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1 developed directly from Kras (G12D)-induced chief cells.
2 essed in the gastric pepsinogen-synthesizing chief cells.
3 racing that SPEM evolves from differentiated chief cells.
4 least in part, from transdifferentiation of chief cells.
5 xpression is also a specific marker of human chief cells.
6 ct reprogramming of existing cells-mainly of chief cells.
7 of SPEM derived from transdifferentiation of chief cells.
8 or cell or by transdifferentiation of mature chief cells.
9 at SPEM derived from transdifferentiation of chief cells.
10 cally localized to the secretory granules in chief cells.
11 ed potentiation of cAMP levels in guinea pig chief cells.
12 tion of cAMP levels in cholera toxin-treated chief cells.
13 5'-triphosphate-binding protein, in gastric chief cells.
16 6 mouse showed a marked loss of parietal and chief cells, along with a marked expansion of an aberran
17 c factor expression is both predetermined in chief cells and can be expressed in parietal cells in re
19 Moreover, the parathyroid adenoma subtypes (chief cells and oxyphil cells) were characterized by the
20 associated with preservation of parietal and chief cells and protection from the development of gastr
21 t tumors, preparatively isolated oxyphil and chief cells, and laser-captured microdissected PA specim
22 IST1 as a reliable marker of mature, healthy chief cells, and we provide the first evidence that meta
23 s of FK-506 on cholera toxin-treated gastric chief cells are caused by its inhibitory actions on calc
24 rise in part through transdifferentiation of chief cells as opposed to expansion of mucus neck or pro
29 onfirm MIST1 expression is restricted to the chief cell compartment in normal oxyntic mucosa, rare in
30 Atp4a(-/-) stomachs revealed the presence of chief cells, demonstrating that the lack of acid secreti
32 sia and oxyntic atrophy were sustained while chief cell, enterochromaffin-like cell, and somatostatin
33 e, including a profound loss of parietal and chief cells, focal de novo production of acidic mucins,
35 mine whether SPEM lineages were derived from chief cells in 3 independent models of induction by DMP-
36 ted in an overlapping fashion in parathyroid chief cells in adenoma and hyperplastic glands, and also
37 Intrinsic factor is produced primarily by chief cells in rat and mouse, but 4 to 11% of isolated r
38 sulted in a loss of specialized parietal and chief cells in the corpus and the appearance of a metapl
41 been recognized that the secretion of PTH by chief cells in the parathyroid gland is regulated by ext
42 numbers of parietal cells, a loss of mature chief cells, increased numbers of mucous and undifferent
44 tion of digestive enzyme (zymogen)-secreting chief cells is a normal aspect of stomach function that
45 factor MIST1, normally restricted to mature chief cells, is down-regulated as chief cells undergo ex
47 5), epithelial differentiation to mucous and chief cell lineages was rudimentary, with no expression
48 -4 scale to score inflammation, parietal and chief cell loss, mucus metaplasia, and helicobacter colo
49 munoreactive for TFF2 and the differentiated chief cell markers, Mist1 and intrinsic factor, suggesti
50 sion of the activated form of Ras in gastric chief cells of mice leads to the development of SPEM, as
52 issues such as acinar cells of the pancreas, chief cells of the stomach, and parotid and lacrimal sec
54 olves through either transdifferentiation of chief cells or activation of a basal cryptic progenitor.
55 d glands, we have isolated and characterized chief cells, oxyphil cells, and tumor-infiltrating lymph
58 gen-mediated apoptosis depletes parietal and chief cell populations, leading to architectural distort
59 mitochondrial energy generation, whereas the chief cell predominantly expresses digestive enzymes and
62 sion of myofibroblasts, loss of parietal and chief cells, spasmolytic polypeptide expressing metaplas
63 istribution of the rab3D-like protein in the chief cell suggests that it may play an important role i
64 /+ (Mist1-Kras-mTmG) mice to examine whether chief cells that express active Kras give rise to SPEM a
65 th adenocarcinoma, we found normal zymogenic chief cells that were transitioning into SPEM cells only
66 osure of monolayers of renal collecting duct chief cells to orbital shaking and quantified the forces
67 to mature chief cells, is down-regulated as chief cells undergo experimentally induced metaplasia.
68 e stomach-the parietal, mucus-producing, and chief cells-were harvested from cryosections of infected
71 resence of functionally distinct oxyphil and chief cells within parathyroid primary adenomas and prov
72 s produce approximately 50% more PTH than do chief cells, yet display significantly greater PTH suppr
74 zed secretory vesicles in gastric zymogenic (chief) cells (ZCs) as they differentiate from their muco
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