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1  (LPA; acting through the LPA1 receptor) and endothelin.
2 othelial cells by vasoactive signals such as endothelins.
3 orsal Jag1 expression but also by inhibiting endothelin 1 (Edn1) expression in the pharyngeal endoder
4 perturbations demonstrates complex roles for Endothelin 1 (Edn1) signaling in the intermediate joint-
5 emonstrate rs9349379 regulates expression of endothelin 1 (EDN1), a gene located 600 kb upstream of P
6 etermine the selective affinity of EDNRA for endothelin 1 (EDN1), its major physiological ligand, and
7 ular density) and the potent vasoconstrictor endothelin 1 (EDN1); we assayed the activity of angioten
8                                              Endothelin 1 (ET-1) evokes histamine-independent pruritu
9 des, of which 3 distinct isoforms exist, and endothelin 1 (ET-1) is the most abundant and the best-ch
10                                              Endothelin 1 (ET-1), mainly produced from vascular endot
11 mpaired vasodilator reactivity and increased endothelin 1 (ET-1)-mediated vasoconstriction, two abnor
12 th the concentration of the vasoconstrictor, endothelin 1 (P = 0.0005), and negatively with the conce
13 eased expression of vasoconstrictor molecule endothelin 1 and a concomitant decrease in vasodilatory
14            We propose that downregulation of endothelin 1 and upregulation of vascular endothelial gr
15 ycoprotein to proteolipid protein 1 and both endothelin 1 and vascular endothelial growth factor.
16 heart, vascular remodeling, and raised serum endothelin 1 levels.
17 e C signaling, glutamate receptor signaling, endothelin 1 signaling, and cardiac hypertrophy signalin
18 ects, but not in vascular dementia, in which endothelin 1 tended to be elevated, perhaps reflecting a
19 r analysis of the Bristol cohort showed that endothelin 1 was reduced in the white matter in Alzheime
20 amma inducible protein 10 (IP10; CXCL10) and endothelin 1 were raised and strongly correlated togethe
21 e complement anaphylatoxins C3a and C5a, and endothelin 1, induced human MCs rapidly to secrete small
22 atory BP), arterial stiffness, nitric oxide, endothelin 1, or blood lipid profile.
23 resence of an endothelin-converting enzyme 1/endothelin 1-SphK positive feedback loop.
24 er quartile); pulmonary hypertension and low endothelin-1 <1.7 pg/mL; lower 3 quartiles); no pulmonar
25 ould be explained by an enhanced response to endothelin-1 (20% greater reduction in lumen diameter, P
26 ls of the endothelium-derived C-terminal-pro-endothelin-1 (both p < 0.02).
27 d cardiovascular progenitors using WNT3A and endothelin-1 (EDN1) human recombinant proteins.
28 nduced glomerulosclerosis is associated with endothelin-1 (EDN1) release by podocytes, which mediates
29 (Ednra) expression and increased circulating endothelin-1 (Edn1).
30 newborn arteries also expresses and releases endothelin-1 (ET-1) and initiates endothelium-dependent
31 s, correlate with increased plasma levels of endothelin-1 (ET-1) and other functional markers of PH i
32 creased levels of the potent vasoconstrictor endothelin-1 (ET-1) and PHT.
33                                              Endothelin-1 (ET-1) antagonists are a possibility becaus
34         Gene profiling identified inter alia endothelin-1 (ET-1) as one of the target genes of P2Y4 i
35            Hepatic production and release of endothelin-1 (ET-1) binding to endothelin B (ETB) recept
36                Previous studies suggest that endothelin-1 (ET-1) contributes to the pathogenesis of E
37                                              Endothelin-1 (ET-1) dose and time-dependently up-regulat
38 ivation of endothelin-A receptor (ET(A)R) by endothelin-1 (ET-1) drives epithelial-to-mesenchymal tra
39 (NGAL), kidney injury molecule-1 (KIM-1) and endothelin-1 (ET-1) during EVKP in a series of discarded
40    Endothelial expression and the release of endothelin-1 (ET-1) in levels sufficient to initiate vas
41                                              Endothelin-1 (ET-1) induces matrix-associated gene expre
42                                              Endothelin-1 (ET-1) is a potent endothelial-derived vaso
43                  The vasoconstrictor peptide endothelin-1 (ET-1) is a transcriptional target of TGF-b
44                                        Since endothelin-1 (ET-1) is implicated in blood pressure (BP)
45 termine whether vascular endothelial-derived endothelin-1 (ET-1) is important for skin Na(+) bufferin
46 ceptor mediating the vasodilatory effects of endothelin-1 (ET-1) is induced by OA-NO2 Inasmuch as ET-
47 tic brain injury or subarachnoid hemorrhage, endothelin-1 (ET-1) is induced resulting in cerebral vas
48                                              Endothelin-1 (ET-1) is involved in the pathogenesis of c
49 estigated whether the potent vasoconstrictor endothelin-1 (ET-1) is involved.
50                                              Endothelin-1 (ET-1) is unique among a broad range of hyp
51                                    Increased endothelin-1 (ET-1) levels, disordered thiol protein sta
52 rum concentrations of the vasoactive protein endothelin-1 (ET-1) occur in the setting of systemic inf
53 The present study investigated the effect of endothelin-1 (ET-1) on cholinergic mechanisms of end-org
54 n endogenous inhibitor of NO production, and endothelin-1 (ET-1) oppose the actions of NO, suggesting
55                                              Endothelin-1 (ET-1) promotes renal damage during cardiov
56 edominantly responsible for producing active endothelin-1 (ET-1), a mitogenic peptide implicated in t
57 ) correlated with increased plasma levels of endothelin-1 (ET-1), a potent vasoconstrictor, in sickle
58                  Vasoconstrictors, including endothelin-1 (ET-1), inhibit myocyte BK channels, leadin
59 ed an endogenous inhibitor of remyelination, Endothelin-1 (ET-1), which is highly expressed in reacti
60 isoproterenol (ISO), phenylephrine (PE), and endothelin-1 (ET-1).
61                                  In EOC, the endothelin-1 (ET-1, EDN1)-endothelin A receptor (ETAR, E
62                                              Endothelin-1 (ET1) synthesis is understood to promote ca
63 ubgroup with pulmonary hypertension and high endothelin-1 (high endothelin-1: >/=1.7 pg/mL; upper qua
64 lin-1; and no pulmonary hypertension and low endothelin-1 (log-rank chi2 = 77.16; P < .01 ).
65  these proteins in DN, and demonstrated that endothelin-1 activates podocytes to release heparanase.
66                                              Endothelin-1 activates the phospholipase C pathway, lead
67 of ARHGAP18 resulted in a failure to secrete endothelin-1 and a reduction in neutrophil transmigratio
68 r basal conditions and after the addition of endothelin-1 and abnormal spontaneous Ca(2+) release eve
69 (OPN) in mouse arteries via local release of endothelin-1 and activation of CREB.
70 y PGP levels associate with both circulating endothelin-1 and acute rejection in cardiac transplant p
71 eraction with GRK2 is inversely regulated by endothelin-1 and CAV1 scaffolding domain after liver inj
72 lacylcarnitines correlated with increases in endothelin-1 and creatinine/cystatin C, respectively.
73                           Epithelial-derived endothelin-1 and fibroblast growth factor were also augm
74 -beta1 signaling and increased expression of endothelin-1 and genes involved in VSMC contraction, hig
75                                     However, endothelin-1 and IL-6 increased, and IL-10 decreased, be
76                                    Levels of endothelin-1 and markers of fibrinolysis and inflammatio
77                                       Plasma endothelin-1 and OPN concentrations are positively corre
78     Despite pathophysiological links between endothelin-1 and pulmonary vascular remodeling, to our k
79 e previously showed that both heparanase and endothelin-1 are essential for the development of DN.
80 es of evidence have demonstrated the role of endothelin-1 as both a constrictor of uterine myometrial
81 tor-2, and the potent vasoconstrictive agent endothelin-1 as compared with control cells.
82                             In injured SECs, endothelin-1 blocked CAV1 phosphorylation induced by CAV
83 y in systemic sclerosis after macitentan, an endothelin-1 blocker.
84 emokine Receptor 2 (CXCR2) and production of endothelin-1 both in vitro and in vivo.
85 a) and the neuroendocrine regulatory peptide endothelin-1 by DH82 cells.
86                                Also, whether endothelin-1 can predict future heart failure and mortal
87                  This evidence suggests that endothelin-1 drives development of glomerulosclerosis an
88  Stimulation of primary mouse podocytes with endothelin-1 elicited rapid calcium transients mediated
89       Mediation analysis showed that BNP and endothelin-1 explained 56% and 40%, respectively, of the
90  pain behavior, epidermal tissue damage, and endothelin-1 expression.
91 ivation and angiotensin-induced increases in endothelin-1 expression.
92  fibroblasts were treated with 20 and 100 nM endothelin-1 for 6 and 24 hours and then collected to as
93 en a modest ( approximately 35%) decrease in endothelin-1 gene (Edn1) expression is sufficient to cau
94 dney vasculature and normalized Tgf-beta and endothelin-1 gene expression in aged MWF rats.
95 array analysis showed increased Tgf-beta and endothelin-1 gene expression with age.
96 generated low-expressing and high-expressing endothelin-1 genes (L and H) and have bred mice with fou
97 phy signaling triggered by angiotensin II or endothelin-1 in HEK293T cells as well as in neonatal and
98 the expression of contractile markers and of endothelin-1 in VSMCs.
99                     In vitro, treatment with endothelin-1 increased total beta-catenin and phospho-NF
100 s not known whether elevated serum levels of endothelin-1 indicate future risk of kidney disease in t
101                             We conclude that endothelin-1 is critical for maintaining normal contract
102  0.05), but not in vascular endothelial cell endothelin-1 knockout (VEET KO) mice (76.4 +/- 5.7 pg/mg
103 ular risk in black adults, we measured serum endothelin-1 level at baseline (2000-2004; n=3538).
104    Phenotyping by pulmonary hypertension and endothelin-1 level showed mortality decreasing in order
105                       Log-transformed plasma endothelin-1 level.
106 ur knowledge, the association between plasma endothelin-1 levels and pulmonary hypertension has not b
107 ied African American individuals with plasma endothelin-1 levels and tricuspid regurgitation on echoc
108         In conclusion, higher baseline serum endothelin-1 levels associated with incident CKD and all
109 en-binding activity, soluble E-selectin, and endothelin-1 levels by using ELISA and BRAHMS Kryptor te
110                   Participants with baseline endothelin-1 levels in higher quartiles had a greater in
111                                    Mean (SD) endothelin-1 levels were 1.36 (0.64) pg/mL; 217 of 3223
112 g for potential confounders, log-transformed endothelin-1 levels were associated with increased odds
113                              Log-transformed endothelin-1 levels were associated with mortality (adju
114         Basal and angiotensin-stimulated big endothelin-1 levels were elevated in Tg(Prkcb)apoE-/- mi
115 terminal telopeptide of collagen type I, and endothelin-1 levels were higher in diabetic patients (p
116                                              Endothelin-1 levels were significantly increased 20 hr a
117                              Elevated plasma endothelin-1 levels, especially associated with an eleva
118 tion of the endothelin-A receptor (EDNRA) by endothelin-1 may play a role in the disease because the
119      However, no direct pathogenic effect of endothelin-1 on podocytes has been shown in vivo and end
120 hese results indicate that activation of the endothelin-1 pathways selectively in podocytes mediates
121                                              Endothelin-1 positively associated with all-cause mortal
122                                              Endothelin-1 promotes mesangial cell proliferation and s
123                                              Endothelin-1 promotes vasculopathy in systemic sclerosis
124  Our data do not support the use of the dual endothelin-1 receptor antagonist, bosentan, in patients
125                               Treatment with endothelin-1 receptor antagonists could theoretically im
126 , whereas pretreatment of rats with the dual endothelin-1 receptor blocker, bosentan, improved cell e
127 ion was associated with increased glomerular endothelin-1 receptor type A (Ednra) expression and incr
128 physiologically important thromboxane A2 and endothelin-1 receptors.
129        Of these, the vasoconstrictive factor endothelin-1 serves as an integral point of communicatio
130 in-1 on podocytes has been shown in vivo and endothelin-1 signaling in podocytes has not been investi
131           Our data suggest that in diabetes, endothelin-1 signaling, as occurs in endothelial activat
132                                              Endothelin-1 stimulated the production of MMP1, MMP8, an
133             These pathways were activated by endothelin-1 through the ETB receptor; inhibiting recept
134 anti-angiotensin II type-1 receptor and anti-endothelin-1 type A receptor autoantibodies are associat
135 tatus for angiotensin II type-1 receptor and endothelin-1 type A receptor autoantibodies pre-LT, and
136           The extracellular concentration of endothelin-1 was increased following GLO1-knockdown, whe
137       Moreover, Ca(2+) release stimulated by endothelin-1 was inhibited by Ned-19, ryanodine, or xest
138  the effect of IRL-1620 [Suc-[Glu9,Ala11,15]-Endothelin-1(8-12)] on astrocytes, neurons, and vascular
139 ious pruritogens (histamine, chloroquine, or endothelin-1) and recorded spontaneous scratching before
140 ddressing 1 abnormality (eg, upregulation of endothelin-1) and were not developed specifically for PA
141 en-binding activity, soluble E-selectin, and endothelin-1) were significantly increased during HAE at
142 to histaminergic (histamine, compound 48/80, endothelin-1), not non-histaminergic (chloroquine) pruri
143 creased production of vasoconstrictors (e.g. endothelin-1).
144 ure to vasoconstrictors (50 mM KCl and 20 nM Endothelin-1).
145  (adjusted hazard ratio per log increment in endothelin-1, 1.57, 95% CI, 1.05-2.37; median follow-up,
146 on (adjusted odds ratio per log increment in endothelin-1, 1.66; 95% CI, 1.16-2.37).
147  (adjusted hazard ratio per log increment in endothelin-1, 1.69; 95% CI, 1.27-2.25; median follow-up,
148                                              Endothelin-1, a marker of endothelial dysfunction, is a
149                                              Endothelin-1, a potent vasoconstrictor, plays an importa
150  is determined by venous endothelium-derived endothelin-1, acting through its specific receptor Ednra
151  activation, such as smooth muscle actin and Endothelin-1, and all of these genes play a key role in
152 (ICAM-1), anti-LG3, aminopeptidase N, CXCL9, endothelin-1, and gelsolin.
153 transforming growth factor beta1 (TGFbeta1), endothelin-1, and NAD(P)H oxidase 4 also occur in parall
154 k involving transforming growth factor-beta, endothelin-1, angiotensin II, CCN2 (connective tissue gr
155 procalcitonin, MR-pro-adrenomedullin, CT-pro-endothelin-1, CT-pro-arginine vasopressin, and MR-pro-at
156 such as transforming growth factor beta1 and endothelin-1, enhance RBC NADPH oxidase activity and inc
157 tes production of the potent vasoconstrictor endothelin-1, producing pulmonary hypertension.
158 l as in human disease, including the role of endothelin-1, pulmonary monocytes, and angiogenesis.
159 iewed, including nitric oxide, prostacyclin, endothelin-1, reactive oxygen species, and endothelial a
160 with elevated vasoconstrictor signalling via endothelin-1, reduces the local vasodilatory response to
161 activated gene networks involved in calcium, endothelin-1, renin-angiotensin, and cardiac beta-adrene
162 pro-B-type natriuretic peptide, aldosterone, endothelin-1, troponin I, and C-telopeptide for type I c
163 s elicited by phenylephrine, angiotensin II, endothelin-1, U46619, and K(+)-induced membrane depolari
164 n enhances epidermal expression of TRPV4 and endothelin-1, underscoring the potential of keratinocyte
165 ce has been associated with raised levels of endothelin-1, which are common both before and after Fon
166 es was increased expression and secretion of endothelin-1, which is also a known pruritogen.
167 on of vascular endothelial growth factor and endothelin-1.
168 zed mesenteric arteries pre-constricted with endothelin-1.
169 cluding BNP (B-type natriuretic peptide) and endothelin-1.
170 ary hypertension and high endothelin-1 (high endothelin-1: >/=1.7 pg/mL; upper quartile); pulmonary h
171 artiles); no pulmonary hypertension and high endothelin-1; and no pulmonary hypertension and low endo
172 a and recruitment of vasoconstrictors (e.g., endothelin-1; Edn1) leads to clearance of transplanted c
173 ased pressor responses to angiotensin II and endothelin-1; these effects are prevented by treatment w
174 ise in the expression of the vasoconstrictor endothelin 2 by follicle cells of wild-type mice.
175 e mice, infusion of vasoconstrictors (either endothelin 2 or angiotensin 2) into the bursa restored t
176  responsible for this regenerative effect of endothelin 2, analysis of both remyelination following e
177 etinae identified several cytokines (CXCL13, endothelin 2, CCL20 and CXCL2) to be significantly upreg
178  Although increasing evidence indicates that endothelin-2 (Edn2) has distinct roles in tissue patholo
179                                              Endothelin-2 (EDN2) is a potent vasoconstrictor that is
180 in white mutants a transcriptional defect in endothelin 3 (edn3), encoding a peptide factor that prom
181 d by molecules such as the signaling protein endothelin 3 (EDN3), its receptor (the endothelin recept
182                             Mechanistically, endothelin A receptor (ETAR)-positive macrophages are hi
183 on of its cognate G protein-coupled receptor endothelin A receptor (ETAR).
184        In EOC, the endothelin-1 (ET-1, EDN1)-endothelin A receptor (ETAR, EDNRA) signaling axis regul
185                      Atrasentan, a selective endothelin A receptor antagonist, has been shown to redu
186 ion of similar magnitude (P </= 0.05) of the endothelin A receptor in the lung tissue.
187 dothelin signaling via the activation of the endothelin-A receptor (EDNRA) by endothelin-1 may play a
188                                Activation of endothelin-A receptor (ET(A)R) by endothelin-1 (ET-1) dr
189 o three groups: placebo (RVD+PTRAS), chronic endothelin-A receptor (ET-A) blockade (RVD+PTRAS+ET-A),
190 g-term treatment strategy with the selective endothelin-A receptor (ETA) antagonist, ambrisentan, des
191                              While targeting endothelin and angiotensin, which are upstream regulator
192 factor, vascular endothelial growth factor), endothelin and inhibitors of chemotaxis.
193 increases in angiogenic mediators, including endothelins and endothelin receptor (EDNR) A.
194 tion persists in the absence of endothelium, endothelin, and cyclooxygenase mediators.
195 ion of natriuretic peptides, adrenomedullin, endothelin, and galectin-3 with new-onset HF was stronge
196 n various mediators, including nitric oxide, endothelin, and prostanoids, among others.
197 oncentration of catecholamines, vasopressin, endothelin, and renin activity in 14 patients with CIPA,
198  consisting of prostacyclin and its analogs, endothelin antagonists, phosphodiesterase-5 inhibitors,
199                                              Endothelins are a family of vasoactive peptides, of whic
200                                              Endothelins are potent vasoconstrictors and signaling mo
201                                          The endothelin axis and in particular the two endothelin rec
202 development of novel therapies targeting the endothelin axis.
203                                          The endothelin B (ETB) receptor is a G-protein-coupled recep
204 nd release of endothelin-1 (ET-1) binding to endothelin B (ETB) receptors, overexpressed in the lung
205 lular loop (IL2 or IL3, respectively) of the endothelin B receptor (ETB).
206  to a cysteine sulfenic acid modification in endothelin B receptor and consequently decreased endothe
207 BR-4628 against IR was lost when a selective endothelin B receptor antagonist was coadministered.
208 a nicotinic receptor (CHRNG, 6 subjects) and endothelin converting enzyme-like 1 (ECEL1, 4 subjects).
209                               Members of the endothelin-converting enzyme (ECE) family are considered
210 nists (BQ123 plus BQ788) or by inhibition of endothelin-converting enzyme (phosphoramidon or SM19712)
211              Here, we have identified neural endothelin-converting enzyme 1 (ECE-1) as a key regulato
212 ned whether agonist degradation by endosomal endothelin-converting enzyme 1 (ECE-1) controls SSTR2A t
213 -1 expression, indicating the presence of an endothelin-converting enzyme 1/endothelin 1-SphK positiv
214                                              Endothelin-converting enzyme-1 (ECE-1) is the enzyme pre
215                                              Endothelin-converting enzyme-1 (Ece-1), a crucial compon
216 t inhibition of SphK leads to suppression of endothelin-converting enzyme-1 expression, indicating th
217 ltiplex consanguineous family to identify in endothelin-converting enzyme-like 1 (ECEL1) mutations th
218 th virulence and has a putative action as an endothelin-converting enzyme.
219                      We further identify the endothelin/Ednra pathway as an autocrine activator of Gq
220                      This study investigated endothelin effects in podocytes during experimental diab
221 strictive and vascular remodeling actions of endothelin (ET) 1 and angiotensin (Ang) II via endotheli
222 nd tumor necrosis factor-alpha, to stimulate endothelin (ET) and ET receptor (ETR) expression in brea
223  receptors (GPCRs), including adrenergic and endothelin (ET) receptors, after elevated neurohormonal
224 n the renin-angiotensin system (RAS) and the endothelin (ET) system as dual vasopeptidase inhibitors
225 layed a vasoconstriction response to KCl and endothelin for each experimental group.
226 osis factor-alpha, IL-1b, troponin, vascular endothelin growth factor, IL-17a, matrix metallopeptidas
227                                              Endothelin-induced vasoconstriction by hepatic stellate
228 C-dependent, positive-feedback mechanism for Endothelin induction and establish MEF2C as an immediate
229 est enhancer from the mouse genome abolishes Endothelin induction of Mef2c expression.
230 alyzed the expression of the complete set of endothelin ligands and receptors in the jawless vertebra
231 S/MS to identify NT-proET-1 (ppET-1[18-50]), Endothelin-Like Domain Peptide (ELDP, ppET-1[93-166]) an
232     ELDP contains the evolutionary conserved endothelin-like domain sequence, which potentially confe
233           Moreover, the results suggest that endothelin pathways have a role in the pathogenesis of M
234 iogenic mediators, including endothelins and endothelin receptor (EDNR) A.
235 y by Jagged-Notch signaling and ventrally by endothelin receptor A (EDNRA) signaling.
236                                              Endothelin receptor A (ETA), a G protein-coupled recepto
237                                              Endothelin receptor A blockade in vitro did not improve
238  angiogenesis by Edn2 requires expression of Endothelin receptor A but not Endothelin receptor B in t
239                          Conditional loss of endothelin receptor A in granulosa cells also decreased
240                                          The endothelin receptor antagonist is among the most effecti
241 us epoprostenol were weaned off post-LT, and endothelin receptor antagonist or phosphodiesterase type
242 mendation for either prostacyclin agonist or endothelin receptor antagonist therapy and a strong reco
243                                              Endothelin receptor antagonists (ERA) and phosphodiester
244 s of disease-targeted therapy (predominantly endothelin receptor antagonists [47.3%] or phosphodieste
245                                              Endothelin receptor antagonists have emerged as a novel
246                    Additionally, infusion of endothelin receptor antagonists into the bursa of wild-t
247 were receiving riociguat in combination with endothelin receptor antagonists or prostanoids, or both.
248 erent classes of drugs are now available-ie, endothelin receptor antagonists, phosphodiesterase-5 inh
249 se biological effects that are unaffected by endothelin receptor antagonists.
250                             We observed that endothelin receptor B [ET-B (gene name EDNRB)], the rece
251  expression of Endothelin receptor A but not Endothelin receptor B in the neural retina.
252 ts may constitute the mechanism of action of endothelin receptor blockers in DN.
253   In mice, podocyte-specific knockout of the endothelin receptor prevented the diabetes-induced incre
254                                          The endothelin receptor type A (EDNRA) signaling pathway is
255 dothelin (ET) 1 and angiotensin (Ang) II via endothelin receptor type A (ETAR) and Ang receptor type-
256                 These cells highly expressed endothelin receptor type B (ETB(R)) and Jagged1, a Notch
257 otein endothelin 3 (EDN3), its receptor (the endothelin receptor type B [EDNRB]), and the transcripti
258                               Antagonists of endothelin receptor type B also inhibited remyelination
259 n post-mortem tissue revealed high levels of endothelin receptor type B in oligodendrocyte lineage ce
260 genome sequencing, we discovered that EDNRB (Endothelin receptor type B) is a candidate gene involved
261 development and suggest that modification of endothelin receptor-ligand specificity was a key step in
262 essed the efficacy of macitentan, a new dual endothelin-receptor antagonist, using a primary end poin
263                                              Endothelin-receptor antagonists are in clinical use to t
264 hypertension and patients who were receiving endothelin-receptor antagonists or (nonintravenous) pros
265  the disease and in those who were receiving endothelin-receptor antagonists or prostanoids.
266 c receptors, alpha-adrenergic receptors, and endothelin receptors (among others) have been associated
267 d podocyte loss through direct activation of endothelin receptors and NF-kappaB and beta-catenin path
268                                              Endothelin receptors are also expressed on the human ecc
269  ednra and ednrb, the genes encoding the two Endothelin receptors in mice, were born at predicted Men
270 he endothelin axis and in particular the two endothelin receptors, ETA and ETB, are targets for thera
271                                 We show that Endothelin signaling activates Mef2c expression in the n
272                Moreover, we demonstrate that Endothelin signaling activates neural crest expression o
273     These data suggest that OA-NO2 modulates endothelin signaling by increasing Nrf2-dependent expres
274 duplication and specialization of vertebrate Endothelin signaling coincided with the appearance of hi
275  ednr expression, we also analyzed all known Endothelin signaling components in the African clawed fr
276                To test the potential role of endothelin signaling diversification in the evolution of
277 nscriptional effectors directly activated by Endothelin signaling during neural crest development rem
278 he cardiac conduction system in mice lacking Endothelin signaling has not been previously addressed.
279 amine in more detail the effect of OA-NO2 on endothelin signaling in human endothelial cells.
280                         However, the role of Endothelin signaling in mammalian conduction system deve
281 tream transcriptional target and effector of Endothelin signaling in the neural crest.
282 diate transcriptional effector and target of Endothelin signaling in the neural crest.
283                        In jawed vertebrates, Endothelin signaling involves multiple functionally dist
284 r neural crest development, and dysregulated Endothelin signaling is associated with several neural c
285 thin the developing mammalian heart and that Endothelin signaling is dispensable for specification an
286                                              Endothelin signaling is essential for neural crest devel
287                                              Endothelin signaling is required for neural crest migrat
288  primarily on gain-of-function studies, that Endothelin signaling is responsible for myocyte-to-Purki
289 enzyme-1 (Ece-1), a crucial component of the Endothelin signaling pathway, is required for embryonic
290                                              Endothelin signaling regulates several aspects of NCC de
291                                              Endothelin signaling via the activation of the endotheli
292 ETA), a G protein-coupled receptor, mediates endothelin signaling, which is regulated by GRK2.
293 nduction system in mouse embryos lacking all Endothelin signaling.
294                                          The endothelin system has emerged as a novel target for the
295       We hypothesized that activation of the endothelin system via EDNRA plays a causal role in patho
296  FRET-based biosensors, we show that LPA and endothelin transiently activate Cdc42 through Gi, concur
297 es to angiotensin type 1 receptor (AT1R) and endothelin type A receptor (ETAR) is associated with all
298 s significantly increased by blockade of the endothelin type A receptor with ABT-627 (0.116 +/- 0.006
299 licited rapid calcium transients mediated by endothelin type A receptors (ETARs) and endothelin type
300 d by endothelin type A receptors (ETARs) and endothelin type B receptors (ETBRs).

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