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1 t is detected in bronchial epithelial cells (Clara cells).
2 of nonciliated respiratory epithelial cells (Clara cells).
3 of an abundant airway progenitor such as the Clara cell.
4 1 cells, a cell line with characteristics of Clara cells.
5 P-D were expressed in both type II cells and Clara cells.
6 irway branch points and gave rise to nascent Clara cells.
7 d CC-10 expression of mRNA was restricted to Clara cells.
8 ep, originating from type II pneumocytes and Clara cells.
9 dyloxobutylating species are concentrated in Clara cells.
10 1 cells, a cell line with characteristics of Clara cells.
11 critical for differentiation and function of Clara cells.
12 the distribution and function of bronchiolar Clara cells.
13 in Foxm1-deficient airways were derived from Clara cells.
14 y hyperplasia and increased proliferation of Clara cells.
15 pe, and fewer basal stem cells, ciliated and Clara cells.
16  hyperplasias were primarily made of CC10(+) Clara cells.
17 from less complete processing in bronchiolar Clara cells.
18 so secreted tonically from human bronchiolar Clara cells.
19 cells or nonciliated bronchiolar epithelial (Clara) cells.
20  cell proliferation mainly confined to Club (Clara) cells.
21 by a circadian clock within epithelial club (Clara) cells.
22 he murine IL-9 cDNA was regulated by the rat Clara cell 10 protein promoter.
23 urine cDNA for IL-4 was regulated by the rat Clara cell 10 protein promoter.
24                                  We used the clara cell 10-kD protein (CC10) promoter and the reverse
25 define its potential effector functions, the Clara cell 10-kD protein promoter was used to express IL
26 ssociated with drastically reduced levels of Clara cell 10-kDa protein (CC10), a multifunctional secr
27 mily that includes rabbit uteroglobin, human Clara Cell 10-kDa protein (CC10), and the multimeric rat
28 D39 under the control of the airway-specific Clara cell 10-kDa protein gene promoter.
29 ts potential in vivo effector functions, the Clara cell 10-kDa protein promoter was used to express I
30 kidney capsules self-organized into distinct Clara cell 10-kDa secretory protein (CC10+) airway-like
31 ic steroid-binding protein subunit C3, human Clara cell 10-kilodalton protein, and rabbit uteroglobin
32                                      Urinary Clara Cell 16 (CC16) and 15-isoprostane F2t (8-iso-PGF2a
33  fixed tissue, and urinary biomarkers (KIM-1/clara cell 16) assessed tubular cell structure and funct
34 C treatment decreased O6-mG levels by 52% in Clara cells, 19% in Type II cells and small cells, and 3
35 reased pyridyloxobutyl DNA adducts by 57% in Clara cells, 51% in Type II cells, 40% in small cells, a
36 elial regeneration after naphthalene-induced Clara cell ablation occurred preferentially at airway br
37  several mucosal tissues appear engorged and Clara cells accumulated Clara cell secretory protein (CC
38                                              Clara cells also function as stem/progenitor cells for r
39 o selectively disrupt the IL-4Ralpha gene in Clara cells, an airway epithelial cell population that g
40                            A 75% decrease in Clara cells and a 25% decrease in ciliated cells were co
41 ll population that maintains the bronchiolar Clara cells and alveolar cells of the distal lung and th
42 he collagen-like domain (DeltaG8-P80) in the Clara cells and alveolar type II cells of SP-A(-/-) mice
43 llowing lung injury, PNECs can contribute to Clara cells and ciliated cells.
44 Deletion of Foxm1 inhibited proliferation of Clara cells and disrupted the normal patterning of epith
45 of native epithelial Na(+) channels in human Clara cells and human alphabetagammadelta ENaCs expresse
46 CCSP) is specifically expressed in pulmonary Clara cells and is widely used as a Clara cell marker.
47 eration of the airway epithelium: 1) nascent Clara cells and NEBs localize to the same spatial domain
48 zation, perhaps by facilitating migration of Clara cells and other bronchiolar cells into the regions
49 ry nonciliated bronchiolar epithelial cells (Clara cells) and alveolar type II (AT II) epithelial cel
50  mucin synthesis is massively upregulated in Clara cells, and stored mucin granules come to dominate
51 tein C (SPC)(+) alveolar type 2 cells and in Clara cell antigen 10 (CC10)(+) Clara cells by use of ce
52 ithelial cells, including ciliated cells and Clara cells, appears to be unaffected.
53                                              Clara cells are also known as progenitor or stem cells d
54                                              Clara cells are non-ciliated, secretory bronchiolar epit
55                                              Clara cells are primary targets for metabolically activa
56  that direct effects of IL-4 and/or IL-13 on Clara cells are required for allergen-induced mucus prod
57 iliated secretory epithelial cells, known as Clara cells, as the progenitors of goblet cells induced
58 ted proteins A (SP-A), SP-B, SP-C, and SP-D; Clara cell-associated protein CC-10; and thyroid transcr
59  shows normal differentiation of bronchiolar Clara cells but a reduction in the number of differentia
60 d us to explore the possibility of enriching Clara cells by flow cytometry.
61 nthetase (gamma-GCS) was induced in tolerant Clara cells by repeated exposures to NA.
62 cells and in Clara cell antigen 10 (CC10)(+) Clara cells by use of cell-type-restricted recombinant A
63 function in vivo and that SP-B expression in Clara cells cannot substitute for this function.
64 asm of alveolar epithelial type II (ATII) or Clara cells caused by a type D/B chimeric retrovirus, ja
65  Furthermore, in vivo expression of SPDEF in Clara cells caused rapid and reversible goblet cell diff
66 ditional Cre-recombinase expression from the Clara cell (CC10) promoter.
67 ly-appropriate airway epithelial cell types, Clara cells, ciliated cells and basal cells, and activat
68 ation, and significantly decreased levels of Clara cells, Clara cell secretory protein, and surfactan
69  Pyridyloxobutyl DNA adducts were highest in Clara cells compared to alveolar Type II cells, alveolar
70           Conditional deletion of Foxm1 from Clara cells, controlled by the Scgb1a1 promoter, dramati
71                    Repeated exposures to the Clara cell cytotoxicant naphthalene (NA) result in targe
72 e embryonic lung; and 4) NEBs harbor variant Clara cells deficient in cytochrome P450 2F2-immunoreact
73 ing to renewal of terminal bronchioles after Clara cell depletion.
74 ys using nuclear extracts from MLE-15 murine Clara cell-derived mtCC1-2 cells with probes correspondi
75 Clara cell marker expression indicating that Clara cell development is also affected.
76                            The mechanisms of Clara cell differentiation are largely unknown.
77                      Absence of Alk5 blocked Clara cell differentiation but had no effect on ciliated
78 ling pathway by which TGFbeta/ALK5 regulates Clara cell differentiation may entail inhibition of Pten
79 tion of NA tolerance does not markedly alter Clara cell differentiation, epithelial organization, or
80 ased apoptosis of alveolar type II cells and Clara cells, disrupted alveolar development, decreased v
81           Many bronchiolized cells displayed Clara cell features by electron microscopy.
82 ucture and internal organelle composition in Clara cells from tolerant mice were similar compared to
83  who subsequently developed BPD suggest that Clara cell function and CCSP expression may be critical
84 ithelial repair, whereas c-Myc ablation from Clara cells has no effect on airway epithelial regenerat
85 ng alveolar type 2 cells and CC10-expressing Clara cells have the ability to initiate malignant trans
86 th Scgb1a1 promoter was sufficient to induce Clara cell hyperplasia.
87 nd/or function of the secretory apparatus in Clara cells in mouse lung.
88   These findings suggest a role for CCSP and Clara cells in regulating lung inflammatory and immune r
89 od for investigating the function of primary Clara cells in stem cell research and mouse models.
90                          From E18.5 to PN20, Clara cells in the bronchiolar epithelium co-expressed C
91 d PSMCs as a stem cell niche for the variant Clara cells in the lung and established that paracrine F
92 olar type II cells, alveolar macrophages and Clara cells in the lung.
93 otein are restricted to alveolar Type II and Clara cells in the respiratory epithelium.
94 ysis of these mice identifies type II cells, Clara cells in the terminal bronchioles, and putative br
95 ient to cause goblet cell differentiation of Clara cells in vivo.
96  cell secretory protein (CCSP), a marker for Clara cells, in lung transplant recipients with BOS, BOS
97 that regulate bronchiolar regeneration after Clara cell injury are not known.
98 nt in up-regulating cell proliferation after Clara cell injury in the mouse.
99 ntal pollutant naphthalene to induce massive Clara cell injury.
100 rs growing in wild-type mice and bronchiolar Clara cells isolated from normal mouse lungs, but was un
101                                              Clara cell isolation by flow cytometry sorting is a usef
102 rp2 gene expression in the mouse transformed Clara cell line, mtCC, in a time- and dose-dependent man
103 arkers MUC1 and surfactant protein-A and the Clara cell lineage marker CC10, also occurred.
104 tion in NCI-H441 cells, a human cell line of Clara cell lineage.
105 clear factor/forkhead homologue 4 (Hfh4) and Clara cell marker CC10, and the distal marker Sp-C.
106 oximal lung, E2f4 loss causes a reduction in Clara cell marker expression indicating that Clara cell
107 ulmonary Clara cells and is widely used as a Clara cell marker.
108  proliferating bronchiolar epithelial cells (Clara cells) may be the initiated sites for pulmonary tu
109 ansgenic lines which expressed human SP-B in Clara cells (mCCSP/hSP-B).
110 ucous cell numbers was primarily a result of Clara cell metaplasia.
111 l lines derived from type II pneumocytes and Clara cells (MLE-15 and mtCC1-2 mouse cell lines).
112 lated, baseline secretory pathway, such that Clara cell Muc5b, normally secreted soon after synthesis
113 e testes, Paneth cell of the intestines, and Clara cell of the airway protect surrounding parenchymal
114  small airways and likely interacts with the Clara cells of bronchioles.
115  (W82219) whose expression is induced within Clara cells of CCSP knockout mice.
116                                              Clara cells of mammalian airways have multiple functions
117  Selective restoration of SP-B expression in Clara cells of SP-B -/- mice resulted in respiratory dys
118 selectively express SP-B in Type II cells or Clara cells of SP-B -/- mice.
119 was selectively restored in Type II cells or Clara cells of SP-B -/- mice.
120 eep that arises from type II pneumocytes and Clara cells of the lung epithelium.
121                 COX-2 protein was present in Clara cells of wild-type and COX-1(-/-) terminal bronchi
122 body indicated the presence of this mucin in Clara cells of wildtype (WT) control mice, and increased
123 lial cells and bronchiolar epithelial cells (Clara cells) of adult lung.
124 cells and the nonciliated bronchiolar cells (Clara cells) of the lungs; these cells are where JSRV is
125                                              Clara cell pathophysiology was evident from decreased cy
126 onal cloning of a novel protein required for Clara cell physiology in mouse lung development.
127                         The highly secretory Clara cells play a pivotal role in protecting the lung a
128 cation and if diversity is established among Clara cell precursors.
129 ess the SV40 large T antigen (TAg) under the Clara cell promoter, develop bilateral, multifocal, and
130 -1, CXCL8 mRNA, sputum neutrophils and serum Clara cell protein-16 (CC-16) were significantly higher
131 a concentrations of surfactant protein A and Clara cell protein.
132                                        Club (Clara) cell protein 16 (CC-16) is a protein that is synt
133 y/Enhancer of Split-1, which is expressed in Clara cell putative ;progenitors' was found to be a down
134 tion of PNECs has no apparent consequence on Clara cell recovery.
135 reduced potential for bronchiolar stem-cell (Clara cell)-related repair in the setting of an ever-pre
136  alveolar epithelial cells (Aqp5 and Sftpc), Clara cells (Scgb1a1) and ciliated cells (Foxj1) in E18.
137                                              Clara cell secretory protein (CC10) is a steroid-inducib
138 erating a conditional mutant mouse with both Clara cell secretory protein (CC10)-Cre recombinase and
139   GWAS was performed for two pneumoproteins, Clara cell secretory protein (CC16) and surfactant prote
140                                              Clara cell secretory protein (CC16) is associated with T
141 edly expressed in lung epithelial cells [via Clara cell secretory protein (CCSP(cre))].
142                                              Clara cell secretory protein (CCSP) and interleukin 8 le
143 n in the proximal airways of the fetus; both Clara cell secretory protein (CCSP) and MUC5AC/5B mRNA a
144 the human surfactant protein-C (SP-C) or rat Clara cell secretory protein (ccsp) genes.
145                                              Clara cell secretory protein (CCSP) has been shown to ha
146                                          The Clara cell secretory protein (CCSP) imparts a protective
147  appear engorged and Clara cells accumulated Clara cell secretory protein (CCSP) in Munc13-2-deficien
148                                              Clara cell secretory protein (CCSP) is expressed abundan
149                                              Clara cell secretory protein (CCSP) is specifically expr
150 e growth factor (NGF) from the lung-specific Clara cell secretory protein (CCSP) promoter exhibit hyp
151 activity of a protein that was identified as Clara cell secretory protein (CCSP) was observed more co
152 protein and lung fluid protein expression of Clara cell secretory protein (CCSP), a marker for Clara
153 en-1 (SSEA-1), the alveolar stem cell marker Clara cell secretory protein (Ccsp), and the epithelial
154 vious studies identified pollutant-resistant Clara cell secretory protein (CCSP)-expressing stem cell
155 by pronuclear microinjection, were bred with Clara cell secretory protein (CCSP)-rtTA activator mice.
156             These studies used bi-transgenic Clara cell secretory protein (CCSP)/IL-1beta mice that c
157 s in the bronchiolar epithelium co-expressed Clara cell secretory protein and alpha(7).
158 des cells that are dually immunopositive for Clara cell secretory protein and calcitonin gene-related
159  in the bronchiolar epithelium including the clara cell secretory protein gene and the HNF-3alpha gen
160 ary epithelium, the surfactant protein A and Clara cell secretory protein genes, serve as useful para
161 ry epithelial cells under the control of the Clara cell secretory protein promoter (CCSP-IL-4 mice) w
162 potentiates expression of the HNF-3alpha and clara cell secretory protein promoter regions.
163 oglobin epitope tag under the control of the Clara cell secretory protein promoter, which largely lim
164 factant protein B, surfactant protein C, the Clara cell secretory protein, and Foxj1, was inhibited.
165 the differentiation markers beta-tubulin-IV, Clara cell secretory protein, and Foxj1.
166 gnificantly decreased levels of Clara cells, Clara cell secretory protein, and surfactant proteins B
167 However, surfactant proteins SP-B, SP-C, and Clara cell secretory protein, normally produced by nonci
168 the same spatial domain; 2) within NEB, both Clara cell secretory protein- and calcitonin gene-relate
169 8, surfactant protein D, C-reactive protein, Clara cell secretory protein-16, IL-6 and -8, and tumor
170    We previously defined a critical role for Clara cell secretory protein-expressing (CE) cells in re
171 se model with inducible expression of p52 in Clara cell secretory protein-expressing airway epithelia
172                                         When Clara cell secretory protein-membrane hen egg lysozyme/h
173 ice and controls, but increased apoptosis of Clara cell secretory protein-positive airway epithelial
174             Administration of doxycycline to Clara cell secretory protein-reverse tetracycline-contro
175 get genes including surfactant protein C and Clara cell secretory protein.
176 m including pulmonary surfactant A, B, C and Clara cell secretory protein.
177 fferentiation, assessed by the expression of Clara cell secretory protein2 and pro-SP-C, was inhibite
178 ext applied the KP(Het)C model, in which the Clara cell-specific CCSP-driven Cre activates KRASG12D a
179                                              Clara cell-specific IL-4Ralpha-deficient mice and contro
180         However, compared with control mice, Clara cell-specific IL-4Ralpha-deficient mice were nearl
181 ggest a role for Notch in the induction of a Clara cell-specific program of gene expression, and reve
182 kground expressing KC under the control of a Clara cell-specific promoter within the lung.
183 expression of peripheral epithelial markers (Clara cell-specific protein, surfactant protein C, and a
184 se cells, it is unclear how Notch influences Clara cell specification and if diversity is established
185 involve preferential injury to the secretory Clara cells that function in innate defense and epitheli
186 s essential for activating surviving variant Clara cells (the cells in the airway epithelium from whi
187 pressed by alveolar type II (ATII) cells and Clara cells, the primary producers of pulmonary surfacta
188                                   Similarly, Clara cells, the primary secretory cell in the mouse air
189                                           In Clara cells, the relative lack of staining for mucosubst
190 e that conditionally overexpress IL-1beta in Clara cells to determine whether IL-1beta can promote an
191                                              Clara cells, together with ciliated and pulmonary neuroe
192                                    Extent of Clara cell toxicity and exfoliation was identical in the
193 e numbers, Muc5ac and Muc5b mRNA levels, and Clara cell ultrastructure (except for increased secretor
194 lands, the finding that Muc5b is secreted by Clara cells under control conditions may indicate that i
195 od for the isolation of CCSP-expressing cell Clara cells using a combination of mechanical and enzyma
196 s, and some were pulmonary epithelial cells (Clara cells), vascular endothelial cells, and smooth mus
197 veolar type II cells were SP-A-positive, and Clara cells were negative by immunohistochemistry in hTG
198         Electron microscopy illustrated that Clara cells were undergoing metaplasia to mucous cells.
199 induce Snai1 expression in surviving variant Clara cells, which subsequently underwent a transient ep
200 ype characterized by an absence of secretory Clara cells without evidence of cell death, and showed a

 
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