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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.
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
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
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
39 o selectively disrupt the IL-4Ralpha gene in Clara cells, an airway epithelial cell population that g
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
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
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
62 cells and in Clara cell antigen 10 (CC10)(+) Clara cells by use of cell-type-restricted recombinant A
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
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
72 e embryonic lung; and 4) NEBs harbor variant Clara cells deficient in cytochrome P450 2F2-immunoreact
74 ys using nuclear extracts from MLE-15 murine Clara cell-derived mtCC1-2 cells with probes correspondi
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
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
88 These findings suggest a role for CCSP and Clara cells in regulating lung inflammatory and immune r
91 d PSMCs as a stem cell niche for the variant Clara cells in the lung and established that paracrine F
94 ysis of these mice identifies type II cells, Clara cells in the terminal bronchioles, and putative br
96 cell secretory protein (CCSP), a marker for Clara cells, in lung transplant recipients with BOS, BOS
100 rs growing in wild-type mice and bronchiolar Clara cells isolated from normal mouse lungs, but was un
102 rp2 gene expression in the mouse transformed Clara cell line, mtCC, in a time- and dose-dependent man
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
108 proliferating bronchiolar epithelial cells (Clara cells) may be the initiated sites for pulmonary tu
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
117 Selective restoration of SP-B expression in Clara cells of SP-B -/- mice resulted in respiratory dys
122 body indicated the presence of this mucin in Clara cells of wildtype (WT) control mice, and increased
124 cells and the nonciliated bronchiolar cells (Clara cells) of the lungs; these cells are where JSRV is
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
133 y/Enhancer of Split-1, which is expressed in Clara cell putative ;progenitors' was found to be a down
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.
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
143 n in the proximal airways of the fetus; both Clara cell secretory protein (CCSP) and MUC5AC/5B mRNA a
147 appear engorged and Clara cells accumulated Clara cell secretory protein (CCSP) in Munc13-2-deficien
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.
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
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.
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
173 ice and controls, but increased apoptosis of Clara cell secretory protein-positive airway epithelial
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
181 ggest a role for Notch in the induction of a Clara cell-specific program of gene expression, and reve
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
190 e that conditionally overexpress IL-1beta in Clara cells to determine whether IL-1beta can promote an
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
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