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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
10           Plasminogen activator inhibitor-2 (PAI-2), a member of the serpin gene family, is thought t
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
16                        Our results establish PAI-2 and TG2 as downstream mediators in the antiapoptot
17 ls but not in HeLa cells that do not express PAI-2, and overexpression of FosB, c-Fos, or c-Jun in He
18                               High levels of PAI-2 are found in keratinocytes, monocytes, and the hum
19                     In addition, we identify PAI-2 as an antiviral SERPIN that reduces infectivity of
20 is revealed that both intracellular forms of PAI-2 bind to the ZNF198/FGFR1 kinase.
21 een PAI-2 and RhlR, we demonstrated that [3H]PAI-2 binds to E. coli cells expressing RhlR and not to
22 elaxed form was identical with that of total PAI-2, but in vitro the relaxed form was detected in a s
23         Likewise, overexpressing Beclin 1 in PAI-2-deficient cells rescued the suppression of NLRP3 a
24 ial functions of PAI-2 in vivo, we generated PAI-2-deficient mice by gene targeting in embryonic stem
25                                   Homozygous PAI-2-deficient mice exhibited normal development, survi
26 monstrated that HEK-293 cells do not express PAI-2 endogenously, but in ZNF198/FGFR1-expressing cells
27         This site specifically binds FosB in PAI-2-expressing U937 cells but not in HeLa cells that d
28 t for PMA-induced transactivator activity in PAI-2-expressing U937 cells.
29                 TLR2 or TLR4 agonist induced PAI-2 expression, which subsequently stabilized the auto
30 , which directs synthesis of the autoinducer PAI-2 (formerly referred to as factor 2).
31         Second, we showed that PAI-1 blocked PAI-2 from binding to RhlR, thereby inhibiting the expre
32  In experiments with a bacterially expressed PAI-2 fusion protein, [3H]thymidine incorporation by ker
33 for the transcriptional control of the human PAI-2 gene and further our understanding of the molecula
34  (PKC) pathway that is a powerful inducer of PAI-2 gene expression in monocytes, macrophages, and mye
35  the plasminogen activator inhibitor type-2 (PAI-2) gene is a major response to cellular stress.
36  signaling, and the plasminogen activator 2 (PAI-2) gene, a target for CREB, in maintenance of macrop
37 ected cell lines that express high levels of PAI-2 have suggested that this inhibitor may confer prot
38 biopsy samples revealed a high expression of PAI-2 in both normal and dysplastic epithelium with a ma
39 Immunostaining also revealed the presence of PAI-2 in its relaxed (i.e., cleaved) conformation.
40 subpopulation of keratinocytes also contains PAI-2 in its relaxed (i.e., cleaved) conformation.
41  death, we determined expression patterns of PAI-2 in murine hair and nail.
42                        Altered expression of PAI-2 in the different cultured cells was validated via
43   This consistent, selective distribution of PAI-2 in the postmitotic, maturing cells prior to termin
44        To examine the potential functions of PAI-2 in vivo, we generated PAI-2-deficient mice by gene
45 inhibitor plasminogen activator inhibitor 2 (PAI-2), in the IL-5-producing, infected wild-type mice o
46 ker for many epithelial cell types, and (ii) PAI-2 is appropriately positioned to protect epithelial
47            At least in vitro, all detectable PAI-2 is cell associated, with a cytoplasmic distributio
48 e present results are the first to show that PAI-2 is found in normal human corneal epithelium in viv
49                            The expression of PAI-2 is induced by a variety of cytokines and growth fa
50          These results strongly suggest that PAI-2 is involved in the regulation of keratinocyte prol
51      Plasminogen activator inhibitor type 2 (PAI-2) is an unusual serine proteinase inhibitor in that
52 2 or plasminogen activator inhibitor type 2 (PAI-2) is highly induced in macrophages in response to i
53  contrast, there was a marked abnormality in PAI-2 levels in patients with HAE-N that is not seen in
54                                 In contrast, PAI-2 levels showed a steady increase, even after conflu
55                                              PAI-2 levels varied from 25 to 87 ng/mL (mean, 53.8 ng/m
56                                              PAI-2 limits caspase-3 activation through stabilization
57 l keratinization and death suggests that (i) PAI-2 may be considered as a differentiation marker for
58                  To test the hypothesis that PAI-2 may protect epithelial cells in vivo from prematur
59 GFR1 fusion gene is associated with specific PAI-2-mediated resistance to apoptosis which may contrib
60                                              PAI-2 mRNA and protein were detected in the differentiat
61 -(3-oxododecanoyl)-L-homoserine lactone) and PAI-2 (N-butyryl-L-homoserine lactone) respectively.
62 tem (i.e. HeLa cells) that neither expresses PAI-2 nor PI10.
63 Epidermal wound healing was equivalent among PAI-2 -/- null and control mice.
64 pling, there were no differences in PAI-1 to PAI-2 or MMA ratios between trial arms, but there was a
65  which lack the ability to synthesize PAI-1, PAI-2, or both autoinducers were significantly or greatl
66 ogen activator inhibitors 1 and 2 (PAI-1 and PAI-2), over a several-day holding period.
67                              It appears that PAI-2 plays a crucial role in twitching motility and pha
68 regulated plasminogen activator inhibitor-2 (PAI-2) production which suppressed cancer stem-like cell
69 tic cells also induced the expression of the PAI-2 protein.
70                                         When PAI-2, purified from human cornified cells, was added to
71  associated with a 21% decrease in the PAI-1/PAI-2 ratio during gestation (95% CI 4-35, p=0.015).
72                               Orthologues of PAI-2 (SERPINB2), MNEI (SERPINB1), PI-6 (SERPINB6), and
73 dicted host targets for PAI-1 (SERPINE1) and PAI-2 (SERPINB2).
74 on of the plasminogen activator inhibitor-2 (PAI-2/SERPINB2) was highly increased in cells expressing
75 ed serpin plasminogen activator inhibitor 2 (PAI-2) to protect cells against tumor necrosis factor al
76 d in transactivator-mediated derepression of PAI-2 transcription in macrophage-like cells, as exempli
77                                              PAI-2 was also detected in the permanent portion of the
78 ermore, the interaction of ch-uPA(RRHR) with PAI-2 was also substantially enhanced, while the interac
79                                              PAI-2 was analyzed by immunohistochemistry and western b
80 tern blot analysis revealed that most of the PAI-2 was cell associated and functionally active.
81                                 In the nail, PAI-2 was detected in the differentiating cells of the m
82                        In vivo and in vitro, PAI-2 was immunohistochemically localized to the superfi
83  the telogen phase of the hair growth cycle, PAI-2 was limited to the postmitotic cells of the outer
84 homoserine lactone (C4-HSL) (formerly called PAI-2), was studied by using tritium-labeled signals.
85 es (maspin, SCCA1, SCCA2, hurpin, megsin and pAI-2) were commonly differentially expressed in primary
86 ibitor 1 [PAI-1]) and placental dysfunction (PAI-2) were measured every month until delivery.
87  known as plasminogen activator inhibitor-2, PAI-2), which stabilizes p21 in senescent cells.
88 aspect of the function of corneal epithelial PAI-2, which may be relevant to terminal differentiation
89 /FGFR1-expressing cells 2 molecular forms of PAI-2, which were 47 kDa and 32 kDa, were expressed intr
90                            Finally, crossing PAI-2 -/- with PAI-1 -/- mice to generate animals defici