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1 s the type I pneumocyte markers, T1alpha and aquaporin-5.
2 secretion accompanied by down-regulation of aquaporin 5 and an increase in anti-M3R autoantibodies.
4 yzed by Western blotting for the presence of aquaporin 5 (AQP5) and 120-kDa fragments of alpha-fodrin
7 nocked-in Cre recombinase through control of aquaporin 5 (Aqp5) promoter/enhancer (Aqp5-Cre) allows u
9 st, expression of TMEM16A, the water channel aquaporin 5 (AQP5), and other regulators of sweat gland
10 sport, we asked whether targeted deletion of Aquaporin 5 (AQP5), the major transcellular water transp
12 hese changes lead to a selective decrease in aquaporin-5 (AQP5) abundance because of protein internal
13 submucosal glands, where fluid secretion is aquaporin-5 (AQP5) dependent, we postulated that aquapor
19 orphology and decreased expression of TTF-1, aquaporin-5 (AQP5), zonula occludens-1 (ZO-1), and cytok
22 ecently identified by us (CD44, CD24, EpCAM, aquaporin 5, claudin-4, secretin receptor, claudin-7, V-
23 ed with decreased expression of T1-alpha and aquaporin 5, consistent with a delay of type I cell diff
25 mma markedly improved salivary secretion and aquaporin 5 expression in anti-PD-L1-treated NOD/ShiLtJ
29 hese mice showed an atypical distribution of aquaporin 5 in their salivary glands, suggesting likely
30 novirus (AdrAQP5) mediated the expression of aquaporin-5 in rat and human salivary cell lines and in
32 tenuated type I cells, and reduced levels of aquaporin-5 mRNA and protein, a type I cell water channe
35 carinic Acetylcholine receptor M3) and AQP5 (Aquaporin 5) protein expression, b) decreased saliva sec
38 ot protein kinase C or casein kinase II, and aquaporin-5 was phosphorylated in cultured cells after l
39 expression of both surfactant protein-C and aquaporin-5 were inhibited in cultured TACE-mutant embry
40 nt receptor potential vanalloid 4) and AQP5 (aquaporin 5), which is required for regulating water per
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