ライフサイエンスコーパス: thyrocyte

1 tive of thyroid peroxidase (TPO) behavior in thyrocytes.

2 at thyroid cell line FRTL5 and primary human thyrocytes.

3 wn in a variety of cell types in addition to thyrocytes.

4 cent and thyroid-stimulating hormone-treated thyrocytes.

5 hyrotropin (TSH)/cAMP-mediated repression in thyrocytes.

6 g Ganciclovir causes the death (ablation) of thyrocytes.

7 l cell invasion and by BMP-Smad signaling in thyrocytes.

8 epressed TTF-1 expression in PPFP-expressing thyrocytes.

9 increases and TSH-dependent iodide efflux in thyrocytes.

10 kinase (MAPK) pathway activation in Tg-Braf thyrocytes.

11 thways similar to those observed in cultured thyrocytes.

12 n is used to specifically delete Pten in the thyrocytes.

13 c and dramatic decrease in NIS expression in thyrocytes.

14 with iodine to enhance ICAM-1 expression on thyrocytes.

15 apoptotic inflammatory cells in proximity to thyrocytes.

16 ranscription factor 1 (TTF-1), in rat FRTL-5 thyrocytes.

17 ble expression of TPO at the cell surface of thyrocytes.

18 ma(-/-)NOD.H-2h4 mice expressing TGF-beta on thyrocytes all develop fibrosis and moderate to severe T

19 wer in thyroid tumor cells than in wild-type thyrocytes, allowing more effective binding of PV to p85

20 he secretory pathway of TSHR-hyperstimulated thyrocytes alters the structure of the iodination substr

21 tiated thyroid carcinomas, but not in normal thyrocytes and benign thyroid nodules.

22 end of RP3 induces signaling pathways within thyrocytes and causes cellular transformation.

23 ion, up-regulated MHC class II expression on thyrocytes and decreased thyrocyte proliferation.

24 s of TAO and control orbital fibroblasts and thyrocytes and explore the physical and functional relat

25 SMCT was reported in the apical surface of thyrocytes and formerly proposed also to transport I(-)

26 ociated with increased megalin expression on thyrocytes and increased serum Tg levels, with reduced s

27 lls resulted in decreased FasL expression by thyrocytes and inflammatory cells, but had no effect on

28 relates with their ability to bind to FRTL-5 thyrocytes and is inhibited by a specific antibody to th

29 ve I(-) uptake in the basolateral surface of thyrocytes and other cells.

30 is localized at the basolateral membrane of thyrocytes and that the serum TH concentration is reduce

31 that RET/PTC3 induces Il24 expression in rat thyrocytes and that this expression is dependent on the

32 oblasts are considerably lower than those on thyrocytes and that this receptor associates with IGF-1R

33 ime PCR analyses reveal that human and mouse thyrocytes and the Nthy-Ori 3-1 human thyrocyte line exp

34 When thyroglobulin (Tg) is endocytosed by thyrocytes and transported to lysosomes, thyroid hormone

35 duce sustained proliferation in normal human thyrocytes, and provides the first direct evidence that

36 In pull-down studies using fibroblasts, thyrocytes, and thyroid tissue, Abs directed specificall

37 d genes is thus mediated by the ASPGR on the thyrocyte apical membrane and regulated by a signal syst

38 oid enlargement (goiter) implicates death of thyrocytes as part of disease pathogenesis.

39 ed in mice expressing transgenic TGF-beta on thyrocytes, at least in part, because there is an increa

40 duces mostly benign lesions, Braf-expressing thyrocytes become transformed and progress to invasive c

41 In primary cultures of human thyrocytes, both TSH and the agonists increase mRNA leve

42 tes, showed up-regulation of MHC class II on thyrocytes, but did not develop spontaneous thyroiditis.

43 ounts of Il24 following expression in murine thyrocytes, but its expression is dramatically reduced i

44 cytoplasmic compartments in fibroblasts and thyrocytes by confocal microscopy.

45 n both EAGD mouse thyroids and human primary thyrocytes, CD40 mediates this effect by activating down

46 n aggregates may set the stage for apoptotic thyrocyte cell death, preventing thyroid goiter formatio

47 Although the FRTL5 (and PC Cl3) rat thyrocyte cell line also exhibits almost no endo H-resis

48 To examine TPO surface distribution in thyrocyte cell lines, we prepared new antibodies against

49 on iodination of TG secreted from PCCL3 (rat thyrocyte) cells was augmented from cells previously exp

50 on, and decreased MHC class II expression on thyrocytes compared with WT mice.

51 scence that in stable clones of PC Cl3 (rat) thyrocytes, considerably more ( approximately 50%) of th

52 , a small percentage ( approximately 10%) of thyrocytes constitutively expressed ICAM-1.

53 ession of inhibitory Smad-7 by proliferating thyrocytes correlate with the severity of TEC H/P.

54 IFN-gamma as lymphocytes from WT donors, and thyrocytes could respond to IFN-gamma.

55 Furthermore, TG secreted from human thyrocyte cultures hyperstimulated with TSH also showed

56 immune infiltrate, we treated mouse primary thyrocyte cultures with 0.01 mM sodium iodine and showed

57 Adult zebrafish expressing BRAF(V600E) in thyrocytes developed invasive carcinoma.

58 autoimmune thyroid disease, characterized by thyrocyte epithelial cell (TEC) hyperplasia and prolifer

59 storage disease characterized by a distended thyrocyte ER containing misfolded Tg, along with induced

60 iferating cell nuclear antigen and the dying thyrocytes exhibited the ultrastructural features of apo

61 Five different agonists for thyrocyte-expressed TAS2Rs reduced TSH-dependent Ca(2+)

62 genes were extensively repressed in primary thyrocytes from a bitransgenic murine model (Bi-Tg) of t

63 ne, we analyzed CD45 and ICAM-1expression on thyrocytes from NOD.H2(h4) wild-type and NOD.H2(h4) thyr

64 , we performed cell culture experiments with thyrocytes from the PPFP mouse thyroid cancers.

65 irus thymidine kinase (HSVI-TK) is driven in thyrocytes from the thyroglobulin promoter, the drug Gan

66 e cyclic AMP pathway is a major regulator of thyrocyte function and proliferation and, predictably, i

67 on of bitter-tasting compounds to changes in thyrocyte function and T3/T4 production.

68 In normal thyrocytes, GRP94 interacts transiently with thyroglobul

69 Thyrocytes had intense FasL immunoreactvity, and many CD

70 of adult BBDR thymi in the presence of BBDR thyrocytes had no effect on the ability of recovered cel

71 D.H-2h4 mice and inhibits the development of thyrocyte hyperplasia and proliferation (TEC H/P).

72 s the role of TGF-beta in the development of thyrocyte hyperplasia.

73 ater develop severe thyroid epithelial cell (thyrocyte) hyperplasia and proliferation (TEC H/P) and f

74 expression of ICAM-1, we analyzed NOD.H2(h4) thyrocytes in baseline conditions (day 0) and at several

75 duced these genes directly into normal human thyrocytes in primary culture using amphotropic retrovir

76 In contrast, FLIP was mainly expressed by thyrocytes in resolving G-EAT, the expression of active

77 TNF-alpha promotes proliferation of thyrocytes in vitro, and anti-TNF-alpha inhibits develop

78 ation of thyroid epithelial cells (TECs), or thyrocytes, in IFN-gamma(-/-) autoimmune-prone NOD and N

79 IFN-alpha treatment of cultured thyrocytes increased expression of thyroid differentiati

80 In PC Cl3 thyrocytes, inducible overexpression of ERp72 increased

81 rts iodide across the apical membrane of the thyrocyte into the colloid space.

82 Finally, transfer of RP3-expressing thyrocytes into mice in vivo attracted dense macrophage

83 RET/PTC1 not only increased proliferation of thyrocytes, it also altered morphogenesis and differenti

84 g hormone-stimulated, constitutively active, thyrocyte K+ channel required for normal thyroid hormone

85 mouse thyrocytes and the Nthy-Ori 3-1 human thyrocyte line express several TAS2Rs.

86 stimulation of DNA synthesis was observed in thyrocytes, matched by an almost perfectly reciprocal in

87 hese results suggested that CD8+ T cells and thyrocytes may kill inflammatory cells through the Fas p

88 These results suggest that thyrocytes must be able to respond to IFN-gamma for the

89 transiently with thyroglobulin (Tg), and in thyrocytes of animals suffering from congenital hypothyr

90 Proliferating thyrocytes of IFN-gamma(-/-) mice with TEC H/P produce T

91 However, thyrocytes of normal NOD.H-2h4 thyroids did express late

92 significant repression of DDR genes in Bi-Tg thyrocytes (P=2.4 x 10(-4)) compared with either PBF- (P

93 her PBF- (P=1.5 x 10(-3)) or PTTG-expressing thyrocytes (P=NS).

94 ice given anti-TGF-beta had markedly reduced thyrocyte proliferation and decreased fibrosis compared

95 ontribution of these pathways to TSH-induced thyrocyte proliferation and thyroid hyperplasia.

96 le of estrogens in controlling the increased thyrocyte proliferation index in mutant females.

97 Ablation occurred in the absence of thyrocyte proliferation or nuclear DNA synthesis, but wa

98 ability of purified CD8(+) T cells to induce thyrocyte proliferation, CD4(+) T cells or CD8 T cell-de

99 on through mechanisms that include increased thyrocyte proliferation.

100 ss II expression on thyrocytes and decreased thyrocyte proliferation.

101 oid results in a significant increase in the thyrocyte proliferative index, which is more prominent i

102 en resulted in a significant increase in the thyrocyte proliferative index, which was more prominent

103 , but did not develop L-SAT, suggesting that thyrocytes responding to IFN-gamma are important for inh

104 es the hyperplastic but not the hypertrophic thyrocyte responses to TSH, thus functionally uncoupling

105 roid gland, are delineated by a monolayer of thyrocytes resting on a continuous basement membrane.

106 contrast, expression of the mutants in human thyrocytes resulted in defects in adhesion and migration

107 ar analysis indicate that absence of NEMO in thyrocytes results in a dramatic loss of the thyroid gla

108 caused by PTEN deficiency in nontransformed thyrocytes results in a global downregulation of Krebs c

109 6.5% of non-injected thyrocytes showed NE irregularity.

110 nder questionable the notion that I(-) exits thyrocytes solely via the Cl(-)/I(-) exchanger Pendrin (

111 To model PTC, we bred mice with adult-onset, thyrocyte-specific expression of BRAF(V600E).

112 Here we show that thyrocyte-specific NEMO knock-out mice gradually develop

113 extent the proliferation index of the female thyrocytes, suggesting that a relevant part of the thyro

114 ative regulation of the TSH receptor gene in thyrocytes, suppression of MHC class II, and up-regulati

115 TSHR levels are 11-fold higher on thyrocytes than on TAO or control fibroblasts.

116 the production of Ganciclovir phosphates in thyrocytes that express HSV1-TK.

117 cells and expanded numbers of proliferating thyrocytes that highly express CD40.

118 ine whether responsiveness of lymphocytes or thyrocytes to IFN-gamma is important for the development

119 g both a human thyroid cell line and primary thyrocytes, we investigated the mechanism by which IR in

120 imarily by inflammatory cells; some enlarged thyrocytes were also Fas+.

121 typic consequences of RET/PTC1 expression in thyrocytes were determined.

122 s, genetic instability was greatest in Bi-Tg thyrocytes with a mean genetic instability (GI) index of

123 Treatment of primary thyrocytes with recombinant human TSH results in rapid E