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1 h angiotensin II () as a substrate than with angiotensin I ().
2 activity was assessed by radioimmunoassay of angiotensin I.
3 brid, a resolution of 33,200 is achieved for angiotensin I.
4 d substrates with P1 Phe and does not cleave angiotensin I.
5 was preferred over [15N]10-microcystin-YR or angiotensin I.
8 lysyl-proline (AcSDKP), urine AcSDKP, plasma angiotensin I (AI), plasma angiotensin II (AII), or the
10 with the use of brachial artery infusions of angiotensin I and angiotensin II at two doses, with and
11 oprotein of 120 kDa, which is able to cleave angiotensin I and angiotensin II but not bradykinin or H
13 activated neutrophils 1) converts both human angiotensin I and angiotensinogen to angiotensin II; 2)
14 atubular concentrations of AngII, as well as angiotensin I and angiotensinogen, are much greater than
15 ading capacities, approximately 100 fmol for angiotensin I and approximately 50 fmol for insulin, wer
16 acid, the known metal-binding amino acids of angiotensin I and bacitracin A are oxidized, while no ox
17 of cleaving the two hemoregulatory peptides angiotensin I and bradykinin, but differ in their affini
18 e, and a marked increase in constrictions to angiotensin I and II despite continuously increased plas
21 cting peptides from physiological solutions, angiotensin I and insulin in artificial seawater are loa
22 iently extract two different peptides, human angiotensin I and MRFA, individually from an SDS contain
27 recursor species such as multiply protonated angiotensin I and ubiquitin dissociated across a variety
28 oint of view is that the bioactive peptides, angiotensins I and II and vasoactive intestinal peptide,
30 nalysis of back-exchange in the decapeptide, angiotensin I, and a hexapeptide derived by digestion of
32 cter, antagonized the contractile effects of angiotensin I, and, importantly, caused a decrease in th
34 se inhibitors on the contractile response to angiotensin I (Ang I) in human resistance arteries to in
35 duced vascular endothelial growth factor and angiotensin I (Ang I) production in RA ST fibroblasts an
36 is primarily known for its ability to cleave angiotensin I (Ang I) to the vasoactive octapeptide angi
41 els of immunoreactive angiotensinogen (AGT), angiotensin I (AngI), and angiotensin II (AngII) were me
42 2-C12 tetra-alkyl ammonium ions, bradykinin, angiotensin I, angiotensin II, bovine ubiquitin, and two
43 tidyl 4-nitroanilides, and avidly hydrolyzes angiotensin I at Phe8 to generate bioactive angiotensin
44 pertrophy caused by a subpressor infusion of angiotensin is attenuated in mice deficient in the gp91p
45 giotensin-converting enzyme (ACE) can cleave angiotensin I, bradykinin, neurotensin and many other pe
46 te fluid homeostasis, cleaves the vasoactive angiotensin-I, bradykinin, and a number of other physiol
47 al effect of CNP on the vascular response to angiotensin I but not to angiotensin II suggest that CNP
48 system, we studied the enzymatic cleavage of angiotensin I by angiotensin converting enzyme and monit
50 ssociation efficiencies for fragmentation of angiotensin I by resonance excitation are investigated a
52 )/cell; and 3) has similar high affinity for angiotensin I compared with free cathepsin G (Km = 5.9 x
53 in, and (3) stimulation of adrenal cortex by angiotensin is consistent with all the information avail
55 he angiotensin II (Ang II)-breakdown enzyme, angiotensin I converting enzyme (ACE) 2, suggests the im
56 shed Amadori ketoses showed moderate to weak angiotensin I converting enzyme (ACE) inhibitory activit
57 identify peptides with dual antioxidant and angiotensin I converting enzyme (ACE) inhibitory activit
59 he activity of the peptide inhibitors of the angiotensin I converting enzyme (ACE), and the antiradic
60 othelin 1 (EDN1); we assayed the activity of angiotensin I converting enzyme (ACE), which catalyses t
63 e N- and C-terminal domains of human somatic angiotensin I converting enzyme (sACE-1) demonstrate dis
65 II type 1 receptor antagonist (AT1RA) and/or angiotensin I converting enzyme inhibitor (ACEI) were in
68 egation analysis have shown that circulating angiotensin-I converting enzyme (ACE) levels are influen
74 fraction of the heart and skeletal muscles, angiotensin I-converting enzyme (ACE) and neutral endope
75 g white, and (ii) evaluate the inhibition of angiotensin I-converting enzyme (ACE) by the obtained hy
76 n expended to determine whether the gene for angiotensin I-converting enzyme (ACE) confers susceptibi
83 To investigate further the relationship of angiotensin I-converting enzyme (ACE) inhibitors to acti
84 es, majority of them were found identical to angiotensin I-converting enzyme (ACE) inhibitors, antiox
87 In addition, the effects of digestion on the angiotensin I-converting enzyme (ACE) inhibitory activit
88 hiols content but at the same time increased angiotensin I-converting enzyme (ACE) inhibitory activit
90 showed different amino acid compositions and angiotensin I-converting enzyme (ACE) inhibitory potenti
94 Although both LFHs <3 kDa showed in vitro angiotensin I-converting enzyme (ACE)-inhibitory activit
100 eported previously a novel mode of action of angiotensin I-converting enzyme (kininase II; ACE) inhib
103 as associated with a significant decrease in angiotensin I-converting enzyme activity and a small, bu
104 pairs, we identified 91 that had discordant angiotensin I-converting enzyme and glutathione S-transf
105 nd an insertion/deletion polymorphism of the angiotensin I-converting enzyme gene (ACE) may be relate
106 These results confirm the association of the angiotensin I-converting enzyme indel with Alzheimer's d
107 amino groups, GABA content, antioxidant and angiotensin I-converting enzyme inhibitory (ACEI) activi
108 ffect on proteolysis and negatively affected angiotensin I-converting enzyme inhibitory activity of f
109 acids), bioactivity (antioxidant effect and angiotensin I-converting enzyme inhibitory activity), rh
111 system gene regions (angiotensinogen, renin, angiotensin I-converting enzyme, and angiotensin II rece
112 nst alpha-glucosidase, pancreatic lipase and angiotensin I-converting enzyme, using in vitro models.
114 -binding proteins were identified as porcine angiotensin-I-converting enzyme (ACE I) and aminopeptida
115 work in animals suggests that inhibitors of angiotensin-I-converting enzyme (ACE) protect against ca
116 l phenotype [C1Inh, C4, spontaneous amidase, angiotensin-I-converting enzyme (ACE), aminopeptidase P
117 eutral endopeptidase (NEP, EC 3.4.24.11) and angiotensin-I-converting enzyme (ACE, EC 2.4.15.1), have
121 tidase that cleaves a single amino acid from angiotensin I, des-Arg bradykinin, and many other bioact
122 mast cell degranulation released enzyme with angiotensin I-forming activity blocked by the selective
128 he HDX rates for a small 10-residue peptide, angiotensin I, in aqueous droplets, from which we found
130 ward their receptors, CPA6 converts inactive angiotensin I into the biologically active angiotensin I
131 P1) is a zinc metallopeptidase that converts angiotensin I into the vasoactive and aldosterone-stimul
134 io (10-fold enhancement) in the detection of angiotensin I is demonstrated using the DRILL interface
135 nogen have normal fertility, indicating that angiotensin I is not a necessary substrate for testis AC
137 andards of polycyclic aromatic hydrocarbons, angiotensin I, lidocaine, ferrocene, diesel, and rosemar
138 cleavage of the peptide bond at proline for angiotensin I, Lys-bradykinin, and myoglobin are demonst
139 e state distributions was investigated using angiotensin I (M(r) = 1296), insulin (M(r) = 5774), and
140 ation of recombinant L-type Ca2+ channels by angiotensin is mediated by inositol trisphosphate-induce
141 in higher levels (16 +/- 6 versus 6 +/- 3 ng angiotensin I/ml per h, group 1 versus group 2, P = 0.01
144 amide), but did not display activity towards angiotensin I (NRVYIHPFHL), des-Arg bradykinin and AF1 (
148 response to ACE inhibition (-0.4+/-0.4 ng of angiotensin I per milliliter per hour, as compared with
149 CNP inhibited the vasoconstrictive effect of angiotensin I (reduction in overall effect with CNP, 56.
150 ttomole detection limits of a model peptide (angiotensin I) spiked into a complex mixture (in this ca
151 d ACE2 activity toward its natural substrate angiotensin I, suggesting that they would be functional
153 is responsible for proteolytic activation of angiotensin I to angiotensin II (Ang II), a potent vasoc
154 y plasma proteinase inhibitors and converted angiotensin I to angiotensin II even in undiluted plasma
155 of serine proteases are enzymes that convert angiotensin I to angiotensin II, as well as others that
156 zyme (ACE) act by blocking the conversion of angiotensin I to angiotensin II, which is catalysed by t
157 hydrolyzes the carboxy terminal leucine from angiotensin I to generate angiotensin 1-9, which is conv
158 the carboxy terminal His-Leu dipeptide from angiotensin I to produce a potent vasopressor octapeptid
159 so known as ACE) catalyses the conversion of angiotensin I to the physiologically active peptide angi
160 ts to trigger the Ace2-to-Ace enzyme switch, angiotensin I-to-II conversion, and cardiac hypertrophy.
161 detection limit of 400 amol was achieved for angiotensin I using the nanofibrous carbon ME-SALDI subs
162 ion of fragments produced in the cleavage of angiotensin I was obtained using liquid chromatography-m
164 total ion current peak areas of 500 fmol of angiotensin I were improved by a factor of 2.6 when the
165 rdiac myocytes produce increasing amounts of angiotensin I, which is converted to angiotensin II by t
166 ns accessible to small substrates, including angiotensin I, with activity in serum that is stable wit
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