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1 or of cytokine signaling-3, lipocalin-2, and alpha1-antichymotrypsin.
2 inhibitors, alpha1-proteinase inhibitor and alpha1-antichymotrypsin.
3 s with raised concentrations (16% higher for alpha1-antichymotrypsin, 18% for alpha1-acid-glycoprotei
4 n to TIGR/MYOC, a serine protease inhibitor (alpha1-antichymotrypsin), a neuroprotective factor (pigm
5 athepsin G can also be completely blocked by alpha1 antichymotrypsin, a specific inhibitor of chymotr
7 Inhibition of human chymase by the serpins alpha1-antichymotrypsin (ACT) and alpha1-proteinase inhi
8 se (AD) based on immunochemical detection of alpha1-antichymotrypsin (ACT) in amyloid plaques from th
9 omosome 14q32.1 allow a single gene encoding alpha1-antichymotrypsin (ACT) to be expressed in astrocy
11 nd/or that are known to interact with Abeta: alpha1-antichymotrypsin (ACT), interleukin-1beta (IL-1be
12 nes on chromosome 14, presenilin 1 (PS1) and alpha1-antichymotrypsin (ACT), with the risk of sporadic
13 in the liver, including alpha1-antitrypsin, alpha1-antichymotrypsin, alpha-fetal protein, ceruloplas
14 g the pH dependence of the conversion of the alpha1-antichymotrypsin.alpha-chymotrypsin encounter com
16 idly bound by protease inhibitors, primarily alpha1-antichymotrypsin, although a fraction is inactiva
17 main protects cathepsin G from inhibition by alpha1-antichymotrypsin and squamous cell carcinoma anti
18 nase inhibitors alpha1-proteinase inhibitor, alpha1-antichymotrypsin, and alpha2-macroglobulin functi
19 ons (ie, cyclin D3, tissue transglutaminase, alpha1-antichymotrypsin, and STAT1), which have not prev
20 eact strongly for desmin, alphaB-crystallin, alpha1-antichymotrypsin, and ubiquitin and variably for
21 orescent derivatives of cysteine variants of alpha1-antichymotrypsin at the P11 and P13 residues.
22 te-phase proteins (alpha1-acid-glycoprotein, alpha1-antichymotrypsin, C-reactive protein, or serum am
23 tion of prostate specific antigen (PSA), PSA-alpha1-antichymotrypsin, carcinoembryonic antigen and mu
24 prothrombin, beta amyloid precursor protein, alpha1-antichymotrypsin, cystic fibrosis transmembrane c
25 hymotrypsin with a fluorescent derivative of alpha1-antichymotrypsin (derivatized at position P7 of t
28 t mice given cathepsin G/chymase inhibitors (alpha1-antichymotrypsin or Z-Gly-Leu-Phe-CH(2)Cl), were
29 f E*I* formation from alpha-chymotrypsin and alpha1-antichymotrypsin using two approaches: first, by
31 tio to Abeta of another acute phase protein, alpha1-antichymotrypsin, was not active in preventing fi
32 zyme also is inactivated more effectively by alpha1-antichymotrypsin, which features P1 Leu in the re
33 2A and other isoforms of endopins related to alpha1-antichymotrypsin, yet endopin 2C differs in its t
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