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1                                              C1INH also suppressed LPS-induced up-regulation of TNF-a
2                                              C1INH concentrations (0.0-2.5 muM) decreased but did not
3                                              C1INH consists of two distinct domains: a serpin domain
4                                              C1INH in which N-linked carbohydrate was removed by usin
5                                              C1INH is a crucial regulator of enzymatic cascades in th
6                                              C1INH is a key inhibitor of enzymes controlling compleme
7                                              C1INH is a relatively weak contact system enzyme inhibit
8                                              C1INH is the main inhibitor of the contact system.
9                                              C1INH may be important in protection from sepsis through
10                                              C1INH sialylated-N- and -O-glycans were not only essenti
11                                              C1INH-deficient mice (C1INH-/- mice) subjected to CLP ha
12                                              C1INH-deficient mice showed no obvious phenotypic abnorm
13                                              C1INH-deficient mice, which have been used as a model of
14               Investigators have generated a C1INH-/- mouse model that has demonstrated the importanc
15 due to acquired C1-inhibitor deficiency (AAE-C1INH) is a rare disorder characterized by recurrent epi
16 2021-000720-36), all 3 participants with AAE-C1INH had complete control of angioedema during 8 weeks
17 n-label, single-arm study, patients with AAE-C1INH received deucrictibant 40 mg extended-release tabl
18                       Four patients with AAE-C1INH were enrolled, 3 of whom were rolled over from the
19 nted angioedema attacks in patients with AAE-C1INH, with no safety concerns.
20  prophylactic treatment in patients with AAE-C1INH.
21 this study, we demonstrated that both active C1INH and reactive center-cleaved, inactive C1INH protec
22                                 In addition, C1INH was shown to bind to diphosphoryl lipid A (dLPA) b
23 ure model of endothelial-leukocyte adhesion, C1INH showed inhibition in a dose-dependent manner.
24 minant-negative disease mechanisms affecting C1INH plasma levels in HAE type I patients, and may pave
25 ation on HMVECs was modulated by the ambient C1INH concentration.
26 ng to RAW 264.7 cells was reversed with anti-C1INH Ab and was more efficient when C1INH was incubated
27 sion biopsies showed positive intra-arterial C1INH staining and reduced C4d staining in C1INH-treated
28                                However, both C1INH and iC1INH enhanced the bactericidal activity of b
29                 Mice with deficiency of both C1INH and Bk2R demonstrated diminished vascular permeabi
30 pond well to modest increases of circulating C1INH activity levels because inhibition of fluid-phase
31 oth native C1INH and reactive center cleaved C1INH significantly inhibit selectin-mediated leukocyte
32         Furthermore, reactive-center-cleaved C1INH attenuated pulmonary damage evoked by intravenous
33 trated by the use of reactive-center-cleaved C1INH, but dependent on its glycosylation status.
34                                Collectively, C1INH administration provides a new therapeutic option f
35                        In humans, congenital C1INH deficiency results in a rare episodic bradykinin-m
36                             N-deglycosylated C1INH also failed to suppress fluorescein isothiocyanate
37 ed immunosorbent assay, the N-deglycosylated C1INH bound to LPS very poorly.
38 and in vivo models, whereas N-deglycosylated C1INH loses such activities.
39 with intact LPS, binding of N-deglycosylated C1INH to dLPA and mLPA was diminished in comparison with
40 (TEE) have been reported with plasma-derived C1INH, but so far none with recombinant human C1INH (rhC
41 d prophylactic treatment with plasma-derived C1INH.
42              Our results recommend high-dose C1INH complement blockade in transplant recipients as an
43 findings highlight a key role for endogenous C1INH as a negative regulator of contact pathway-mediate
44     Further, this work identifies endogenous C1INH as an important negative regulator of venous throm
45 (C1-INH-HAE) includes therapy with exogenous C1INH.
46                                       First, C1INH bound to glycan moieties within P. falciparum glyc
47                           Heterozygosity for C1INH deficiency results in hereditary angioedema, which
48                In addition, whole blood from C1INH-deficient mice supported significantly increased c
49 duction in the levels of secreted functional C1INH, thereby manifesting in the condition that allows
50 tients with C1INH deficiency-associated HAE (C1INH-HAE) have increased circulating markers of activat
51 ended cohort of 80 HAE patients (60 with HAE-C1INH type 1, 20 with HAE-C1INH type 2), including sampl
52 ients (60 with HAE-C1INH type 1, 20 with HAE-C1INH type 2), including samples taken during attack and
53 s blue dye, both homozygous and heterozygous C1INH-deficient mice revealed increased vascular permeab
54                             In vivo, histone-C1INH complexes were detected in bronchoalveolar lavage
55 ed HMVECs constitutively coexpressed PK, HK, C1INH, and PRCP.
56 reversed by treatment with intravenous human C1INH, with a Kunitz domain plasma kallikrein inhibitor
57                  Furthermore, purified human C1INH normalized contact pathway-mediated thrombin gener
58 1INH, but so far none with recombinant human C1INH (rhC1INH).
59                          We found that human C1INH, at therapeutically relevant doses, blocks severe
60                                 Importantly, C1INH-deficient mice exhibited significantly enhanced ve
61        The data suggest that the mutation in C1INH-Ta results in a folding abnormality that behaves a
62 l C1INH staining and reduced C4d staining in C1INH-treated grafts compared with controls.
63 thrombin generation and venous thrombosis in C1INH-deficient mice.
64 on because reactive center-cleaved, inactive C1INH (iC1INH) also was effective.
65  C1INH and reactive center-cleaved, inactive C1INH protected mice from lethal Gram-negative endotoxem
66 ently due to absent or reduced C1 inhibitor (C1INH) activity.
67 y the ambient concentration of C1 inhibitor (C1INH) and prolylcarboxypeptidase (PRCP).
68             Heterozygosity for C1 inhibitor (C1INH) deficiency results in hereditary angioedema.
69                                C1 inhibitor (C1INH) is a multifunctional serine protease inhibitor th
70                         Plasma C1 inhibitor (C1INH) is a natural inhibitor of complement and contact
71                                C1 inhibitor (C1INH) is beneficial in animal models of endotoxemia and
72                                C1 inhibitor (C1INH) prevents endotoxin shock in mice via a direct int
73                            The C1 inhibitor (C1INH) promoter is unusual in two respects: 1) It contai
74                                C1 inhibitor (C1INH) protects mice from lethal Gram-negative bacterial
75 the SERPING1 gene encoding the C1 inhibitor (C1INH) that leads to plasma deficiency, resulting in rec
76                                C1 inhibitor (C1INH), a member of the serine proteinase inhibitor (ser
77                            The C1 inhibitor (C1INH), a plasma complement regulatory protein, prevents
78 SERPING1 gene that encodes the C1 inhibitor (C1INH), a serine protease inhibitor (serpin).
79                  Dysfunctional C1 inhibitor (C1INH)-Ta is a naturally occurring mutant from a patient
80 iciency of the encoded protein C1 inhibitor (C1INH).
81  by a deficiency of functional C1-inhibitor (C1INH) becomes clinically manifest as attacks of angioed
82                          Human C1-inhibitor (C1INH) is a multifunctional protease inhibitor that regu
83  of first component of complement-inhibitor (C1INH).
84       HAE with normal C1 esterase inhibitor (C1INH) activity includes the form with mutations in the
85     Recombinant human C1 esterase inhibitor (C1INH) serves as a promising future alternative to curre
86    To explore whether C1 esterase inhibitor (C1INH), an endogenous inhibitor of the contact phase, ma
87 aft administration of C1 esterase inhibitor (C1INH, a lectin/classical pathway inhibitor) into deceas
88                       C1 esterase-inhibitor (C1INH) deficiency or gain-of-function mutations in facto
89                                 Insufficient C1INH activity leads to uncontrolled activation of plasm
90 minal domain, mutations were introduced into C1INH at the three N-linked glycosylation sites and at t
91 nant-negative manner and forms intracellular C1INH aggregates.
92 ding to the creation of larger intracellular C1INH aggregates that were trapped in the endoplasmic re
93 y effects of full-length or near full-length C1INH encoded by 28 disease-associated SERPING1 variants
94 s by which they result in pathologically low C1INH plasma levels remain largely unknown.
95 , but the cellular mechanisms leading to low C1INH levels (20%-30% of normal) in heterozygous HAE typ
96 se Factor XIIa and kallikrein requires lower C1INH levels than inhibition of activator-bound factors.
97 P small interfering RNA knockdowns magnified C1INH inhibitory activity on PK activation, and PRCP tra
98                        C1INH-deficient mice (C1INH-/- mice) subjected to CLP had a higher mortality t
99 73 m(2), IQR: 34-50; P = .02) and 30 months (C1INH median: 54 mL/min/1.73 m(2), IQR: 47-66; placebo m
100 rate than recipients of placebo at 6 months (C1INH median: 55 mL/min/1.73 m(2), interquartile range [
101                                    Moreover, C1INH-HAE patients had elevated plasma levels of PLC, wh
102                     In the presence of 2 muM C1INH, only 50% of the HK became cleaved.
103 otein interactions between normal and mutant C1INH, leading to the creation of larger intracellular C
104 simultaneous expression of normal and mutant C1INH.
105  subset of patients with type I HAE, mutated C1INH encoded by HAE-causing SERPING1 acts upon wildtype
106                Here we show that both native C1INH and reactive center cleaved C1INH significantly in
107 found that coexpression of mutant and normal C1INH negatively affected the overall capacity to target
108 ERPING1 alleles affected secretion of normal C1INH protein in a dominant-negative fashion by triggeri
109                               The ability of C1INH to control the inflammatory processes was studied
110                            In the absence of C1INH, forming PKa on HMVECs cleaved 120-kDa HK complete
111        Notably, intracellular aggregation of C1INH and ER abnormality were observed in fibroblasts fr
112     Here, we demonstrate that application of C1INH alleviates bleomycin-induced lung injury via direc
113                  In addition, the binding of C1INH mutants to diphosphoryl lipid A was decreased in c
114 ere modulated by the local concentrations of C1INH and PRCP.
115 eavily glycosylated amino-terminal domain of C1INH.
116 as significantly increased with two doses of C1INH, one given immediately following CLP, and the seco
117 he multifaceted anti-inflammatory effects of C1INH in various animal models and human diseases.
118                          Optimal efficacy of C1INH therapy is achieved at doses >/=50 U/kg.
119 ent of HAE attacks suggests that efficacy of C1INH therapy is optimal when C1INH activity levels are
120 mLPA had any effect on the rate or extent of C1INH complex formation with C1s or on cleavage of the r
121 bset of variants, intracellular formation of C1INH foci was detectable only in heterozygous configura
122                                Both forms of C1INH blocked the LPS-binding protein-dependent binding
123 a demonstrate that N-linked glycosylation of C1INH is essential to mediate its interaction with the L
124         To further investigate the impact of C1INH deficiency on activation of coagulation and thromb
125                Therefore, the interaction of C1INH with gram-negative bacterial LPS is dependent both
126                           The interaction of C1INH with LPS was directly demonstrated both by ELISA a
127                        Direct involvement of C1INH in modulation of selectin-mediated cell adhesion m
128                          The target level of C1INH activity needed to achieve optimal efficacy, howev
129            We determined the plasma level of C1INH associated with optimal clinical efficacy in the t
130                     Reduced plasma levels of C1INH lead to enhanced activation of the contact system,
131 ent mice, which have been used as a model of C1INH-HAE, had significantly increased baseline circulat
132               However, no multimerization of C1INH-Ta isolated from serum or of C1INH-Ta in serum, wa
133                              The mutation of C1INH at all four positively charged amino acid residues
134 zation of C1INH-Ta isolated from serum or of C1INH-Ta in serum, was observed.
135 observed no effect on DGF, but recipients of C1INH-treated allografts showed higher estimated glomeru
136 ract might be important in the regulation of C1INH promoter activity.
137 activation on HMVECs by PRCP and the role of C1INH to regulate it, high-molecular-weight kininogen (H
138                 However, the mechanism(s) of C1INH protection remain(s) ill-defined.
139         Extensive and comparative studies of C1INH expression, secretion, functionality, and intracel
140                                  Survival of C1INH-/- mice was significantly increased with two doses
141 ation was 1 h with icatibant and 2 h with pd-C1INH and median time from drug administration to comple
142                   This dose increases plasma C1INH activity in almost all patients to values >/=0.7 U
143 sent studies test the hypothesis that plasma C1INH bears sialyl Lewis(x)-related moieties and therefo
144               The data also show that plasma C1INH can bind to P- and E-selectins by FACS and immunop
145                  We demonstrated that plasma C1INH does express sialyl Lewis(x)-related moieties on i
146                        Treatment with plasma C1INH is effective not only in patients with hereditary
147                                  Recombinant C1INH-Ta revealed an intermediate thermal stability in c
148                                  Recombinant C1INH-Ta, on 7.5% SDS-polyacrylamide gel electrophoresis
149 ect of weekly administrations of recombinant C1INH (rhC1INH).
150                Plasma-derived or recombinant C1INH products are approved for the treatment of such an
151 AE with either plasma-derived or recombinant C1INH products, tested at various doses.
152 K activation, and PRCP transfections reduced C1INH inhibition at any given concentration.
153                                      Second, C1INH bound to host CD36 and chondroitin sulfate A molec
154 ne is able to restore the levels of secreted C1INH, thereby opening up a novel mechanism justifying g
155         The data support the hypothesis that C1INH plays a direct role in leukocyte-endothelial cell
156                      This study reveals that C1INH is a potential therapeutic antimalarial molecule a
157                         Here, we showed that C1INH encoded by a subset of HAE-causing SERPING1 allele
158                           We have shown that C1INH expresses the sialyl-Lewis(x) tetrasaccharide on i
159              This discovery may suggest that C1INH plays a role in the endothelial-leukocyte interact
160                                          The C1INH gene also contains a number of potential regulator
161                                          The C1INH mutants that did not bind to LPS also did not supp
162                                          The C1INH-Ta dimer expressed the epitopes that normally are
163                            Disruption of the C1INH gene by gene trapping enabled the generation of ho
164  role of these elements in regulation of the C1INH promoter was examined.
165                In addition, treatment of the C1INH-deficient mice with an angiotensin-converting enzy
166                                   Therefore, C1INH, in addition to its function as a serine protease
167  alpha1AT-SMTR/V and -SLLR/V are superior to C1INH in reducing bradykinin production in plasma.
168 omparison with that of recombinant wild-type C1INH.
169 to receive allografts treated with 500 units C1INH or placebo (normal saline) into the transplant ren
170 The differences in half-lives of the various C1INH products do not have an obvious effect on clinical
171                                    In vitro, C1INH bound to bacteria cultured from blood or peritonea
172                                    In vitro, C1INH was found to bind all histone types.
173                                     In vivo, C1INH and iC1INH both reduced the number of viable bacte
174 th anti-C1INH Ab and was more efficient when C1INH was incubated first with LPS rather than with the
175 at efficacy of C1INH therapy is optimal when C1INH activity levels are restored to the normal range.
176 ine some types of hereditary angioedema with C1INH deficiency as serpinopathies driven by dominant-ne
177  complementing the phenotype associated with C1INH-HAE.
178 hed vascular permeability in comparison with C1INH-deficient, Bk2R-sufficient mice.
179                                Patients with C1INH deficiency-associated HAE (C1INH-HAE) have increas
180 ore, we recently reported that patients with C1INH-HAE had a moderate but significant increased risk
181                   Plasmas from patients with C1INH-HAE had significantly increased contact pathway-me
182 LP) model for sepsis in mice, treatment with C1INH improved survival in comparison with untreated con
183                               Treatment with C1INH may provide a useful additional therapeutic approa
184 enient acute and prophylactic treatment with C1INH.
185 HAE-causing SERPING1 acts upon wildtype (WT) C1INH in a dominant-negative manner and forms intracellu

 
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