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1 or proliferative and functional stimulus for thyroid follicular cells.
2 that express constitutively IFN-gamma in the thyroid follicular cells.
3 o cancer cells to mimic the iodide uptake of thyroid follicular cells.
4 larly in rNIS-transduced tumor cells and rat thyroid follicular cells.
5 e of p27 in mediating estrogen action in the thyroid follicular cells.
6 logically relevant model, the differentiated thyroid follicular cells, a system that requires thyroid
7 sion and function of this pathway in primary thyroid follicular cells and a papillary thyroid carcino
8 sable for TSH/TSHR-mediated proliferation of thyroid follicular cells and biosynthesis of thyroid hor
9 ng was mostly weak in comparison with normal thyroid follicular cells and FAs.
10 n genetic instability, we transfected FTC133 thyroid follicular cells and observed increased genetic
11 id hormone biosynthesis and proliferation of thyroid follicular cells and uncovers a mechanism by whi
12 tion of the chimeric RET/PTC oncoproteins in thyroid follicular cells, are frequently found in radiat
13 n iodide transport at the apical membrane of thyroid follicular cells, but experimental evidence for
14 o determine whether programmed cell death in thyroid follicular cells can be related to activation of
15 with Thrb(PV), an established mouse model of thyroid follicular cell carcinogenesis, significantly in
16 ce programmed cell death (PCD) in any of the thyroid follicular cells examined.
17  F1 adult males, and increased incidences of thyroid follicular cell hypertrophy in adult females.
18 apillary thyroid carcinomas (BRAF(V600E)) in thyroid follicular cells in a doxycycline-inducible (dox
19 nes facilitates the apoptotic destruction of thyroid follicular cells in experimental autoimmune thyr
20 nal epithelial cells in Crohn's disease, and thyroid follicular cells in Graves' disease (GD).
21               The occurrence of apoptosis in thyroid follicular cells induced by Fas activation has b
22 n that conditional loss of Pten in the mouse thyroid follicular cells is sufficient to stimulate cont
23 ncogenic Braf was appropriately activated in thyroid follicular cells of these mice, they had a lower
24                                    The PCCL3 thyroid follicular cells represent a differentiated and
25 ive results revealed that 6 had a paucity of thyroid follicular cells, suggesting insufficient sampli
26  two pathways, alone, is unable to transform thyroid follicular cells, their simultaneous activation
27  patient with thyroiditis, and unexpectedly, thyroid follicular cells themselves could be induced to
28 drin, cause diminished export of iodide from thyroid follicular cells to the colloid and are associat
29 RAIL in the thyroid that could interact with thyroid follicular cell TRAIL receptors, RNase protectio
30 ion of cell proliferation of GLIS3-deficient thyroid follicular cells was due to the inhibition of TS
31         Furthermore, the number of apoptotic thyroid follicular cells was increased only in the thyro

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