ライフサイエンスコーパス: angiotensin I

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 ence suggests that the metabolic products of angiotensin I and II - initially thought to be biologica

19 nd plasma from 53 individuals and quantified Angiotensin I and II and over 150 proteins including at

20 Furthermore, labile Angiotensin I and II bioactive peptides along with a pan

21 e, and a marked increase in constrictions to angiotensin I and II despite continuously increased plas

22 At this time, constrictions to angiotensin I and II were depressed, but there was no lo

23 nsinogen resulted in increased generation of angiotensin I and II.

24 f angiotensin II (Ang II) from its precursor angiotensin I and inhibit the breakdown of bradykinin, w

25 cting peptides from physiological solutions, angiotensin I and insulin in artificial seawater are loa

26 by angiotensin-converting enzyme (ACE) from angiotensin I and metabolized by ACE 2 (ACE2), plays a p

27 iently extract two different peptides, human angiotensin I and MRFA, individually from an SDS contain

28 Unlabeled angiotensin I and porcine insulin are then deposited on

29 affinity for the 125I-radiolabeled peptides angiotensin I and porcine insulin.

30 r structural characterization/elucidation of angiotensin I and rapamycin is illustrated.

31 a peptidase responsible for the cleavage of angiotensin I and several other peptides.

32 recursor species such as multiply protonated angiotensin I and ubiquitin dissociated across a variety

33 oint of view is that the bioactive peptides, angiotensins I and II and vasoactive intestinal peptide,

34 Plasma renin and angiotensins I and II are undetectable.

35 nalysis of back-exchange in the decapeptide, angiotensin I, and a hexapeptide derived by digestion of

36 tment of High-Output Shock) trial for renin, angiotensin I, and angiotensin II concentrations before

37 by CPA6, including Met- and Leu-enkephalin, angiotensin I, and neurotensin.

38 cter, antagonized the contractile effects of angiotensin I, and, importantly, caused a decrease in th

39 Several enzymes that hydrolyze angiotensin I (Ang I) and Ang II to Ang-(1-7) have been

40 se inhibitors on the contractile response to angiotensin I (Ang I) in human resistance arteries to in

41 duced vascular endothelial growth factor and angiotensin I (Ang I) production in RA ST fibroblasts an

42 is primarily known for its ability to cleave angiotensin I (Ang I) to the vasoactive octapeptide angi

43 In this study, Angiotensin I (ANG I) was directly injected into the SFO

44 Angiotensin I (Ang I) was generated from angiotensinogen

45 sin-converting enzyme on their surface using angiotensin I (Ang-I) as a proligand.

46 Six angiotensin I (Ang-I) variants were selected as model pe

47 med intrarenally from systemically delivered angiotensin I (AngI) and intrarenally formed AngI.

48 els of immunoreactive angiotensinogen (AGT), angiotensin I (AngI), and angiotensin II (AngII) were me

49 te for collecting duct-derived renin to form angiotensin I (ANGI).

50 2-C12 tetra-alkyl ammonium ions, bradykinin, angiotensin I, angiotensin II, bovine ubiquitin, and two

51 tidyl 4-nitroanilides, and avidly hydrolyzes angiotensin I at Phe8 to generate bioactive angiotensin

52 pertrophy caused by a subpressor infusion of angiotensin is attenuated in mice deficient in the gp91p

53 proteins, including bradykinin, neurotensin, angiotensin I, bovine serum albumin (BSA), and the cat a

54 giotensin-converting enzyme (ACE) can cleave angiotensin I, bradykinin, neurotensin and many other pe

55 te fluid homeostasis, cleaves the vasoactive angiotensin-I, bradykinin, and a number of other physiol

56 al effect of CNP on the vascular response to angiotensin I but not to angiotensin II suggest that CNP

57 system, we studied the enzymatic cleavage of angiotensin I by angiotensin converting enzyme and monit

58 bitor BILA 2157, which excludes formation of angiotensin I by proteases other than renin.

59 ssociation efficiencies for fragmentation of angiotensin I by resonance excitation are investigated a

60 Angiotensin I can be directly converted to angiotensin-(

61 Several variants were shown to block angiotensin I cleavage in vitro, highlighting their pote

62 )/cell; and 3) has similar high affinity for angiotensin I compared with free cathepsin G (Km = 5.9 x

63 in, and (3) stimulation of adrenal cortex by angiotensin is consistent with all the information avail

64 e of the most widely studied is the gene for angiotensin I converting enzyme (ACE ).

65 he angiotensin II (Ang II)-breakdown enzyme, angiotensin I converting enzyme (ACE) 2, suggests the im

66 cal use of several therapeutic drugs, mostly angiotensin I converting enzyme (ACE) inhibitors and ang

67 identify peptides with dual antioxidant and angiotensin I converting enzyme (ACE) inhibitory activit

68 shed Amadori ketoses showed moderate to weak angiotensin I converting enzyme (ACE) inhibitory activit

69 Angiotensin I converting enzyme (ACE) inhibitory and ant

70 he activity of the peptide inhibitors of the angiotensin I converting enzyme (ACE), and the antiradic

71 othelin 1 (EDN1); we assayed the activity of angiotensin I converting enzyme (ACE), which catalyses t

72 The most hydrolysed sample showed high angiotensin I converting enzyme (ACE)-inhibitory and ant

73 Angiotensin I converting enzyme (kininase II; ACE) inhib

74 e N- and C-terminal domains of human somatic angiotensin I converting enzyme (sACE-1) demonstrate dis

75 Susceptibility to infection correlated with angiotensin I converting enzyme 2 (ACE2) expression leve

76 encoded residues dominate recognition of the angiotensin I converting enzyme 2 (ACE2)-binding site.

77 ells expressing the SARS-CoV receptor, human angiotensin I converting enzyme 2 (hACE2).

78 II type 1 receptor antagonist (AT1RA) and/or angiotensin I converting enzyme inhibitor (ACEI) were in

79 HE to HE continuum is specifically marked by angiotensin-I converting enzyme (ACE) expression.

80 and mechanism of action towards antioxidant, angiotensin-I converting enzyme (ACE) inhibition, and di

81 activity (DPPH), degree of hydrolysis (DH), angiotensin-I converting enzyme (ACE) inhibitory activit

82 Angiotensin-I converting enzyme (ACE) is a zinc dipeptid

83 Angiotensin-I converting enzyme (ACE) is a zinc metallop

84 egation analysis have shown that circulating angiotensin-I converting enzyme (ACE) levels are influen

85 Angiotensin-I converting enzyme (ACE) regulates the leve

86 Angiotensin-I converting enzyme (ACE) regulates the reni

87 Angiotensin-I converting enzyme (ACE), a two-domain dipe

88 he causes of hypertension is the activity of angiotensin-I converting enzyme (ACEI), making its inhib

89 Previously, we have shown that loss of angiotensin-I converting enzyme 2 (ACE2) promotes the AC

90 An insertion polymorphism of the angiotensin-I converting enzyme gene (ACE) is common in

91 or FT was assessed to release peptides with angiotensin-I converting enzyme inhibition (ACEi) and di

92 are also less responsive to monotherapy with angiotensin-I converting enzyme inhibitors or angiotensi

93 sk diverse population where monotherapy with angiotensin-I converting enzyme inhibitors or angiotensi

94 sweetness, bitterness and umami, as well as angiotensin-I converting enzyme inhibitory activity.

95 xidant activity persisted, and inhibition of angiotensin-I converting enzyme was improved after the d

96 haracteristics, and in vitro antioxidant and Angiotensin-I converting enzyme-inhibitory activities we

97 ddition to the extract's capacity to inhibit angiotensin I-converting enzyme (ACE) activity.

98 Using inhibitors of angiotensin I-converting enzyme (ACE) and CP, we show th

99 fraction of the heart and skeletal muscles, angiotensin I-converting enzyme (ACE) and neutral endope

100 g white, and (ii) evaluate the inhibition of angiotensin I-converting enzyme (ACE) by the obtained hy

101 n expended to determine whether the gene for angiotensin I-converting enzyme (ACE) confers susceptibi

102 The peptide inhibition of the angiotensin I-converting enzyme (ACE) from its default b

103 The A-240T and I/D polymorphisms in the angiotensin I-converting enzyme (ACE) gene are markers o

104 Angiotensin I-converting enzyme (ACE) hydrolyzes numerou

105 dipeptidyl peptidase-IV (DPP-IV) (0.62) and angiotensin I-converting enzyme (ACE) inhibitor peptides

106 Part of the beneficial effects of angiotensin I-converting enzyme (ACE) inhibitors are due

107 Angiotensin I-converting enzyme (ACE) inhibitors derived

108 To investigate how angiotensin I-converting enzyme (ACE) inhibitors enhance

109 Angiotensin I-converting enzyme (ACE) inhibitors have be

110 To investigate further the relationship of angiotensin I-converting enzyme (ACE) inhibitors to acti

111 es, majority of them were found identical to angiotensin I-converting enzyme (ACE) inhibitors, antiox

112 The angiotensin I-converting enzyme (ACE) inhibitory activit

113 hiols content but at the same time increased angiotensin I-converting enzyme (ACE) inhibitory activit

114 The angiotensin I-converting enzyme (ACE) inhibitory activit

115 In addition, the effects of digestion on the angiotensin I-converting enzyme (ACE) inhibitory activit

116 This study aimed to screen novel angiotensin I-converting enzyme (ACE) inhibitory peptide

117 Angiotensin I-converting enzyme (ACE) inhibitory peptide

118 showed different amino acid compositions and angiotensin I-converting enzyme (ACE) inhibitory potenti

119 We determined the influence of angiotensin I-converting enzyme (ACE) insertion (I)/dele

120 Pedigree analyses have shown that angiotensin I-converting enzyme (ACE) levels are influen

121 Angiotensin I-converting enzyme (ACE), one of the centra

122 Although both LFHs <3 kDa showed in vitro angiotensin I-converting enzyme (ACE)-inhibitory activit

123 anti-obesity, immunomodulatory, antioxidant, angiotensin I-converting enzyme (ACE)-inhibitory, anti-m

124 ion (D) polymorphism (indel) of the gene for angiotensin I-converting enzyme (ACE).

125 bitory effects against alpha-glucosidase and angiotensin I-converting enzyme (ACE).

126 s established for oligopeptides that inhibit angiotensin I-converting enzyme (ACE).

127 Angiotensin I-converting enzyme (ACE)2, a new component

128 Angiotensin I-converting enzyme (ACE, or DCP1) is a zinc

129 Angiotensin I-converting enzyme (ACE, peptidyl dipeptida

130 eported previously a novel mode of action of angiotensin I-converting enzyme (kininase II; ACE) inhib

131 Human somatic angiotensin I-converting enzyme (sACE) has two active si

132 Human somatic angiotensin I-converting enzyme (sACE) is a key regulato

133 valuate transgenic mice expressing the human angiotensin I-converting enzyme 2 (ACE2) receptor driven

134 gain insights into its interactions with the angiotensin I-converting enzyme 2 (ACE2)-solute carrier

135 as associated with a significant decrease in angiotensin I-converting enzyme activity and a small, bu

136 pairs, we identified 91 that had discordant angiotensin I-converting enzyme and glutathione S-transf

137 nd an insertion/deletion polymorphism of the angiotensin I-converting enzyme gene (ACE) may be relate

138 These results confirm the association of the angiotensin I-converting enzyme indel with Alzheimer's d

139 amino groups, GABA content, antioxidant and angiotensin I-converting enzyme inhibitory (ACEI) activi

140 ffect on proteolysis and negatively affected angiotensin I-converting enzyme inhibitory activity of f

141 acids), bioactivity (antioxidant effect and angiotensin I-converting enzyme inhibitory activity), rh

142 y HRV only in the 20 participants using ACE (angiotensin I-converting enzyme) inhibitors.

143 system gene regions (angiotensinogen, renin, angiotensin I-converting enzyme, and angiotensin II rece

144 nst alpha-glucosidase, pancreatic lipase and angiotensin I-converting enzyme, using in vitro models.

145 inc metalloprotease whose closest homolog is angiotensin I-converting enzyme.

146 -binding proteins were identified as porcine angiotensin-I-converting enzyme (ACE I) and aminopeptida

147 hey protein hydrolysates (WPHs) obtained had angiotensin-I-converting enzyme (ACE) and dipeptidyl pep

148 work in animals suggests that inhibitors of angiotensin-I-converting enzyme (ACE) protect against ca

149 l phenotype [C1Inh, C4, spontaneous amidase, angiotensin-I-converting enzyme (ACE), aminopeptidase P

150 eutral endopeptidase (NEP, EC 3.4.24.11) and angiotensin-I-converting enzyme (ACE, EC 2.4.15.1), have

151 Angiotensin-I-converting enzyme (ACE-I) plays a key role

152 Angiotensin-I-converting enzyme activities were 58 (44-7

153 Inhibition of angiotensin is crucial in treatment of chronic kidney di

154 tidase that cleaves a single amino acid from angiotensin I, des-Arg bradykinin, and many other bioact

155 mast cell degranulation released enzyme with angiotensin I-forming activity blocked by the selective

156 The angiotensin I-forming activity of the renin protein was

157 al peptide hormones including bradykinin and angiotensin I have been described as substrates.

158 Angiotensin I, II, and III produced concentration-depend

159 Angiotensin I, II, and III; angiotensin-converting enzym

160 We determined the effect of angiotensin I, II, III, and IV and angiotensin-(1-7) on

161 in concentrations correlated positively with angiotensin I/II ratios (r = 0.39; P < 0.001).

162 he HDX rates for a small 10-residue peptide, angiotensin I, in aqueous droplets, from which we found

163 In response to chronic angiotensin I infusions, ACE 9/9 mice displayed increase

164 ward their receptors, CPA6 converts inactive angiotensin I into the biologically active angiotensin I

165 Angiotensin-converting enzyme (ACE) converts angiotensin I into the potent vasoconstrictor angiotensi

166 P1) is a zinc metallopeptidase that converts angiotensin I into the vasoactive and aldosterone-stimul

167 es were not effective for the enhancement of angiotensin I ions.

168 [Pro(11)(D)-Ala(12)] angiotensin I is an ACE-resistant substrate specific for

169 io (10-fold enhancement) in the detection of angiotensin I is demonstrated using the DRILL interface

170 nogen have normal fertility, indicating that angiotensin I is not a necessary substrate for testis AC

171 The best-known natural substrate, angiotensin I, is cleaved to generate vasoactive angiote

172 andards of polycyclic aromatic hydrocarbons, angiotensin I, lidocaine, ferrocene, diesel, and rosemar

173 cleavage of the peptide bond at proline for angiotensin I, Lys-bradykinin, and myoglobin are demonst

174 e state distributions was investigated using angiotensin I (M(r) = 1296), insulin (M(r) = 5774), and

175 ation of recombinant L-type Ca2+ channels by angiotensin is mediated by inositol trisphosphate-induce

176 in higher levels (16 +/- 6 versus 6 +/- 3 ng angiotensin I/ml per h, group 1 versus group 2, P = 0.01

177 old rats (13.9 +/- 3.8 versus 2.9 +/- 0.8 ng angiotensin I/ml per min), respectively.

178 onditions (1.3 +/- 0.2 versus 1.8 +/- 0.3 ng angiotensin I/ml per min).

179 amide), but did not display activity towards angiotensin I (NRVYIHPFHL), des-Arg bradykinin and AF1 (

180 ed to confirm intact deposition of [Val (5)]-Angiotensin I on a surface.

181 t significantly inhibit the effect of either angiotensin I or angiotensin II.

182 s for limit of detection was performed using angiotensin I peptide.

183 response to ACE inhibition (-0.4+/-0.4 ng of angiotensin I per milliliter per hour, as compared with

184 CNP inhibited the vasoconstrictive effect of angiotensin I (reduction in overall effect with CNP, 56.

185 ttomole detection limits of a model peptide (angiotensin I) spiked into a complex mixture (in this ca

186 d ACE2 activity toward its natural substrate angiotensin I, suggesting that they would be functional

187 Using a solution of angiotensin I, the carbon fiber emitter in 75-microm-i.d

188 is responsible for proteolytic activation of angiotensin I to angiotensin II (Ang II), a potent vasoc

189 y plasma proteinase inhibitors and converted angiotensin I to angiotensin II even in undiluted plasma

190 of serine proteases are enzymes that convert angiotensin I to angiotensin II, as well as others that

191 zyme (ACE) act by blocking the conversion of angiotensin I to angiotensin II, which is catalysed by t

192 hydrolyzes the carboxy terminal leucine from angiotensin I to generate angiotensin 1-9, which is conv

193 the carboxy terminal His-Leu dipeptide from angiotensin I to produce a potent vasopressor octapeptid

194 e (ACE) regulates blood pressure by cleaving angiotensin I to produce angiotensin II.

195 so known as ACE) catalyses the conversion of angiotensin I to the physiologically active peptide angi

196 by blocking the ACE-dependent conversion of angiotensin I to the potent vasoconstrictor angiotensin

197 arate bioactive peptides, notably converting angiotensin-I to angiotensin-II and degrading amyloid be

198 ts to trigger the Ace2-to-Ace enzyme switch, angiotensin I-to-II conversion, and cardiac hypertrophy.

199 detection limit of 400 amol was achieved for angiotensin I using the nanofibrous carbon ME-SALDI subs

200 ion of fragments produced in the cleavage of angiotensin I was obtained using liquid chromatography-m

201 A solution of angiotensin I was quantified using this method, and the

202 total ion current peak areas of 500 fmol of angiotensin I were improved by a factor of 2.6 when the

203 rdiac myocytes produce increasing amounts of angiotensin I, which is converted to angiotensin II by t

204 ns accessible to small substrates, including angiotensin I, with activity in serum that is stable wit