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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 cal cells from prolactin-treated mice become follicular cells.
6 ere expressed almost entirely in surrounding follicular cells.
7  types of the hair follicle as well as upper follicular cells.
8 r significantly from that observed in normal follicular cells.
9 ress constitutively IFN-gamma in the thyroid follicular cells.
10  cells to mimic the iodide uptake of thyroid follicular cells.
11  rNIS-transduced tumor cells and rat thyroid follicular cells.
12 y relevant model, the differentiated thyroid follicular cells, a system that requires thyroid-stimula
13  function of this pathway in primary thyroid follicular cells and a papillary thyroid carcinoma cell
14 r TSH/TSHR-mediated proliferation of thyroid follicular cells and biosynthesis of thyroid hormone.
15 ostly weak in comparison with normal thyroid follicular cells and FAs.
16 ng of additional subsets, including T helper follicular cells and IL-17-producing T helper cells.
17 c instability, we transfected FTC133 thyroid follicular cells and observed increased genetic instabil
18 us ovarian androgen production requires both follicular cells and oocytes themselves.
19       There is an active interaction between follicular cells and the microenvironment that determine
20 ized intercellular communication between the follicular cells and the oocyte.
21 ne biosynthesis and proliferation of thyroid follicular cells and uncovers a mechanism by which GLIS3
22 (BCL6) is required for the development of Th follicular cells, and it has been shown to suppress Th2
23 may induce a destructive thyroiditis through follicular cell apoptosis.
24 the chimeric RET/PTC oncoproteins in thyroid follicular cells, are frequently found in radiation-indu
25 aRKO) exhibited a significant expansion of T follicular cells, as well as increases in TFH to TFR rat
26 lasma membrane of ovarian follicular and non-follicular cells, binds to E and its expression is regul
27  little is known about how these genes alter follicular cell biology.
28  transport at the apical membrane of thyroid follicular cells, but experimental evidence for this con
29 ine whether programmed cell death in thyroid follicular cells can be related to activation of the tum
30                             We conclude that follicular cells can undergo reprogramming to become lon
31 b(PV), an established mouse model of thyroid follicular cell carcinogenesis, significantly increased
32 mouse strains may be due to differences in T follicular cell commitment or intrinsic B cell differenc
33        However, it is generally thought that follicular cells contribute to the wound epidermis only
34 g been demonstrated in thyroid carcinomas of follicular cell derivation, but no consistent relationsh
35       Several lines of evidence suggest that follicular cell-derived thyroid cancers represent a cont
36 vulated oocytes degenerated, the surrounding follicular cells did not begin atresia.
37 reporter virus confirmed the permissivity of follicular cells ex vivo.
38 ammed cell death (PCD) in any of the thyroid follicular cells examined.
39 the cell membrane of both follicular and non-follicular cells, except the oocytes.
40  (familial medullary thyroid cancer) or from follicular cells (familial nonmedullary thyroid cancer).
41 activation specifies three distinct anterior follicular cell fates, suggesting that Upd is a morphoge
42 ape of thyroid cancers that are derived from follicular cells has been substantially elucidated throu
43                                            T follicular cells help B cells generate high-affinity ant
44                                            T follicular cells help B cells to drive germinal center f
45 t males, and increased incidences of thyroid follicular cell hypertrophy in adult females.
46  thyroid carcinomas (BRAF(V600E)) in thyroid follicular cells in a doxycycline-inducible (dox-inducib
47 litates the apoptotic destruction of thyroid follicular cells in experimental autoimmune thyroiditis,
48 helial cells in Crohn's disease, and thyroid follicular cells in Graves' disease (GD).
49  transported DA and cAMP produced by somatic follicular cells in response to NE-induced beta-adrenore
50 ter that is found at the luminal membrane of follicular cells in the thyroid gland as well as in the
51       The occurrence of apoptosis in thyroid follicular cells induced by Fas activation has been a su
52 e-tracing studies and showed an expansion of follicular cells into the interfollicular epidermis, as
53 onditional loss of Pten in the mouse thyroid follicular cells is sufficient to stimulate continuous a
54 ucleotide moieties are located mainly in the follicular cell layer.
55 lume and nuclear-to-cytoplasmic ratio of the follicular cells may provide important information about
56 on pattern; RASAL is highly expressed in the follicular cells of the thyroid and the adrenal medulla
57  Braf was appropriately activated in thyroid follicular cells of these mice, they had a lower mitotic
58              Thyroid tumors arising from the follicular cells often harbor mutations leading to the c
59 s either by directing the differentiation of follicular cells or assisting cells in interpreting a gr
60 somatic genetic changes in thyroid cancer of follicular cell origin (RET/PTC, NTRK, RAS, BRAF, PAX8-P
61                                   Cancers of follicular cell origin are the most common of the endocr
62  the tumor cell biology of thyroid cancer of follicular cell origin has improved and modern genomic t
63                  This analysis confirms that follicular cells participate in the initial resurfacing
64               The DNA-reactive B cells had a follicular cell phenotype.
65 sex determination and differentiation of the follicular cell progenitors, but is downregulated after
66                Thyroid lesions had extensive follicular cell proliferation, large numbers of histiocy
67 1R interactions influence the phenotype of T follicular cells, reducing the expression of CXCR4 and i
68                            The PCCL3 thyroid follicular cells represent a differentiated and physiolo
69 argets are key integrators of antibody and T follicular cell responses.
70 lts revealed that 6 had a paucity of thyroid follicular cells, suggesting insufficient sampling of th
71 hways, alone, is unable to transform thyroid follicular cells, their simultaneous activation is highl
72  with thyroiditis, and unexpectedly, thyroid follicular cells themselves could be induced to express
73                           The ability of the follicular cell to take up iodine permits the use of rad
74 use diminished export of iodide from thyroid follicular cells to the colloid and are associated with
75 the thyroid that could interact with thyroid follicular cell TRAIL receptors, RNase protection assays
76 he use of agents to improve iodine uptake in follicular cell tumors, are in early clinical investigat
77 s, PDE activity was manipulated in different follicular cells using type-specific inhibitors.
78 ell proliferation of GLIS3-deficient thyroid follicular cells was due to the inhibition of TSH-mediat
79 Furthermore, the number of apoptotic thyroid follicular cells was increased only in the thyroids from

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