戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 ient to meet target levels for inhibition of plasma kallikrein.
2 ors that are selective either for or against plasma kallikrein.
3 dimensional views of the catalytic domain of plasma kallikrein.
4 tivity for factor Xa relative to trypsin and plasma kallikrein.
5 binant granzyme A, human thrombin, and human plasma kallikrein.
6 ariants (SMTR/S and SLLR/S) strongly inhibit plasma kallikrein, activated FXII, and plasmin.
7 propose that blocking the B2R and inhibiting plasma kallikrein activity might have an ameliorating ef
8 ll tolerated and led to rapid suppression of plasma kallikrein activity, resulting in increased time
9 ls) for expression of the protease domain of plasma kallikrein, along with the purification and high
10                                              Plasma kallikrein amplifies FXII activation, and its def
11       We determined the relationship between plasma kallikrein and cardiovascular disease (CVD) outco
12 ection from ex vivo stimulated generation of plasma kallikrein and cleavage of high-molecular-weight
13 teases we identified two new HGF activators, plasma kallikrein and coagulation factor XIa (FXIa).
14 f both arms of the system as a substrate for plasma kallikrein and critical cofactor, which forms int
15                In conclusion, the ability of plasma kallikrein and FXIa to activate pro-HGF in vitro
16  the biochemical and enzymatic properties of plasma kallikrein and paves the way for structure-based
17 I-W268R is highly sensitive to activation by plasma kallikrein and plasmin, compared with FXII-WT or
18       We find that HGFA, matriptase, hepsin, plasma kallikrein and trypsin are potently inhibited, an
19 ay inhibitor-2 (TFPI-2) inhibits factor XIa, plasma kallikrein, and factor VIIa/tissue factor; accord
20  is an important inhibitor of complement C1, plasma kallikrein, and factor XIIa, and as such is invol
21  shares high sequence identity with acrosin, plasma kallikrein, and hepsin.
22 oblotting revealed activation of factor XII, plasma kallikrein, and kininogen during the acute phase
23  from the cloned cDNA and inhibited trypsin, plasma kallikrein, and plasmin with IC50 values in the n
24     Thrombin, factor Xa, plasmin, urokinase, plasma kallikrein, and tissue kallikrein had no effect.
25 p-regulated the expression of kallikrein and plasma kallikrein B genes.
26                                              Plasma kallikrein bound to HK cleaves prourokinase to ur
27 min, trypsin, chymotrypsin, cathepsin G, and plasma kallikrein but not urokinase-type plasminogen act
28  thrombin and potentiating the inhibition of plasma kallikrein by antithrombin.
29                                Inhibition of plasma kallikrein by EPI-KAL2 and 13G11 significantly su
30 MPO and HK on cells such that MPO masked the plasma kallikrein cleavage site on HK, and MPO-generated
31 nner and (2) a noncanonical pathway in which plasma kallikrein directly activates FIX, which ultimate
32    In transfected HEK293 cells, we find that plasma kallikrein directly activates G protein-coupled p
33 ions at doses >/=400 mg q8 h met or exceeded plasma kallikrein EC50 values throughout the dosing inte
34  the only inhibitory domain, and it inhibits plasma kallikrein, factor XIa, and plasmin.
35 dy of serum scuPAR levels identified a human plasma kallikrein gene (KLKB1) promoter polymorphism (rs
36  sequence repeat polymorphisms for the human plasma kallikrein gene (KLKB1; previously known as KLK3)
37                                 Like the rat plasma kallikrein gene and the closely related human fac
38 MP-1 levels through the action of plasmin or plasma kallikrein (generated from their added zymogens).
39 ble swelling episodes caused by uncontrolled plasma kallikrein generation and excessive bradykinin re
40              The production of BK from HK by plasma kallikrein has been implicated in the pathogenesi
41                                     Although plasma kallikrein has been purified for 40 years, its st
42 bolytic zymogens plasminogen, urokinase, and plasma kallikrein have all been shown to cleave and acti
43 n or pharmacologic inhibition of factor XII, plasma kallikrein, high-molecular-weight kininogen, or t
44 on was found for plasmin (IC50 = 399 nm) and plasma kallikrein (IC50 = 686 nm).
45 BCX7353) is an oral, once-daily inhibitor of plasma kallikrein in development for the prophylaxis of
46                          A critical role for plasma kallikrein in the pathogenesis of autoantibody-in
47 ontact pathway: factor XIa, factor XIIa, and plasma kallikrein, in the presence and absence of high m
48 ntravenous human C1INH, with a Kunitz domain plasma kallikrein inhibitor (DX88), and with a bradykini
49  The role of plasma KKS was examined using a plasma kallikrein inhibitor (EPI-KAL2) and an antikallik
50 apse following treatment with ecallantide, a plasma kallikrein inhibitor approved for HAE attack trea
51          Berotralstat (BCX-7353) is a potent plasma kallikrein inhibitor developed to prevent heredit
52                          Using the selective plasma kallikrein inhibitor P8720, we investigate whethe
53 s those for the investigational agents, oral plasma kallikrein inhibitor sebetralstat and oral bradyk
54 -guided drug design strategy) is a synthetic plasma kallikrein inhibitor that is potent and highly se
55   Avoralstat is a potent small-molecule oral plasma kallikrein inhibitor under development for treatm
56 nsions from 4 different therapeutic classes (plasma kallikrein inhibitor, receptor tyrosine kinase in
57            We aimed to assess the novel oral plasma kallikrein inhibitor, sebetralstat, which is in d
58 evidence has shown that potent and selective plasma kallikrein inhibitors that block the generation o
59                                              Plasma kallikrein is a serine protease that has many imp
60 human tissue kallikrein (Ki = 0.1 nM), human plasma kallikrein (Ki = 0.3 nM) and human factor XIa (Ki
61                                          The plasma kallikrein-kinin system (KKS) consists of serine
62 ws that monoclonal antibody C11C1 attenuates plasma kallikrein-kinin system activation, local and sys
63 ctions between MPO and the components of the plasma kallikrein-kinin system resulted in decreased bra
64 ays an important role in the assembly of the plasma kallikrein-kinin system.
65 otein for the assembly of the vasoregulatory plasma kallikrein-kinin system; thus we explored whether
66 athway for thrombosis risk reduction via the plasma kallikrein/kinin and renin angiotensin systems.
67 r physiologic assembly and activation of the plasma kallikrein/kinin system and discusses its influen
68        The relevance and significance of the plasma kallikrein/kinin system as a risk factor for the
69                            Here, we identify plasma kallikrein (KK) as a specific direct modulator of
70 ting enzyme 2 (ACE-2), neprilysin (NEP), and plasma kallikrein (KLKB1) cleave and inactivate it, with
71 ypeptidase (PRCP) activates prekallikrein to plasma kallikrein, leading to bradykinin liberation, and
72           These novel findings indicate that plasma kallikrein level associates with the risk of any
73                      The association between plasma kallikrein levels and the risk of any CVD remaine
74 sion models assessed the association between plasma kallikrein levels and the risk of CVD.
75 d to robust and sustained reduction in total plasma kallikrein levels in patients with hereditary ang
76                 In unadjusted models, higher plasma kallikrein levels were associated with higher ris
77                             For MACE, higher plasma kallikrein levels were associated with higher ris
78                                              Plasma kallikrein levels were measured longitudinally in
79 e-dependent, and durable reductions in total plasma kallikrein levels, and no severe adverse events w
80  and human recombinant tissue kallikrein and plasma kallikrein on [Ca(2+)](i) mobilization and [(3)H]
81 ence of prekallikrein (PK), the proenzyme of plasma kallikrein, on vascular endothelial cells is not
82 rted to FXIIa (activated factor XII) by PKa (plasma kallikrein) or its unique ability to autoactivate
83 WT, the KD1-L17R did not inhibit factor XIa, plasma kallikrein, or factor VIIa/tissue factor.
84 mer (p < 0.0001), P-selectin (p < 0.05), and plasma kallikrein (p < 0.001).
85 o [HR] = 1.16 per 20 nmol/L higher levels of plasma kallikrein; P = 0.0177) as well as over the EDIC-
86                                              Plasma kallikrein (PK) cleaves high-molecular-weight kin
87                                              Plasma kallikrein (PK) has been identified in vitreous f
88 t this augmented expansion is ameliorated by plasma kallikrein (PK) inhibition or deficiency.
89 Intravitreal injections of autologous blood, plasma kallikrein (PK), bradykinin, and collagenase were
90 itary angioedema are attributed to excessive plasma kallikrein (PKa) activity, which cleaves high-mol
91  of swelling and pain caused by uncontrolled plasma kallikrein (PKa) activity.
92 ding to increased generation of the protease plasma kallikrein (PKa) and excessive release of the nan
93 hibitor, the main regulator of the proteases plasma kallikrein (PKa) and factor XIIa (FXIIa).
94          HAE is associated with uncontrolled plasma kallikrein (PKa) enzyme activity and generation o
95 -affinity, high-specificity binders to human plasma kallikrein (pKAL) and human thrombin (THBN) can b
96                                     Although plasma kallikrein (PKal) has been implicated in contribu
97                                              Plasma kallikrein (pKal) proteolytically cleaves high mo
98 tissue-type plasminogen activator (tPA), and plasma kallikrein (PKal).
99 was demonstrated against the serine protease plasma kallikrein (Pkal).
100                          In addition, formed plasma kallikrein promotes single-chain urokinase activa
101  or high-molecular-weight kininogen, but not plasma kallikrein, protected mice from prostasome-induce
102       Dose-dependent reductions in the total plasma kallikrein protein level were observed between ba
103 ics (i.e., the change from baseline in total plasma kallikrein protein level); exploratory end points
104             The mean percent change in total plasma kallikrein protein levels from baseline to week 1
105  regulate the catalytic activity of FXIa and plasma kallikrein, respectively, despite the inability t
106  cleavage of FXI and PK to generate FXIa and plasma kallikrein, respectively.
107                            Cleavage of HK by plasma kallikrein results in release of the nonapeptide
108 ere susceptible to activation by plasmin and plasma kallikrein, they were ineffective in supporting a
109 ecular-weight kininogen can be hydrolysed by plasma kallikrein to bradykinin and cleaved high-molecul
110 rine proteases (thrombin, tPA, FXa, plasmin, plasma kallikrein, trypsin, FVIIa).
111                                Inhibition of plasma kallikrein was observed at all doses, and the deg
112 a contact system leads to elevated levels of plasma kallikrein, which cleaves high molecular weight k
113               Activated factor XII generates plasma kallikrein, which proteolyzes kininogen, leading
114 e relatively open active site of plasmin and plasma kallikrein, while it is rejected from sterically
115 -triazole derivative 10 inhibits plasmin and plasma kallikrein with K(i) of 0.77 and 2.4 nM, respecti
116 ic inhibition of PRCP with Z-Pro-Prolinal or plasma kallikrein with soybean trypsin inhibitor, Pro-Ph

 
Page Top