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1 ranscription factor 1 (TTF-1), in rat FRTL-5 thyrocytes.
2 ble expression of TPO at the cell surface of thyrocytes.
3 tive of thyroid peroxidase (TPO) behavior in thyrocytes.
4 at thyroid cell line FRTL5 and primary human thyrocytes.
5 c and dramatic decrease in NIS expression in thyrocytes.
6 wn in a variety of cell types in addition to thyrocytes.
7 cent and thyroid-stimulating hormone-treated thyrocytes.
8 hyrotropin (TSH)/cAMP-mediated repression in thyrocytes.
9 g Ganciclovir causes the death (ablation) of thyrocytes.
10 f its microRNA products in the participants' thyrocytes.
11 l cell invasion and by BMP-Smad signaling in thyrocytes.
12 epressed TTF-1 expression in PPFP-expressing thyrocytes.
13 increases and TSH-dependent iodide efflux in thyrocytes.
14  kinase (MAPK) pathway activation in Tg-Braf thyrocytes.
15 thways similar to those observed in cultured thyrocytes.
16 n is used to specifically delete Pten in the thyrocytes.
17  with iodine to enhance ICAM-1 expression on thyrocytes.
18 apoptotic inflammatory cells in proximity to thyrocytes.
19 ma(-/-)NOD.H-2h4 mice expressing TGF-beta on thyrocytes all develop fibrosis and moderate to severe T
20 wer in thyroid tumor cells than in wild-type thyrocytes, allowing more effective binding of PV to p85
21 he secretory pathway of TSHR-hyperstimulated thyrocytes alters the structure of the iodination substr
22 iated thyroid cancer types but not in normal thyrocytes and benign thyroid lesions.
23 tiated thyroid carcinomas, but not in normal thyrocytes and benign thyroid nodules.
24 end of RP3 induces signaling pathways within thyrocytes and causes cellular transformation.
25 ion, up-regulated MHC class II expression on thyrocytes and decreased thyrocyte proliferation.
26 s of TAO and control orbital fibroblasts and thyrocytes and explore the physical and functional relat
27   SMCT was reported in the apical surface of thyrocytes and formerly proposed also to transport I(-)
28 ociated with increased megalin expression on thyrocytes and increased serum Tg levels, with reduced s
29 lls resulted in decreased FasL expression by thyrocytes and inflammatory cells, but had no effect on
30 relates with their ability to bind to FRTL-5 thyrocytes and is inhibited by a specific antibody to th
31 ve I(-) uptake in the basolateral surface of thyrocytes and other cells.
32  is localized at the basolateral membrane of thyrocytes and that the serum TH concentration is reduce
33 that RET/PTC3 induces Il24 expression in rat thyrocytes and that this expression is dependent on the
34 oblasts are considerably lower than those on thyrocytes and that this receptor associates with IGF-1R
35 ime PCR analyses reveal that human and mouse thyrocytes and the Nthy-Ori 3-1 human thyrocyte line exp
36    When thyroglobulin (Tg) is endocytosed by thyrocytes and transported to lysosomes, thyroid hormone
37 duce sustained proliferation in normal human thyrocytes, and provides the first direct evidence that
38      In pull-down studies using fibroblasts, thyrocytes, and thyroid tissue, Abs directed specificall
39 d genes is thus mediated by the ASPGR on the thyrocyte apical membrane and regulated by a signal syst
40 oid enlargement (goiter) implicates death of thyrocytes as part of disease pathogenesis.
41 ed in mice expressing transgenic TGF-beta on thyrocytes, at least in part, because there is an increa
42 duces mostly benign lesions, Braf-expressing thyrocytes become transformed and progress to invasive c
43                 In primary cultures of human thyrocytes, both TSH and the agonists increase mRNA leve
44 tes, showed up-regulation of MHC class II on thyrocytes, but did not develop spontaneous thyroiditis.
45 ounts of Il24 following expression in murine thyrocytes, but its expression is dramatically reduced i
46  cytoplasmic compartments in fibroblasts and thyrocytes by confocal microscopy.
47 isphenol A (TBBPA)) of the thyroid axis, the thyrocytes can change their size and express lower or hi
48 n both EAGD mouse thyroids and human primary thyrocytes, CD40 mediates this effect by activating down
49 n aggregates may set the stage for apoptotic thyrocyte cell death, preventing thyroid goiter formatio
50          Although the FRTL5 (and PC Cl3) rat thyrocyte cell line also exhibits almost no endo H-resis
51       To examine TPO surface distribution in thyrocyte cell lines, we prepared new antibodies against
52 on iodination of TG secreted from PCCL3 (rat thyrocyte) cells was augmented from cells previously exp
53 on, and decreased MHC class II expression on thyrocytes compared with WT mice.
54 scence that in stable clones of PC Cl3 (rat) thyrocytes, considerably more ( approximately 50%) of th
55 , a small percentage ( approximately 10%) of thyrocytes constitutively expressed ICAM-1.
56 ession of inhibitory Smad-7 by proliferating thyrocytes correlate with the severity of TEC H/P.
57 IFN-gamma as lymphocytes from WT donors, and thyrocytes could respond to IFN-gamma.
58          Furthermore, TG secreted from human thyrocyte cultures hyperstimulated with TSH also showed
59  immune infiltrate, we treated mouse primary thyrocyte cultures with 0.01 mM sodium iodine and showed
60 tor cells (TPCs-day 22), which maturate into thyrocytes (day 30).
61                       Mouse HrasG12V/Rbm1OKO thyrocytes develop metastases that are reversed by RBM10
62    Adult zebrafish expressing BRAF(V600E) in thyrocytes developed invasive carcinoma.
63 type with predominant dedifferentiation-like thyrocytes, enriched cancer-associated fibroblasts, wors
64 autoimmune thyroid disease, characterized by thyrocyte epithelial cell (TEC) hyperplasia and prolifer
65 storage disease characterized by a distended thyrocyte ER containing misfolded Tg, along with induced
66 iferating cell nuclear antigen and the dying thyrocytes exhibited the ultrastructural features of apo
67                  Five different agonists for thyrocyte-expressed TAS2Rs reduced TSH-dependent Ca(2+)
68  also discover three phenotypes of malignant thyrocytes (follicular-like, partial-epithelial-mesenchy
69 ole in promoting the migration of vertebrate thyrocytes for follicle generation.
70  genes were extensively repressed in primary thyrocytes from a bitransgenic murine model (Bi-Tg) of t
71 ne, we analyzed CD45 and ICAM-1expression on thyrocytes from NOD.H2(h4) wild-type and NOD.H2(h4) thyr
72 , we performed cell culture experiments with thyrocytes from the PPFP mouse thyroid cancers.
73 irus thymidine kinase (HSVI-TK) is driven in thyrocytes from the thyroglobulin promoter, the drug Gan
74 e cyclic AMP pathway is a major regulator of thyrocyte function and proliferation and, predictably, i
75 on of bitter-tasting compounds to changes in thyrocyte function and T3/T4 production.
76                                    In normal thyrocytes, GRP94 interacts transiently with thyroglobul
77                                              Thyrocytes had intense FasL immunoreactvity, and many CD
78  of adult BBDR thymi in the presence of BBDR thyrocytes had no effect on the ability of recovered cel
79 Cs arise by engineering TPCs, whereas mature thyrocytes have a very limited tumorigenic capacity.
80 D.H-2h4 mice and inhibits the development of thyrocyte hyperplasia and proliferation (TEC H/P).
81 s the role of TGF-beta in the development of thyrocyte hyperplasia.
82 ater develop severe thyroid epithelial cell (thyrocyte) hyperplasia and proliferation (TEC H/P) and f
83 expression of ICAM-1, we analyzed NOD.H2(h4) thyrocytes in baseline conditions (day 0) and at several
84 duced these genes directly into normal human thyrocytes in primary culture using amphotropic retrovir
85    In contrast, FLIP was mainly expressed by thyrocytes in resolving G-EAT, the expression of active
86          TNF-alpha promotes proliferation of thyrocytes in vitro, and anti-TNF-alpha inhibits develop
87 ation of thyroid epithelial cells (TECs), or thyrocytes, in IFN-gamma(-/-) autoimmune-prone NOD and N
88              IFN-alpha treatment of cultured thyrocytes increased expression of thyroid differentiati
89                                    In PC Cl3 thyrocytes, inducible overexpression of ERp72 increased
90 rts iodide across the apical membrane of the thyrocyte into the colloid space.
91          Finally, transfer of RP3-expressing thyrocytes into mice in vivo attracted dense macrophage
92            The fluorescence expressed in the thyrocytes is inversely proportional to the thyroid axis
93 RET/PTC1 not only increased proliferation of thyrocytes, it also altered morphogenesis and differenti
94 g hormone-stimulated, constitutively active, thyrocyte K+ channel required for normal thyroid hormone
95  mouse thyrocytes and the Nthy-Ori 3-1 human thyrocyte line express several TAS2Rs.
96 e identify a subgroup of NF-kappaB-activated thyrocytes located at the center of thyroid tissues in p
97 stimulation of DNA synthesis was observed in thyrocytes, matched by an almost perfectly reciprocal in
98 hese results suggested that CD8+ T cells and thyrocytes may kill inflammatory cells through the Fas p
99     Suppressing NF-kappaB signaling affected thyrocyte migration and follicle formation, leading to a
100 oid cells played a crucial role in promoting thyrocyte migration by maintaining close contact and sec
101 h all myeloid cells were depleted, exhibited thyrocyte migration defects.
102                   These results suggest that thyrocytes must be able to respond to IFN-gamma for the
103  transiently with thyroglobulin (Tg), and in thyrocytes of animals suffering from congenital hypothyr
104                                Proliferating thyrocytes of IFN-gamma(-/-) mice with TEC H/P produce T
105                                     However, thyrocytes of normal NOD.H-2h4 thyroids did express late
106 significant repression of DDR genes in Bi-Tg thyrocytes (P=2.4 x 10(-4)) compared with either PBF- (P
107 her PBF- (P=1.5 x 10(-3)) or PTTG-expressing thyrocytes (P=NS).
108 ta identifies a "cancer-primed" premalignant thyrocyte population with normal morphology but altered
109 ice given anti-TGF-beta had markedly reduced thyrocyte proliferation and decreased fibrosis compared
110 ontribution of these pathways to TSH-induced thyrocyte proliferation and thyroid hyperplasia.
111 le of estrogens in controlling the increased thyrocyte proliferation index in mutant females.
112          Ablation occurred in the absence of thyrocyte proliferation or nuclear DNA synthesis, but wa
113 ability of purified CD8(+) T cells to induce thyrocyte proliferation, CD4(+) T cells or CD8 T cell-de
114 on through mechanisms that include increased thyrocyte proliferation.
115 ss II expression on thyrocytes and decreased thyrocyte proliferation.
116 oid results in a significant increase in the thyrocyte proliferative index, which is more prominent i
117 en resulted in a significant increase in the thyrocyte proliferative index, which was more prominent
118 , but did not develop L-SAT, suggesting that thyrocytes responding to IFN-gamma are important for inh
119 es the hyperplastic but not the hypertrophic thyrocyte responses to TSH, thus functionally uncoupling
120 roid gland, are delineated by a monolayer of thyrocytes resting on a continuous basement membrane.
121 contrast, expression of the mutants in human thyrocytes resulted in defects in adhesion and migration
122 ar analysis indicate that absence of NEMO in thyrocytes results in a dramatic loss of the thyroid gla
123  caused by PTEN deficiency in nontransformed thyrocytes results in a global downregulation of Krebs c
124                         6.5% of non-injected thyrocytes showed NE irregularity.
125 nder questionable the notion that I(-) exits thyrocytes solely via the Cl(-)/I(-) exchanger Pendrin (
126                                              Thyrocyte-specific double-mutant BRAF(V600E) PIK3CA(H104
127 To model PTC, we bred mice with adult-onset, thyrocyte-specific expression of BRAF(V600E).
128                            Here we show that thyrocyte-specific NEMO knock-out mice gradually develop
129 extent the proliferation index of the female thyrocytes, suggesting that a relevant part of the thyro
130 ative regulation of the TSH receptor gene in thyrocytes, suppression of MHC class II, and up-regulati
131            TSHR levels are 11-fold higher on thyrocytes than on TAO or control fibroblasts.
132  the production of Ganciclovir phosphates in thyrocytes that express HSV1-TK.
133  cells and expanded numbers of proliferating thyrocytes that highly express CD40.
134 ine whether responsiveness of lymphocytes or thyrocytes to IFN-gamma is important for the development
135             Upon thyroglobulin delivery from thyrocytes to the follicular lumen of the thyroid gland
136 expresses green fluorescent protein (GFP) in thyrocytes, under the control of the medaka thyroglobuli
137                 Primary-cultured PVPV-Akt1KO thyrocytes uniquely displayed a reduced cell motility.
138 g both a human thyroid cell line and primary thyrocytes, we investigated the mechanism by which IR in
139 imarily by inflammatory cells; some enlarged thyrocytes were also Fas+.
140 typic consequences of RET/PTC1 expression in thyrocytes were determined.
141 s, genetic instability was greatest in Bi-Tg thyrocytes with a mean genetic instability (GI) index of
142                         Treatment of primary thyrocytes with recombinant human TSH results in rapid E

 
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