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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.
6                  For small peptides, such as angiotensin I (Agt I) and [Gln11]-amyloid-beta-protein f
7            The pressor response to exogenous angiotensin I (AI) was measured and normalized for the p
8 lysyl-proline (AcSDKP), urine AcSDKP, plasma angiotensin I (AI), plasma angiotensin II (AII), or the
9 lipid vesicle-bound angiotensin II (AII) and angiotensin I (AI).
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
12 sed by the differential vascular response to angiotensin I and angiotensin II.
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
19               At this time, constrictions to angiotensin I and II were depressed, but there was no lo
20 nsinogen resulted in increased generation of angiotensin I and II.
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
23                                    Unlabeled angiotensin I and porcine insulin are then deposited on
24  affinity for the 125I-radiolabeled peptides angiotensin I and porcine insulin.
25 r structural characterization/elucidation of angiotensin I and rapamycin is illustrated.
26  a peptidase responsible for the cleavage of angiotensin I and several other peptides.
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,
29                             Plasma renin and angiotensins I and II are undetectable.
30 nalysis of back-exchange in the decapeptide, angiotensin I, and a hexapeptide derived by digestion of
31  by CPA6, including Met- and Leu-enkephalin, angiotensin I, and neurotensin.
32 cter, antagonized the contractile effects of angiotensin I, and, importantly, caused a decrease in th
33               Several enzymes that hydrolyze angiotensin I (Ang I) and Ang II to Ang-(1-7) have been
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
37                               In this study, Angiotensin I (ANG I) was directly injected into the SFO
38                                              Angiotensin I (Ang I) was generated from angiotensinogen
39                                          Six angiotensin I (Ang-I) variants were selected as model pe
40 med intrarenally from systemically delivered angiotensin I (AngI) and intrarenally formed 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
49 bitor BILA 2157, which excludes formation of angiotensin I by proteases other than renin.
50 ssociation efficiencies for fragmentation of angiotensin I by resonance excitation are investigated a
51                                              Angiotensin I can be directly converted to angiotensin-(
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
54 e of the most widely studied is the gene for angiotensin I converting enzyme (ACE ).
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
58                                              Angiotensin I converting enzyme (ACE) inhibitory and ant
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
61       The most hydrolysed sample showed high angiotensin I converting enzyme (ACE)-inhibitory and ant
62                                              Angiotensin I converting enzyme (kininase II; ACE) inhib
63 e N- and C-terminal domains of human somatic angiotensin I converting enzyme (sACE-1) demonstrate dis
64 ells expressing the SARS-CoV receptor, human angiotensin I converting enzyme 2 (hACE2).
65 II type 1 receptor antagonist (AT1RA) and/or angiotensin I converting enzyme inhibitor (ACEI) were in
66                                              Angiotensin-I converting enzyme (ACE) is a zinc dipeptid
67                                              Angiotensin-I converting enzyme (ACE) is a zinc metallop
68 egation analysis have shown that circulating angiotensin-I converting enzyme (ACE) levels are influen
69                                              Angiotensin-I converting enzyme (ACE), a two-domain dipe
70             An insertion polymorphism of the angiotensin-I converting enzyme gene (ACE) is common in
71  sweetness, bitterness and umami, as well as angiotensin-I converting enzyme inhibitory activity.
72 ddition to the extract's capacity to inhibit angiotensin I-converting enzyme (ACE) activity.
73                          Using inhibitors of angiotensin I-converting enzyme (ACE) and CP, we show th
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
77      The A-240T and I/D polymorphisms in the angiotensin I-converting enzyme (ACE) gene are markers o
78                                              Angiotensin I-converting enzyme (ACE) hydrolyzes numerou
79            Part of the beneficial effects of angiotensin I-converting enzyme (ACE) inhibitors are due
80                                              Angiotensin I-converting enzyme (ACE) inhibitors derived
81                           To investigate how angiotensin I-converting enzyme (ACE) inhibitors enhance
82                                              Angiotensin I-converting enzyme (ACE) inhibitors have be
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
85                                          The angiotensin I-converting enzyme (ACE) inhibitory activit
86                                          The angiotensin I-converting enzyme (ACE) inhibitory activit
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
89                                              Angiotensin I-converting enzyme (ACE) inhibitory peptide
90 showed different amino acid compositions and angiotensin I-converting enzyme (ACE) inhibitory potenti
91               We determined the influence of angiotensin I-converting enzyme (ACE) insertion (I)/dele
92            Pedigree analyses have shown that angiotensin I-converting enzyme (ACE) levels are influen
93                                              Angiotensin I-converting enzyme (ACE), one of the centra
94    Although both LFHs <3 kDa showed in vitro angiotensin I-converting enzyme (ACE)-inhibitory activit
95 s established for oligopeptides that inhibit angiotensin I-converting enzyme (ACE).
96 ion (D) polymorphism (indel) of the gene for angiotensin I-converting enzyme (ACE).
97                                              Angiotensin I-converting enzyme (ACE)2, a new component
98                                              Angiotensin I-converting enzyme (ACE, or DCP1) is a zinc
99                                              Angiotensin I-converting enzyme (ACE, peptidyl dipeptida
100 eported previously a novel mode of action of angiotensin I-converting enzyme (kininase II; ACE) inhib
101                                Human somatic angiotensin I-converting enzyme (sACE) has two active si
102                                Human somatic angiotensin I-converting enzyme (sACE) is a key regulato
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
110 y HRV only in the 20 participants using ACE (angiotensin I-converting enzyme) inhibitors.
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.
113 inc metalloprotease whose closest homolog is angiotensin I-converting enzyme.
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
118                                              Angiotensin-I-converting enzyme (ACE-I) plays a key role
119                                              Angiotensin-I-converting enzyme activities were 58 (44-7
120                                Inhibition of angiotensin is crucial in treatment of chronic kidney di
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
123                                          The angiotensin I-forming activity of the renin protein was
124 al peptide hormones including bradykinin and angiotensin I have been described as substrates.
125                                              Angiotensin I, II, and III produced concentration-depend
126                                              Angiotensin I, II, and III; angiotensin-converting enzym
127                  We determined the effect of angiotensin I, II, III, and IV and angiotensin-(1-7) on
128 he HDX rates for a small 10-residue peptide, angiotensin I, in aqueous droplets, from which we found
129                       In response to chronic angiotensin I infusions, ACE 9/9 mice displayed increase
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
132 es were not effective for the enhancement of angiotensin I ions.
133                         [Pro(11)(D)-Ala(12)] angiotensin I is an ACE-resistant substrate specific for
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
136            The best-known natural substrate, angiotensin I, is cleaved to generate vasoactive angiote
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
142 old rats (13.9 +/- 3.8 versus 2.9 +/- 0.8 ng angiotensin I/ml per min), respectively.
143 onditions (1.3 +/- 0.2 versus 1.8 +/- 0.3 ng angiotensin I/ml per min).
144 amide), but did not display activity towards angiotensin I (NRVYIHPFHL), des-Arg bradykinin and AF1 (
145 ed to confirm intact deposition of [Val (5)]-Angiotensin I on a surface.
146 t significantly inhibit the effect of either angiotensin I or angiotensin II.
147 s for limit of detection was performed using angiotensin I peptide.
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
152                          Using a solution of angiotensin I, the carbon fiber emitter in 75-microm-i.d
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
163                                A solution of angiotensin I was quantified using this method, and the
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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