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1 and five nuclear receptors in murine primary follicular cells.
2  Dally causes ectopic accumulation of Upd in follicular cells.
3  in mediating estrogen action in the thyroid follicular cells.
4 ferative and functional stimulus for thyroid follicular cells.
5 cellular matrix swelling in both stromal and follicular cells.
6 cal cells from prolactin-treated mice become follicular cells.
7 ere expressed almost entirely in surrounding follicular cells.
8  types of the hair follicle as well as upper follicular cells.
9 r significantly from that observed in normal follicular cells.
10 ress constitutively IFN-gamma in the thyroid follicular cells.
11  cells to mimic the iodide uptake of thyroid follicular cells.
12  rNIS-transduced tumor cells and rat thyroid follicular cells.
13 NA cluster specifically expressed in somatic follicular cells.
14 y relevant model, the differentiated thyroid follicular cells, a system that requires thyroid-stimula
15  function of this pathway in primary thyroid follicular cells and a papillary thyroid carcinoma cell
16 and oncocytic (~2%) forms arise from thyroid follicular cells and are termed well-differentiated thyr
17 r TSH/TSHR-mediated proliferation of thyroid follicular cells and biosynthesis of thyroid hormone.
18  deprotected from their surrounding layer of follicular cells and expressing the epidermal growth fac
19 ostly weak in comparison with normal thyroid follicular cells and FAs.
20 ng of additional subsets, including T helper follicular cells and IL-17-producing T helper cells.
21 c instability, we transfected FTC133 thyroid follicular cells and observed increased genetic instabil
22 us ovarian androgen production requires both follicular cells and oocytes themselves.
23 on of the retrotransposon ZAM in the somatic follicular cells and subsequent germline genome invasion
24       There is an active interaction between follicular cells and the microenvironment that determine
25 ever, the effects of the interaction between follicular cells and the oocyte surface on meiotic proce
26 the bi-directional communication between the follicular cells and the oocyte, which is partly mediate
27 ized intercellular communication between the follicular cells and the oocyte.
28 ne biosynthesis and proliferation of thyroid follicular cells and uncovers a mechanism by which GLIS3
29 (BCL6) is required for the development of Th follicular cells, and it has been shown to suppress Th2
30 may induce a destructive thyroiditis through follicular cell apoptosis.
31 f OGT) amplifies oocyte spindle defects when follicular cells are absent highlighting a control of th
32 the chimeric RET/PTC oncoproteins in thyroid follicular cells, are frequently found in radiation-indu
33 aRKO) exhibited a significant expansion of T follicular cells, as well as increases in TFH to TFR rat
34 lasma membrane of ovarian follicular and non-follicular cells, binds to E and its expression is regul
35  little is known about how these genes alter follicular cell biology.
36  transport at the apical membrane of thyroid follicular cells, but experimental evidence for this con
37       Luteal cells were distinguishable from follicular cells by the presence of LDs, LD-associated p
38 ine whether programmed cell death in thyroid follicular cells can be related to activation of the tum
39                             We conclude that follicular cells can undergo reprogramming to become lon
40 b(PV), an established mouse model of thyroid follicular cell carcinogenesis, significantly increased
41 mouse strains may be due to differences in T follicular cell commitment or intrinsic B cell differenc
42        However, it is generally thought that follicular cells contribute to the wound epidermis only
43 g been demonstrated in thyroid carcinomas of follicular cell derivation, but no consistent relationsh
44 imaging for direct analysis and diagnosis of follicular cell-derived neoplasia tissues and FNA biopsi
45 ocytic (Hurthle cell) thyroid carcinoma is a follicular cell-derived neoplasm that accounts for appro
46                              Here, we create follicular cell-derived TCs of all the different histoty
47                          Aggressive forms of follicular cell-derived thyroid cancer are poorly differ
48       Several lines of evidence suggest that follicular cell-derived thyroid cancers represent a cont
49 vulated oocytes degenerated, the surrounding follicular cells did not begin atresia.
50 reporter virus confirmed the permissivity of follicular cells ex vivo.
51 ammed cell death (PCD) in any of the thyroid follicular cells examined.
52 the cell membrane of both follicular and non-follicular cells, except the oocytes.
53  determined that oocytes surrounded by their follicular cells expressing EGFR-Grb7 exhibit normal mei
54  (familial medullary thyroid cancer) or from follicular cells (familial nonmedullary thyroid cancer).
55 activation specifies three distinct anterior follicular cell fates, suggesting that Upd is a morphoge
56 a-6 PUFA (corn oil, N6) on blood, muscle and follicular cell fatty acid composition and mitochondrial
57                Here, we investigated Xenopus follicular cell function using oocyte signaling and hete
58 rtant leukocyte-derived factors that promote follicular cell function, thereby facilitating ovulation
59 ape of thyroid cancers that are derived from follicular cells has been substantially elucidated throu
60                                            T follicular cells help B cells generate high-affinity ant
61                                            T follicular cells help B cells to drive germinal center f
62 t males, and increased incidences of thyroid follicular cell hypertrophy in adult females.
63               Tumours can arise from thyroid follicular cells if they acquire driver mutations that c
64  thyroid carcinomas (BRAF(V600E)) in thyroid follicular cells in a doxycycline-inducible (dox-inducib
65  Drosophila melanogaster larvae, and ovarian follicular cells in adult Drosophila, discovering ultras
66 nar polarization and collective migration of follicular cells in Drosophila.
67 litates the apoptotic destruction of thyroid follicular cells in experimental autoimmune thyroiditis,
68 helial cells in Crohn's disease, and thyroid follicular cells in Graves' disease (GD).
69 te subpopulations and their interaction with follicular cells in ovulatory follicles, especially in h
70  transported DA and cAMP produced by somatic follicular cells in response to NE-induced beta-adrenore
71 ter that is found at the luminal membrane of follicular cells in the thyroid gland as well as in the
72       The occurrence of apoptosis in thyroid follicular cells induced by Fas activation has been a su
73 e-tracing studies and showed an expansion of follicular cells into the interfollicular epidermis, as
74 t of EVs in mediating the stress response in follicular cells is not fully understood.
75 onditional loss of Pten in the mouse thyroid follicular cells is sufficient to stimulate continuous a
76 rovides further insight into the role of the follicular cell layer in oocyte meiosis progression.
77 ucleotide moieties are located mainly in the follicular cell layer.
78 lume and nuclear-to-cytoplasmic ratio of the follicular cells may provide important information about
79 combination of targeted nutrients to improve follicular cell metabolism.
80 ay, compared with wild type marginal zone or follicular cells of the spleen.
81 on pattern; RASAL is highly expressed in the follicular cells of the thyroid and the adrenal medulla
82  Braf was appropriately activated in thyroid follicular cells of these mice, they had a lower mitotic
83  differentiated cancers derived from thyroid follicular cells offers unique insights into how oncogen
84              Thyroid tumors arising from the follicular cells often harbor mutations leading to the c
85 s either by directing the differentiation of follicular cells or assisting cells in interpreting a gr
86 somatic genetic changes in thyroid cancer of follicular cell origin (RET/PTC, NTRK, RAS, BRAF, PAX8-P
87                                   Cancers of follicular cell origin are the most common of the endocr
88  the tumor cell biology of thyroid cancer of follicular cell origin has improved and modern genomic t
89                  This analysis confirms that follicular cells participate in the initial resurfacing
90               The DNA-reactive B cells had a follicular cell phenotype.
91 sex determination and differentiation of the follicular cell progenitors, but is downregulated after
92                Thyroid lesions had extensive follicular cell proliferation, large numbers of histiocy
93 er (NIS) mediates iodide uptake into thyroid follicular cells, providing the basis for radioiodine (R
94 1R interactions influence the phenotype of T follicular cells, reducing the expression of CXCR4 and i
95                            The PCCL3 thyroid follicular cells represent a differentiated and physiolo
96                                              Follicular cells respond to heat stress (HS) by activati
97 argets are key integrators of antibody and T follicular cell responses.
98 lts revealed that 6 had a paucity of thyroid follicular cells, suggesting insufficient sampling of th
99 tissue representing murine and human thyroid follicular cells (TFCs).
100 enopus oocytes are encompassed by a layer of follicular cells that contribute to oocyte growth and me
101 hways, alone, is unable to transform thyroid follicular cells, their simultaneous activation is highl
102  with thyroiditis, and unexpectedly, thyroid follicular cells themselves could be induced to express
103                           The ability of the follicular cell to take up iodine permits the use of rad
104 use diminished export of iodide from thyroid follicular cells to the colloid and are associated with
105 the thyroid that could interact with thyroid follicular cell TRAIL receptors, RNase protection assays
106 , demonstrating an increase in its levels as follicular cells transition into the luteal phase.
107 he use of agents to improve iodine uptake in follicular cell tumors, are in early clinical investigat
108 terize the changes in the metabolism of each follicular cell type (i.e., oocyte, granulosa cells, inc
109 s, PDE activity was manipulated in different follicular cells using type-specific inhibitors.
110 ell proliferation of GLIS3-deficient thyroid follicular cells was due to the inhibition of TSH-mediat
111 Furthermore, the number of apoptotic thyroid follicular cells was increased only in the thyroids from

 
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