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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  (~4%), and oncocytic (~2%) forms arise from thyroid follicular cells and are termed well-differentia
9 sable for TSH/TSHR-mediated proliferation of thyroid follicular cells and biosynthesis of thyroid hor
10 ng was mostly weak in comparison with normal thyroid follicular cells and FAs.
11 n genetic instability, we transfected FTC133 thyroid follicular cells and observed increased genetic
12 id hormone biosynthesis and proliferation of thyroid follicular cells and uncovers a mechanism by whi
13 tion of the chimeric RET/PTC oncoproteins in thyroid follicular cells, are frequently found in radiat
14 n iodide transport at the apical membrane of thyroid follicular cells, but experimental evidence for
15 o determine whether programmed cell death in thyroid follicular cells can be related to activation of
16 with Thrb(PV), an established mouse model of thyroid follicular cell carcinogenesis, significantly in
17 ce programmed cell death (PCD) in any of the thyroid follicular cells examined.
18  F1 adult males, and increased incidences of thyroid follicular cell hypertrophy in adult females.
19                       Tumours can arise from thyroid follicular cells if they acquire driver mutation
20 apillary thyroid carcinomas (BRAF(V600E)) in thyroid follicular cells in a doxycycline-inducible (dox
21 nes facilitates the apoptotic destruction of thyroid follicular cells in experimental autoimmune thyr
22 nal epithelial cells in Crohn's disease, and thyroid follicular cells in Graves' disease (GD).
23               The occurrence of apoptosis in thyroid follicular cells induced by Fas activation has b
24 n that conditional loss of Pten in the mouse thyroid follicular cells is sufficient to stimulate cont
25 ncogenic Braf was appropriately activated in thyroid follicular cells of these mice, they had a lower
26 icity of differentiated cancers derived from thyroid follicular cells offers unique insights into how
27  symporter (NIS) mediates iodide uptake into thyroid follicular cells, providing the basis for radioi
28                                    The PCCL3 thyroid follicular cells represent a differentiated and
29 ive results revealed that 6 had a paucity of thyroid follicular cells, suggesting insufficient sampli
30 thyroid tissue representing murine and human thyroid follicular cells (TFCs).
31  two pathways, alone, is unable to transform thyroid follicular cells, their simultaneous activation
32  patient with thyroiditis, and unexpectedly, thyroid follicular cells themselves could be induced to
33 drin, cause diminished export of iodide from thyroid follicular cells to the colloid and are associat
34 RAIL in the thyroid that could interact with thyroid follicular cell TRAIL receptors, RNase protectio
35 ion of cell proliferation of GLIS3-deficient thyroid follicular cells was due to the inhibition of TS
36         Furthermore, the number of apoptotic thyroid follicular cells was increased only in the thyro