and occasio

103 of undiagnosed autosomally dominant cases of amelogenesis imperfecta.

104 enamel are grouped under the classification amelogenesis imperfecta.

105 es the need for family-specific diagnosis of amelogenesis imperfecta.

106 the enamelin gene in kindreds suffering from amelogenesis imperfecta.

107 hreonine, as in some cases of human X-linked amelogenesis imperfecta.

108 ation identified in a case of human X-linked amelogenesis imperfecta.

109 consistent with the diagnosis of hypoplastic amelogenesis imperfecta.

110 Amelx and Mmp20 mutations cause amelogenesis imperfecta.

111 because defects in KLK4 cause hypomaturation amelogenesis imperfecta.

112 human enamelin gene cause autosomal dominant amelogenesis imperfecta.

113 tosomal-recessive hypoplastic-hypomaturation amelogenesis imperfecta.

114 efects have been identified in kindreds with amelogenesis imperfecta.

115 tivities that define the maturation stage of amelogenesis include ion (e.g., calcium and phosphate) t

116 y which the enamel organ regulates pH during amelogenesis is largely unknown.

117 upting incisor enamel was normal, suggesting amelogenesis is only sensitive to MIH-causing agents dur

118 Amelogenesis is the process of dental enamel formation,

119 Enamel formation (amelogenesis) is the result of highly orchestrated extra

120 ages of tooth development, especially during amelogenesis, it is unclear how mutant forms cause ARS d

121 hat, while FAM20C is a molecule essential to amelogenesis, its inactivation in the dental epithelium

122 tooth number, crown and root morphology and amelogenesis that is likely due to a functional role of

123 from the secretory and maturation stages of amelogenesis, the serine protease chymotrypsin C (caldec

124 ogical role in organizing ameloblasts during amelogenesis, this study strengthens the hypothesis that

125 The enamel matrix pH during amelogenesis was studied in 10 normal and 10 CF mice.

126 l-time PCR showed DPPI expression throughout amelogenesis, with highest expression at maturation, and