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1 e synthesis of N-butyryl homoserine lactone (PAI-2).
2 ing even to closely related proteins such as PAI-2.
3 plasminogen activator inhibitor (PAI)-1 and PAI-2.
4 ern indicated a cytoplasmic localization for PAI-2.
5 ising antibodies that recognize all forms of PAI-2.
6 , confirming an anti-proliferative effect of PAI-2.
7 restored by exposure to exogenous PAI-1 and PAI-2.
8 of genes, plasminogen activator inhibitor-2 (PAI-2), a gene whose expression has been linked to cell
9 ession of plasminogen activator inhibitor-2 (PAI-2), a member of the serpin family with known antiapo
11 n of plasminogen activator inhibitor type 2 (PAI-2), a serine protease inhibitor, resulted in NLRP3-
12 The primarily intracellular distribution of PAI-2 also may indicate a unique regulatory role in a pr
13 f plasminogen-activator inhibitor (PAI) 1 to PAI-2 and mean uterine-artery resistance index (UtARI)]
14 ay in Escherichia coli and demonstrated that PAI-2 and RhlR are required and sufficient for expressio
15 haracterize the putative interaction between PAI-2 and RhlR, we demonstrated that [3H]PAI-2 binds to
17 ls but not in HeLa cells that do not express PAI-2, and overexpression of FosB, c-Fos, or c-Jun in He
20 een PAI-2 and RhlR, we demonstrated that [3H]PAI-2 binds to E. coli cells expressing RhlR and not to
21 elaxed form was identical with that of total PAI-2, but in vitro the relaxed form was detected in a s
23 ial functions of PAI-2 in vivo, we generated PAI-2-deficient mice by gene targeting in embryonic stem
25 monstrated that HEK-293 cells do not express PAI-2 endogenously, but in ZNF198/FGFR1-expressing cells
31 In experiments with a bacterially expressed PAI-2 fusion protein, [3H]thymidine incorporation by ker
32 for the transcriptional control of the human PAI-2 gene and further our understanding of the molecula
33 (PKC) pathway that is a powerful inducer of PAI-2 gene expression in monocytes, macrophages, and mye
35 signaling, and the plasminogen activator 2 (PAI-2) gene, a target for CREB, in maintenance of macrop
36 ected cell lines that express high levels of PAI-2 have suggested that this inhibitor may confer prot
37 biopsy samples revealed a high expression of PAI-2 in both normal and dysplastic epithelium with a ma
42 This consistent, selective distribution of PAI-2 in the postmitotic, maturing cells prior to termin
44 inhibitor plasminogen activator inhibitor 2 (PAI-2), in the IL-5-producing, infected wild-type mice o
45 ker for many epithelial cell types, and (ii) PAI-2 is appropriately positioned to protect epithelial
47 e present results are the first to show that PAI-2 is found in normal human corneal epithelium in viv
51 2 or plasminogen activator inhibitor type 2 (PAI-2) is highly induced in macrophages in response to i
52 contrast, there was a marked abnormality in PAI-2 levels in patients with HAE-N that is not seen in
56 l keratinization and death suggests that (i) PAI-2 may be considered as a differentiation marker for
58 GFR1 fusion gene is associated with specific PAI-2-mediated resistance to apoptosis which may contrib
60 -(3-oxododecanoyl)-L-homoserine lactone) and PAI-2 (N-butyryl-L-homoserine lactone) respectively.
63 pling, there were no differences in PAI-1 to PAI-2 or MMA ratios between trial arms, but there was a
64 which lack the ability to synthesize PAI-1, PAI-2, or both autoinducers were significantly or greatl
71 on of the plasminogen activator inhibitor-2 (PAI-2/SERPINB2) was highly increased in cells expressing
72 ed serpin plasminogen activator inhibitor 2 (PAI-2) to protect cells against tumor necrosis factor al
73 d in transactivator-mediated derepression of PAI-2 transcription in macrophage-like cells, as exempli
75 ermore, the interaction of ch-uPA(RRHR) with PAI-2 was also substantially enhanced, while the interac
80 the telogen phase of the hair growth cycle, PAI-2 was limited to the postmitotic cells of the outer
81 homoserine lactone (C4-HSL) (formerly called PAI-2), was studied by using tritium-labeled signals.
82 es (maspin, SCCA1, SCCA2, hurpin, megsin and pAI-2) were commonly differentially expressed in primary
84 aspect of the function of corneal epithelial PAI-2, which may be relevant to terminal differentiation
85 /FGFR1-expressing cells 2 molecular forms of PAI-2, which were 47 kDa and 32 kDa, were expressed intr
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