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1 dulate TGF beta-induced IL-8 secretion in CF bronchial epithelia.
2 tr(F508/F508) immortalized and primary human bronchial epithelia.
3 onal expression at the apical PM in human CF bronchial epithelia.
4 focus of the resulting viral infection is in bronchial epithelia.
5 ffects in the mucociliary differentiation of bronchial epithelia.
6 nel in primary CFTRDeltaF508/DeltaF508 human bronchial epithelia.
7 a level 16% of that observed in normal human bronchial epithelia.
8 eration of differentiated human tracheal and bronchial epithelia.
9 K293T cells and in well-differentiated human bronchial epithelia.
10 cells or primary cultures of F508/F508 human bronchial epithelia.
11 Ca(2+)(i) signals in CF compared with normal bronchial epithelia, a response that reflects endoplasmi
12 differentiated primary cultures of tracheal/bronchial epithelia and found that transepithelial condu
13 not increased in these cultured CF tracheal/bronchial epithelia and point to loss of anion transport
14 sites were significantly increased in normal bronchial epithelia and tumor cells derived from p18(-/-
16 clearly demonstrated OPN3 expression in lung bronchial epithelia as well as immune cells, while CHML
17 DeltaF508-CFTR in DeltaF508/DeltaF508 human bronchial epithelia but did not correct a different temp
18 ance tRNA that is particularly rare in human bronchial epithelia, but not in other human tissues, sug
21 ell-differentiated primary cultures of human bronchial epithelia grown at an air-liquid interface.
22 s of primary human nasal epithelia and human bronchial epithelia have established many of the biophys
23 creased Cl(-) secretion in cultured human CF bronchial epithelia (HBE) carrying the G551D gating muta
24 s-treated) normal, and cystic fibrosis human bronchial epithelia (HBE), and a proliferating, single-c
27 ion transport in newborn nasal and tracheal/bronchial epithelia in tissues, cultures, and in vivo.
28 apeutically targeting either TLR2 or IL17 in bronchial epithelia, in the context of morphine, can res
29 30-40-day-old) primary cultures of DeltaF508 bronchial epithelia, indicating this response was indepe
30 xcision repair (NER) pathway in normal human bronchial epithelia (NHBE) and lung fibroblasts (NHLF).
31 first time the stressed mitochondria in the bronchial epithelia of high-fat- or high-fructose-fed mi
33 (6-11-day-old) primary cultures of DeltaF508 bronchial epithelia was lost in long-term (30-40-day-old
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