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1 hannels must occur at the apical pole of the parietal cell.
2 ivity of H K -ATPase, the proton pump of the parietal cell.
3 ctive proton pump at the pH of the secreting parietal cell.
4 on during the secretory cycle of the gastric parietal cell.
5 e necessary for active acid secretion by the parietal cell.
6 e associated with the apical membrane of the parietal cell.
7 e for stimulation of acid secretion from the parietal cell.
8 n maintaining the long-term viability of the parietal cell.
9 e mature progeny lineage, the acid-secreting parietal cell.
10 ctivity of HK-ATPase, the proton pump of the parietal cell.
11 culi and by regulating chloride secretion in parietal cells.
12 ovilli due to the loss of ezrin integrity in parietal cells.
13 types, including chief cells and functional parietal cells.
14 itecture, and secretory membrane dynamics in parietal cells.
15 servation of overall tissue architecture and parietal cells.
16 whether gastrin regulates Shh expression in parietal cells.
17 and is thus required to maintain functional parietal cells.
18 er medullary collecting duct and the gastric parietal cells.
19 tric cancer, involves loss of acid-producing parietal cells.
20 e potassium channel (K(ATP)) is expressed in parietal cells.
21 essed on the basolateral membrane of gastric parietal cells.
22 h mediates some of the actions of EGF in the parietal cells.
23 land lumens and a reduction in the number of parietal cells.
24 b gene, in the progenitors of acid-producing parietal cells.
25 cular and tubulovesicular membranes in mouse parietal cells.
26 istributed to the apical membrane of gastric parietal cells.
27 s, IQGAP1 and IQGAP2, are present in gastric parietal cells.
28 ntain the H,K-ATPase in unstimulated gastric parietal cells.
29 activation of polarized secretion in gastric parietal cells.
30 icated functional activity and regulation of parietal cells.
31 erences in the composition of acid-producing parietal cells.
32 rface pit, mucous neck, chief, endocrine and parietal cells.
33 K-ATPase, into the apical plasma membrane of parietal cells.
34 226 inhibited the acid secretory response of parietal cells.
35 r of G cells and a doubling in the number of parietal cells.
36 king ATP4A, a P-type H+/K+ ATPase in gastric parietal cells.
37 mp responsible for acid secretion by gastric parietal cells.
38 as potently induced by carbachol in the same parietal cells.
39 cated on the basolateral membrane of gastric parietal cells.
40 rface pit, mucous neck, chief, endocrine and parietal cells.
41 s cells appear as sequelae of the absence of parietal cells.
42 wofold increase in intrinsic factor-positive parietal cells.
43 ing the percent of intrinsic factor-positive parietal cells.
44 in high doses leads to the specific loss of parietal cells.
45 onfocal microscopy of [Ca(2+)](i) in ECL and parietal cells.
46 ified one such protein in studies of gastric parietal cells.
47 al cDNA sequences from human lung and rabbit parietal cells.
48 ly achlorhydric and have partially activated parietal cells.
49 ic mucus layer, and increased vacuolation of parietal cells.
50 in-like cells and hepcidin in acid-secreting parietal cells.
51 rane remodeling processes typical of gastric parietal cells.
52 astric cancers), where it is concentrated in parietal cells.
53 f the hydrogen/potassium pump in the gastric parietal cells.
54 tributed throughout the cytoplasm of resting parietal cells.
55 ith EHD proteins in the endocytic pathway of parietal cells.
56 ne trafficking and acid secretion in gastric parietal cells.
57 ullary collecting duct (OMCD) and in gastric parietal cells.
58 isolated rabbit gastric glands and cultured parietal cells.
59 lovesicles to the apical membrane of gastric parietal cells.
60 ion of ezrin from the apical membrane of the parietal cells.
61 ooxygenase-2 and hence prostaglandins within parietal cells, a feedback pathway that may protect the
62 - mice, including sharply reduced numbers of parietal cells, a loss of mature chief cells, increased
66 tal proteins ezrin and moesin participate in parietal cell acid and chief cell pepsinogen secretion,
68 d.Myr-Akt failed to induce changes in either parietal cell actin content, measured by Western blots w
74 sociated with tubulovesicle membranes in the parietal cell and Rab27b may play a role in stimulation-
75 ficance of SNAP-25 as a SNARE protein in the parietal cell and show the dynamic stimulation-associate
76 nd macrophages from the lung and in Bowman's parietal cells and convoluted proximal tubules from the
77 receptor gene, leads to decreased numbers of parietal cells and decreased gastric acid secretion.
78 K-ATPase beta-subunit and CD63 colocalize in parietal cells and form a complex that can be coprecipit
79 membrane of the cortical collecting duct and parietal cells and functions as a coupled Cl(-)/HCO(3)(-
80 gs demonstrate the important roles played by parietal cells and glycan receptors in determining the p
81 s, interacts with muscarinic M3 receptors on parietal cells and has little, if any, effect on histami
83 ation, the differentiation of acid-producing parietal cells and histamine-secreting enterochromaffin-
84 protein fusion construct of pp66 in cultured parietal cells and in Madin-Darby canine kidney cells in
85 part by diminished numbers of acid-producing parietal cells and increased risk for development of gas
89 ct and striking absence of tubulovesicles in parietal cells and reductions in the numbers of parietal
90 ivo, as demonstrated by extensive changes to parietal cells and the gastric epithelium in Hip1r-defic
92 turbations in the secretory membranes of the parietal cell, and metaplasia of the gastric mucosa; how
93 Pase characteristic of the mammalian gastric parietal cell, and the molecular mechanisms of acid gene
94 y ranitidine, showing the absence of PAC1 on parietal cells, and demonstrating functional coupling be
95 lands, cystic structures, reduced numbers of parietal cells, and increased numbers of cells that coex
99 of B cells stimulates the production of anti-parietal cell antibodies, the serological hallmark of AI
101 ng a transgenic TCR specific for the gastric parietal cell antigen, H(+)K(+)-ATPase, to induce autoim
103 intrahepatic cholangiocytes, AQP4 in gastric parietal cells, AQP3 and AQP4 in colonic surface epithel
104 e main stimulants of acid secretion from the parietal cell are histamine, gastrin, and acetylcholine.
106 ngaged in active acid secretion, many of the parietal cells are in various stages of degeneration.
108 nclusions, some of the actions of EGF in the parietal cells are mediated by the sequential activation
111 minopyrine accumulation into isolated rabbit parietal cells, as well as by assessment of DMP 777 effe
113 /- mice, hypochlorhydric G-/- mice developed parietal cell atrophy, significant antral inflammation a
114 le autoantibody, mitochondrial autoantibody, parietal cell autoantibody, and thyroid microsomal autoa
115 E2 is not required for acid secretion by the parietal cell, but is essential for its long-term viabil
117 IL-1beta suppresses Shh gene expression in parietal cells by inhibiting acid secretion and subseque
119 AKAP120 was identified from a rabbit gastric parietal cell cDNA library; however, a monoclonal antibo
120 itopes shared by bacteria and acid-secreting parietal cells, chronic gastritis, and parietal cell los
123 he second-messenger systems activated in the parietal cell converge on H K -ATPase that catalyzes the
129 cultured cells, and localization studies in parietal cells detected its presence in tubulovesicles.
131 mice by expression of noggin causes loss of parietal cells, development of transitional cells that e
134 These pathways regulate the acid-producing parietal cell directly and/or indirectly by regulating t
135 m enterochromaffin-like cells stimulates the parietal cell directly via H-2 receptors coupled to gene
136 ine, released from ECL cells, stimulates the parietal cell directly via H2 receptors and indirectly v
137 anglionic intramural neurons, stimulates the parietal cell directly via M-3 receptors coupled to intr
138 anglionic intramural neurons, stimulates the parietal cell directly via muscarinic M3 receptors and i
141 umulates in the secretory canaliculus of the parietal cell due to pyridine protonation then binds to
142 c mucosa was grossly transformed, with fewer parietal cells due to enhanced apoptotic cell death and
143 ged Notch activation within dedifferentiated parietal cells eventually enhances cell proliferation an
151 gate the hypothesis that AE2 is critical for parietal cell function and to assess its importance in o
152 h factor (EGF) family, which in turn inhibit parietal cell function but stimulate the growth of surfa
153 r stimulatory pathways for acid secretion in parietal cells, gastrin, histamine, and acetylcholine, h
156 2) and eliminated by omeprazole, implicating parietal cell H,K-ATPase as the dominant regulator of su
158 secreting cells similar to mammalian gastric parietal cells has been identified by a unique ultrastru
160 Induced differentiation of acid-secreting parietal cells in hFGOs requires temporal treatment of B
164 mined in chief cells and can be expressed in parietal cells in response to local inflammatory factors
165 se exclusively on the apical pole of gastric parietal cells in Slc26a9(-/-) mice, in contrast to the
166 urface epithelial cells as well as chief and parietal cells in the fundic glands of normal gastric mu
169 nsic factor in 8.9 +/- 3.8% (mean +/- SD) of parietal cells; in inflamed areas of transgenic rats 21
170 eeks of infection, intrinsic factor-positive parietal cells increased from 7.8 +/- 2.8% in the congen
172 canaliculi formation observed in Trpml1(-/-) parietal cells indicate that Trpml1 functions in the for
173 ase in intracellular calcium, stimulates the parietal cell indirectly by activating histidine decarbo
174 c, transgenic overexpression of ML1 in mouse parietal cells induced constitutive acid secretion.
175 that moves protons from the cytoplasm of the parietal cell into the gastric lumen in exchange for pot
185 adenosine triphosphatase (ATPase) of gastric parietal cells is targeted to a regulated membrane compa
188 characterized by the destruction of gastric parietal cells, leading to the loss of intrinsic factor
189 formed a yeast two-hybrid screen of a rabbit parietal cell library with a 3.2-kb segment of AKAP350 (
190 ait in a yeast two-hybrid screen of a rabbit parietal cell library, we have identified a novel AKAP35
192 on, histopathological alterations, including parietal cell loss and gastric atrophy, were noted.
193 obacter infection and contribute to eventual parietal cell loss and progression to gastric cancer.
196 obiotic mouse models of ChAG have shown that parietal cell loss results in amplification of multi- an
197 essing metaplasia with DMP-777-induced acute parietal cell loss revealed that this metaplastic phenot
198 ith Helicobacter felis or induction of acute parietal cell loss with the drug DMP-777 leads to the em
199 ute injury, acute inflammation, or transient parietal cell loss within the stomach do not lead to BMD
200 ed with severe gastric mucosal inflammation, parietal cell loss, atrophy, and metaplastic cell change
201 c inflammation, higher gastric pH, increased parietal cell loss, increased gastric expression of inte
202 t of mice with L-635 for 3 days led to rapid parietal cell loss, induction of a prominent inflammator
203 bit severe mucosal and muscular hypertrophy, parietal cell loss, mucinous epithelial cell metaplasia,
204 Gastric cancer develops in the context of parietal cell loss, spasmolytic polypeptide-expressing m
207 nst human intrinsic factor and H/K ATPase (a parietal cell marker), counting the percent of intrinsic
208 a regression of inflammation, restoration of parietal cell mass, and reestablishment of normal archit
210 e apical pole of other epithelial cells, the parietal cell may represent a model system to characteri
211 sion, repopulation of the glomerular tuft by parietal cells may represent a compensatory response to
212 After extensive podocyte loss, activated parietal cells mediated tuft re-epithelialization by two
213 ced parietal cell proton secretion, abnormal parietal cell morphology, achlorhydria, hypergastrinemia
214 anced proliferation and marginally increased parietal cell mucous metaplasia with oxyntic atrophy.
218 aximal gastric acid secretion, and increased parietal cell number but later progressed to decreased p
219 pus and antrum and a multifocal reduction in parietal cell numbers in the proximal corpus, resulting
220 ocalized miR-324-3p to glomerular podocytes, parietal cells of Bowman's capsule, and most abundantly,
224 year was associated with the reappearance of parietal cells, partial regression of inflammation, and
228 HC class II molecule presentation of gastric parietal cell (PC)-specific H(+)/K(+)-ATPase, which indu
229 c transporter 8, thyroid peroxidase, gastric parietal cells (PCAs), tissue transglutaminase, and 21-h
230 en leads to apoptosis of >90% of all gastric parietal cells (PCs) and metaplasia of zymogenic chief c
234 reroutes the Kcnq1 alpha subunit in vivo in parietal cells (PCs), in which the normally apical locat
236 functional consequences of VacA infection on parietal cell physiology were studied using freshly isol
238 Hip1r is abundantly expressed in the gastric parietal cell, predominantly localizing with F-actin to
241 was associated with transdifferentiation of parietal cell progenitors to a neuroendocrine phenotype,
242 (2) identification of H(+)K(+)-ATPase as the parietal cell proton pump and development of proton pump
243 re gastric phenotype with profoundly reduced parietal cell proton secretion, abnormal parietal cell m
244 ation of parietal cells to show that loss of parietal cells provides an opportunity for a H. pylori i
245 aling with Ca(2+)-dependent TV exocytosis in parietal cells, providing a regulatory mechanism that co
246 primary influence of ACh is directly on the parietal cell receptors rather then the ECL cell recepto
249 n, there was a twofold increase in activated parietal cells resulting in a twofold increase in basal
251 s of expression of Sonic Hedgehog (Shh) from parietal cells results in hypergastrinemia in mice, acco
252 the stomachs of adult mice, loss of Shh from parietal cells results in hypochlorhydria and hypergastr
254 s of superfused gastric glands, but only the parietal cell signal was inhibited by ranitidine, showin
258 hibited aminopyrine accumulation into rabbit parietal cells stimulated with either histamine or forsk
259 of AE2(-/-) gastric mucosa revealed abnormal parietal cell structure, with severely impaired developm
260 ch of the evidence discussed here comes from parietal cell studies, other physiological transport sys
261 mbranes and loss of tubulovesicles in mutant parietal cells, suggesting that Hip1r is necessary for t
262 inlike cells, interacts with H2 receptors on parietal cells that are coupled via separate G proteins
263 Thus, EGF induces a cascade of events in the parietal cells that results in the activation of Akt.
264 ave demonstrated that it is localized to the parietal cell, the acid secretory cell of the gastric gl
265 ocalize initially to the precursor secondary parietal cells then predominantly to daughter tapetal ce
267 expression of a sulfonylurea receptor in the parietal cell, thus further implicating CFTR as the ATP-
268 c mouse model with an engineered ablation of parietal cells to show that loss of parietal cells provi
269 oenriched with Rab11a and H(+)K(+)-ATPase on parietal cell tubulovesicles, and Rab11-FIP1 and Rab11-F
271 w fluorescent protein (YFP) and expressed in parietal cells using adenoviral constructs to study loca
273 e procedure), lymph node primary gastrinoma, parietal cell vagotomy, reoperation and surgery for meta
274 ound in tubular epithelial cells, glomerular parietal cells, vessel walls and some infiltrating cells
275 e absence of the pump appears not to perturb parietal cell viability or chief cell differentiation.
280 nit gene, which is specifically expressed in parietal cells, was used to regulate expression of noggi
281 which is expressed in mucous, zymogenic, and parietal cells, we prepared mice with a null mutation in
282 he stomach and preventing the destruction of parietal cells, we show that iTregs secrete numerous che
283 i) release also stimulates acid secretion in parietal cells, we showed that gadolinium-, thapsigargin
285 l1 and its role in acid secretion by gastric parietal cells were analyzed using biochemical, histolog
286 tructural analyses revealed that Trpml1(-/-) parietal cells were enlarged, had multivesicular and mul
291 c epithelia, AE2 is particularly abundant in parietal cells, where it may be the predominant mechanis
292 2 is polarized to the apical membrane of the parietal cells, whereas IQGAP1 is mainly distributed to
293 noncentrosomal pools of AKAP350, especially parietal cells, which contained multiple cytosolic immun
295 reported that incubation of purified canine parietal cells with epidermal growth factor (EGF) for 6-
300 id secretory dynamics were altered in mutant parietal cells, with enhanced activation and acid trappi