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1 ensin-converting enzyme inhibitor or lacking angiotensinogen.
2 ompletely, compensate for excess circulating angiotensinogen.
3 suppressed the expression of vasoconstrictor angiotensinogen.
4 on of fat-derived peptides (PAI-1 by 4-fold, angiotensinogen 3-fold, leptin 2-fold, resistin 4-fold,
6 eleased by the enzyme renin from the tail of angiotensinogen-a non-inhibitory member of the serpin fa
7 n PE at altitude than at sea level, yet PRR, angiotensinogen (AGT) and AT1R proteins were all increas
10 tes) with two, three, and four copies of the angiotensinogen (Agt) gene (Vpr-Agt-2, Vpr-Agt-3, and Vp
11 oid 2-related factor 2 (Nrf2) stimulation of angiotensinogen (Agt) gene expression and the developmen
12 onucleoprotein F (hnRNP F) overexpression on angiotensinogen (Agt) gene expression, hypertension, and
13 ressure, we sequenced a 6.8 kb region of the angiotensinogen (AGT) gene in 29 male Nigerians with hig
14 k factor for cardiovascular disease, and the angiotensinogen (AGT) gene locus is associated with huma
15 ugh previous studies have suggested that the angiotensinogen (AGT) gene locus is involved in human es
17 ork showed that TGF-beta1 potently increases angiotensinogen (AGT) gene mRNA in primary human lung fi
18 riants in the RREB1 gene, a repressor of the angiotensinogen (AGT) gene previously associated with ki
19 on among the M235T and T174M variants of the angiotensinogen (AGT) gene, plasma AGT, and hypertension
20 hisms in the 5' flanking region of the human angiotensinogen (AGT) gene, the -20 and -217 polymorphis
26 ntisense oligonucleotide (ASO) that inhibits angiotensinogen (Agt) synthesis to lisinopril in adult c
28 osomal regions containing genes for the ACE, angiotensinogen (AGT), and angiotensin II type 1 recepto
29 such as angiotensin-converting enzyme (ACE), angiotensinogen (AGT), and angiotensin receptor type I (
30 cluding angiotensin-converting enzyme (ACE), angiotensinogen (AGT), and the type 1 (AT1) and type 2 (
32 ingle-nucleotide polymorphisms (SNPs) in the angiotensinogen (AGT), angiotensin receptor 1 (AGTR1), a
33 leotide polymorphisms (SNPs) at renin (REN), angiotensinogen (AGT), angiotensin-converting enzyme (AC
35 we explored the role of genetic variants of angiotensinogen (AGT, M235T), ACE (I/D), and angiotensin
36 ta, epidermal growth factor receptor [EGFR], angiotensinogen [AGT]) were tested in urine (Ur) and per
37 ine CC-4, angiotensin-converting enzyme, and angiotensinogen, although the direction of effect was re
41 large increases in plasma concentrations of angiotensinogen and angiotensin peptides (Ang II, III, I
42 lemia was associated with increased systemic angiotensinogen and angiotensin peptides, which were red
43 tribution of mast cells, and the presence of angiotensinogen and angiotensin-converting enzyme in man
44 Inasmuch as myocardial interstitium contains angiotensinogen and angiotensin-converting enzyme, and b
45 h the findings demonstrating the presence of angiotensinogen and angiotensinogen mRNA in proximal tub
46 f p53 was associated with an accumulation of angiotensinogen and AT(1) and enhanced production of ang
48 a significant decrease in circulating human angiotensinogen and markedly blunted the pressor respons
49 ute significantly to the circulating pool of angiotensinogen and provide proof-of-principle that the
50 rting enzyme locus on chromosome 17, nor the angiotensinogen and renin loci on chromosome 1, with eit
51 blot analyses showed increased expression of angiotensinogen and renin protein at 16 to 24 hours of s
53 eed, they express renin, the renin receptor, angiotensinogen, and angiotensin-converting enzyme by mR
54 ("visceral white"), including the resistin, angiotensinogen, and chemerin genes, in addition to indu
55 Increased intracellular levels of Ang II, angiotensinogen, and renin were observed by confocal mic
56 sequence (St domain) in the promoter of the angiotensinogen (ANG) gene and consequently upregulate t
59 53 was characterized by upregulation of Bax, angiotensinogen, Ang type 1 (AT(1)) receptors, and Ang I
61 wn to stimulate expression of the endogenous angiotensinogen, angiotensin-converting enzyme, and endo
64 ma and liver protein using a polyclonal anti-angiotensinogen antibody demonstrated two specific immun
67 pression of p53-dependent genes; quantity of angiotensinogen (Aogen), AT(1), and Bax decreased, where
69 On this basis, p53 DNA binding activity to angiotensinogen (Aogen), bax, and the AT1 receptor was d
70 ance, and renal mRNA levels of its precursor angiotensinogen are increased 2-fold in B-129/Sv-4A11(+/
71 tions of AngII, as well as angiotensin I and angiotensinogen, are much greater than can be explained
74 Angiotensin I (Ang I) was generated from angiotensinogen by cathepsin D in the presence of normal
75 II derived from local synthesis of renin and angiotensinogen can cause an elevation in blood pressure
76 tensin II (Ang II) receptors, we mutated the angiotensinogen cDNA by removing the signal sequence-enc
77 WT-p90RSK-Tg mice, suggesting an increase of angiotensinogen cleavage and subsequent RAS activation i
79 otype is virtually identical to that seen in angiotensinogen-deficient (Agt-/-) and angiotensin-conve
81 es demonstrate that extra-hepatic sources of angiotensinogen do not contribute significantly to the c
82 ssociated with preeclampsia, we investigated angiotensinogen expression in the first trimester uterus
83 further show that repression of resistin and angiotensinogen expression involves recruitment of CtBP1
85 five genetically determined levels of mouse angiotensinogen gene (Agt) expression covering the range
86 nked to differential expression of the human angiotensinogen gene (AGT) gene and hypertension, but th
87 o determine whether common haplotypes in the angiotensinogen gene (AGT), the renin gene, the angioten
89 hose found in mutant mice homozygous for the angiotensinogen gene (Agt-/-), indicating that major bio
91 e- and cell-specific expression of the human angiotensinogen gene and normally produce and process th
92 reduction on renin release, renal renin and angiotensinogen gene expression and the role played by a
93 We conclude that increased NF-kappaB and angiotensinogen gene expression are associated with R-FS
95 t suppressed basal levels of renal renin and angiotensinogen gene expression; (b) acute reduction of
96 generated transgenic mice containing a human angiotensinogen gene flanked by loxP sites (hAGT(flox)).
97 ogic consequences of tissue-specific loss of angiotensinogen gene function in vivo, we constructed an
101 tion in the mice having only one copy of the angiotensinogen gene is greater than twice wild-type.
102 They are hypertensive, and expression of the angiotensinogen gene is increased in their subcutaneous
103 his transgenic mouse model is that the human angiotensinogen gene is inserted into the mouse genome a
106 vity of reporter constructs containing human angiotensinogen gene promoter (with nucleoside A at -20)
109 r alpha (TNFalpha), is a potent activator of angiotensinogen gene transcription in hepatocytes by act
110 mouse model generated by targeting the human angiotensinogen gene upstream of the mouse HPRT locus by
111 S (ACE gene, Angiotensin II receptor 1 gene, Angiotensinogen gene) in 233 liver transplant recipients
112 gen genes can functionally replace the mouse angiotensinogen gene, and provides proof in principle th
113 evidence that individual differences in the angiotensinogen gene, the precursor of the vasoactive ho
117 ransgenic for both the human renin and human angiotensinogen genes (RA+) exhibit appropriate tissue-
118 e studies establish that the human renin and angiotensinogen genes can functionally replace the mouse
119 consisting of both the human renin and human angiotensinogen genes to study further the role played b
120 ice containing a PAC transgene and the human angiotensinogen (hAGT) gene (P+/A+) are moderately hyper
124 ed protein (KAP) promoter fused to the human angiotensinogen (HAGT) gene with the goal of specificall
125 containing the human renin (HREN) and human angiotensinogen (HAGT) genes were bred to mice heterozyg
126 EN) and bred them with mice expressing human angiotensinogen (hAGT) under the control of the same pro
128 Furthermore, male and female mice lacking angiotensinogen have normal fertility, indicating that a
129 lpha, nuclear factor-kappaB (NF-kappaB), and angiotensinogen in 60 biopsies from 27 pediatric renal t
130 tion may not affect intracellular sorting of angiotensinogen in a qualitative manner, it leads to a q
132 y defined, but include enhanced formation of angiotensinogen, increased sodium reabsorption, and incr
133 nogen upregulation and remodeling of cardiac angiotensinogen interaction networks in P21 Kcne2(-/-) m
135 e we show that the reduced unbridged form of angiotensinogen is present in the circulation in a near
137 th R-30P showed a tendency to lowered plasma angiotensinogen level (1563 ng of ANG I/ml (range 1129-1
138 ing that chronic overexpression of renin and angiotensinogen locally in the brain can result in hyper
140 lity that increases in circulating or tissue angiotensinogen may cause an increase in blood pressure
141 ed to determine whether augmented intrarenal angiotensinogen may contribute to the enhanced renal ang
144 y in the transgenic alpha-myosin heavy chain-angiotensinogen mice causes prominent changes in hypertr
145 is revealed the absence of full-length human angiotensinogen mRNA and protein in the liver but not th
147 that chronic AngII infusion increases renal angiotensinogen mRNA and protein levels, thus contributi
149 strating the presence of angiotensinogen and angiotensinogen mRNA in proximal tubule cells, the data
150 circulating AngII levels increase intrarenal angiotensinogen mRNA levels, which may contribute to the
152 This occurs after LPS increases TLR4 and angiotensinogen mRNA, but proximal to AT(1) receptor act
155 induction of left ventricular hypertrophy in angiotensinogen-overexpressing transgenic mice harboring
156 a potential 20-HETE dependence of intrarenal angiotensinogen production and ANGII receptor type 1 act
157 s indicate that SHR have enhanced intrarenal angiotensinogen production that contributes to increased
158 bind to a sequence motif (St-domain) in the angiotensinogen promoter to activate its transcription i
159 inkage disequilibrium with a mutation in the angiotensinogen promoter, G(-6)A, which leads to elevate
162 or 64-kD), renal (52-kD), or hepatic (52-kD) angiotensinogen protein levels; however, there was a sig
163 induction of PRECE was confirmed with serial angiotensinogen protein reduction after perfusion in WT-
164 expression of the highly glycosylated 64-kD angiotensinogen protein, of almost fourfold (densitometr
167 ely inhibited Ang II-induced upregulation of angiotensinogen, renin, and ACE genes, as well as stretc
168 s with Ang II also upregulated expression of angiotensinogen, renin, and ACE genes, whereas it downre
169 four renin-angiotensin system gene regions (angiotensinogen, renin, angiotensin I-converting enzyme,
170 ffect of mechanical stretch on expression of angiotensinogen, renin, angiotensin-converting enzyme (A
172 nal cells in culture with human prorenin and angiotensinogen resulted in increased generation of angi
174 romoter of the gene encoding its prohormone, angiotensinogen, serves as the target site for activated
176 tation at the -30 amino acid position of the angiotensinogen signal peptide, in which an arginine is
178 nvolved the genes governing the structure of angiotensinogen, the substrate in the renin reaction.
179 e loci affecting BP variation are known (eg, angiotensinogen), there are likely to be novel signals t
180 ive reduction in the net secretion of mature angiotensinogen through decreased translocation or incre
181 ose that this redox-responsive transition of angiotensinogen to a form that will more effectively rel
182 stem that permit intracellular processing of angiotensinogen to Ang II and that Ang II generated intr
183 ils 1) converts both human angiotensin I and angiotensinogen to angiotensin II; 2) expresses angioten
185 ed with transgenic mice overexpressing human angiotensinogen to determine if there was a chronic comp
186 ally, we demonstrate the oxidative switch of angiotensinogen to its more active sulphydryl-bridged fo
188 port, we describe the development of a human angiotensinogen transgenic mouse model generated by targ
189 d putative ion channel targets, namely AT1R, angiotensinogen, transient receptor potential channel 6
190 script transcriptomics, we uncovered cardiac angiotensinogen upregulation and remodeling of cardiac a
193 ee system, we found that two forms of native angiotensinogen were generated by alternative initiation
194 tutively secreted proteins IgG, albumin, and angiotensinogen, when added to the assays, remain predom
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