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1 ct reprogramming of existing cells-mainly of chief cells.
2  developed directly from Kras (G12D)-induced chief cells.
3 essed in the gastric pepsinogen-synthesizing chief cells.
4 racing that SPEM evolves from differentiated chief cells.
5  least in part, from transdifferentiation of chief cells.
6 xpression is also a specific marker of human chief cells.
7 of SPEM derived from transdifferentiation of chief cells.
8 or cell or by transdifferentiation of mature chief cells.
9  in both mouse pancreatic acinar and gastric chief cells.
10 at SPEM derived from transdifferentiation of chief cells.
11 cally localized to the secretory granules in chief cells.
12 ed potentiation of cAMP levels in guinea pig chief cells.
13 tion of cAMP levels in cholera toxin-treated chief cells.
14  5'-triphosphate-binding protein, in gastric chief cells.
15                         Compared with normal chief cells, 858 genes were differentially expressed in
16  human parathyroids with varying oxyphil and chief cell abundance and leveraged advanced computationa
17       The PLS-DA model built to discriminate chief cell adenoma from oxyphil cell adenoma allowed us
18 6 mouse showed a marked loss of parietal and chief cells, along with a marked expansion of an aberran
19 c factor expression is both predetermined in chief cells and can be expressed in parietal cells in re
20 ferentiation of fundic cell types, including chief cells and functional parietal cells.
21    Under conditions of chronic inflammation, chief cells and mucous neck cells are plastic and conver
22  Moreover, the parathyroid adenoma subtypes (chief cells and oxyphil cells) were characterized by the
23 associated with preservation of parietal and chief cells and protection from the development of gastr
24 t tumors, preparatively isolated oxyphil and chief cells, and laser-captured microdissected PA specim
25 IST1 as a reliable marker of mature, healthy chief cells, and we provide the first evidence that meta
26 s of FK-506 on cholera toxin-treated gastric chief cells are caused by its inhibitory actions on calc
27 are induced, at which point the reprogrammed chief cells are recognized as mucus-secreting spasmolyti
28 rise in part through transdifferentiation of chief cells as opposed to expansion of mucus neck or pro
29 criptional programs in mucous neck cells and chief cells as they progress to metaplasia mice with chr
30 er pylori (H pylori) infection, parietal and chief cell atrophy in the gastric corpus, a process know
31 irmed rab3D immunoreactivity localization to chief cells but not acid-secreting parietal cells.
32  homeostasis, p57 is constantly expressed in chief cells but rapidly diminishes after injury, followe
33 s, giving rise to parietal, mucous neck, and chief cells, but not to enterochromaffin-like-cell.
34                 We conclude that, in gastric chief cells, calcineurin mediates cross-talk between the
35              After acute parietal cell loss, chief cells can reprogram through an orderly stepwise pr
36  of various types with the exception of rare chief cell carcinoma ( approximately 1%).
37 tamoxifen - or merely the depletion of LGR5+ chief cells - caused an upregulation of RSPO3 expression
38 onfirm MIST1 expression is restricted to the chief cell compartment in normal oxyntic mucosa, rare in
39 Atp4a(-/-) stomachs revealed the presence of chief cells, demonstrating that the lack of acid secreti
40 rs not to perturb parietal cell viability or chief cell differentiation.
41 sia and oxyntic atrophy were sustained while chief cell, enterochromaffin-like cell, and somatostatin
42 e, including a profound loss of parietal and chief cells, focal de novo production of acidic mucins,
43               Although mucous neck cells and chief cells from healthy stomachs each had distinct tran
44                         Thus, mature gastric chief cells have the ability to act as cryptic progenito
45 mine whether SPEM lineages were derived from chief cells in 3 independent models of induction by DMP-
46 ted in an overlapping fashion in parathyroid chief cells in adenoma and hyperplastic glands, and also
47  that imposes the reserve stem cell state of chief cells in homeostasis.
48 ar switch for the reserve stem cell state of chief cells in mice.
49    Intrinsic factor is produced primarily by chief cells in rat and mouse, but 4 to 11% of isolated r
50 sulted in a loss of specialized parietal and chief cells in the corpus and the appearance of a metapl
51 rrectly predict 100% of oxyphil and 99.8% of chief cells in the external validation data set.
52 ls or differentiated, post-mitotic zymogenic chief cells in the gland base.
53 been recognized that the secretion of PTH by chief cells in the parathyroid gland is regulated by ext
54  numbers of parietal cells, a loss of mature chief cells, increased numbers of mucous and undifferent
55             In cholera toxin-treated gastric chief cells, incubation with a cholinergic agonist (carb
56 med the convergence of mucous neck cells and chief cells into a pre-metaplastic phenotype that ultima
57  reprogramming of digestive enzyme-secreting chief cells into deep antral gland-like mucous cells.
58 tion of digestive enzyme (zymogen)-secreting chief cells is a normal aspect of stomach function that
59  factor MIST1, normally restricted to mature chief cells, is down-regulated as chief cells undergo ex
60 a in humans arises at least in part from the chief cell lineage.
61 7 and activation of proliferation within the chief cell lineage.
62 5), epithelial differentiation to mucous and chief cell lineages was rudimentary, with no expression
63 -4 scale to score inflammation, parietal and chief cell loss, mucus metaplasia, and helicobacter colo
64 gnaling caused basal cell expansion, gastric chief cell marker expression, and a decrease in surface
65 mber of cells coexpressing intrinsic factor (chief cell marker), YFP (lineage marker), and GSII lecti
66 munoreactive for TFF2 and the differentiated chief cell markers, Mist1 and intrinsic factor, suggesti
67 sion of the activated form of Ras in gastric chief cells of mice leads to the development of SPEM, as
68               Expression of activated Ras in chief cells of Mist1-Kras mice led to the full range of
69 issues such as acinar cells of the pancreas, chief cells of the stomach, and parotid and lacrimal sec
70 ce, which express the active form of Kras in chief cells on tamoxifen exposure.
71 olves through either transdifferentiation of chief cells or activation of a basal cryptic progenitor.
72 d glands, we have isolated and characterized chief cells, oxyphil cells, and tumor-infiltrating lymph
73 COX defects than the mitochondria-poor clear chief cells (P < 0.001).
74 moesin participate in parietal cell acid and chief cell pepsinogen secretion, respectively.
75 gen-mediated apoptosis depletes parietal and chief cell populations, leading to architectural distort
76 mitochondrial energy generation, whereas the chief cell predominantly expresses digestive enzymes and
77             In the main body of the stomach, chief cells produce digestive enzymes; however, upon inj
78        In pyloric metaplasia, mature gastric chief cells reprogram via an evolutionarily conserved pr
79            Pepsinogen secretion from gastric chief cells requires a series of intracellular vesicle i
80                      Taking advantage of the chief cell-restricted expression of Mist1-Cre-ER(T2), we
81 d by altered niche requirements and a mature chief cell/secretory phenotype.
82  the constitutive expression of p57 in vivo, chief cells showed an impaired injury response.
83 sion of myofibroblasts, loss of parietal and chief cells, spasmolytic polypeptide expressing metaplas
84 istribution of the rab3D-like protein in the chief cell suggests that it may play an important role i
85 /+ (Mist1-Kras-mTmG) mice to examine whether chief cells that express active Kras give rise to SPEM a
86 the expansion of AMCase-expressing zymogenic chief cells that facilitate chitin digestion.
87 th adenocarcinoma, we found normal zymogenic chief cells that were transitioning into SPEM cells only
88 osure of monolayers of renal collecting duct chief cells to orbital shaking and quantified the forces
89  to mature chief cells, is down-regulated as chief cells undergo experimentally induced metaplasia.
90 e stomach-the parietal, mucus-producing, and chief cells-were harvested from cryosections of infected
91 tion in the corpus gland toward parietal and chief cells, while its absence promoted pit cell differe
92 etal cells (PCs) and metaplasia of zymogenic chief cells within 3 days.
93                                              Chief cells within bovine parathyroid glands exhibit a s
94 resence of functionally distinct oxyphil and chief cells within parathyroid primary adenomas and prov
95 s produce approximately 50% more PTH than do chief cells, yet display significantly greater PTH suppr
96 of the digestive enzyme secreting zymogenic (chief) cell (ZC).
97          Adult zymogen-producing (zymogenic) chief cells (ZCs) in the mammalian gastric gland base ar
98 zed secretory vesicles in gastric zymogenic (chief) cells (ZCs) as they differentiate from their muco