ライフサイエンスコーパス: ET-3

1 migrated toward ET-1 and ET-2 but not toward ET-3.

2 ), as judged by a potency rank order of ET-1 ET-3.

3 bitor of guanylate cyclase activation, or by ET-3.

4 residues, 34-38 in big ET-1 and 34-41 in big ET-3.

5 rfusion when injected 10 or 90 min following ET-3.

6 ET-1 and which have the sequence QTVP in big ET-3.

7 ed, using antibodies raised against ET-1 and ET-3.

8 these same sites, but was not stimulated by ET-3.

9 < 0.01) and PLIN5 expression (SIT 2.2-fold, ET 3.1-fold; P < 0.01).

10 c enzyme that processes big ET-3, generating ET-3, a potent bioactive peptide with multiple biologica

11 ET-1 and ET-3 acted through the ETA and ETB receptors, respective

12 e used to determine whether big ET-1 and big ET-3 adopt similar secondary and tertiary structures.

13 d a lesion not different to that produced by ET-3 alone.

14 1 secretion in primary human melanocytes but ET-3, an endothelin isoform, induces a low level of CXCL

15 ET-3, an ETB-selective agonist, also had no effect on pr

16 t to ET-1, which is an ETA receptor agonist, ET-3 and Sarafotoxin-S6c, two ETB receptor agonists, had

17 The increases in ECE-1, ET-1, and ET-3 and their receptor expression after balloon angiopl

18 Competition binding experiments using 125I-ET-3 and unlabeled ET-1, ET-3, S6c, and IRL-1620 suggest

19 the endogenous neuropeptides, endothelin-3 (ET-3) and atrial natriuretic peptide (ANP).

20 died the role of endothelins (ET-1, ET-2 and ET-3) and ET receptors (ET-RA and ET-RB) in the invasive

21 In addition, endothelin-3 (ET-3) and N-succinyl-[Glu9, Ala11, 15]-ET-1-1620, both s

22 the endogenous neuropeptides, endothelin-3 (ET-3), and atrial natriuretic peptide (ANP), modulate th

23 Functional studies showed that ET-1, ET-3, and sarafotoxin 6c displayed similar potencies for

24 thelin-3 (ET-3) at Trp(21)-Ile(22), yielding ET-3, and, to a much lesser extent, also cleaved big ET-

25 roducing the developmental phenotype seen in ET-3-/- and endothelin B receptor (ETB)-/- mice.

26 Big ET-1 and big ET-3 are precursor peptides which render endothelin-1 (E

27 This was mimicked by ET-3 at 28 hours.

28 tein, specifically cleaved big endothelin-3 (ET-3) at Trp(21)-Ile(22), yielding ET-3, and, to a much

29 an ETA-selective antagonist, displaced 125I-ET-3 binding from canine spleen with an IC50 value of 30

30 ker than ET-1 and ET-3 in competing for 125I-ET-3 binding to canine spleen membranes.

31 d after intravitreal injections of different ET-3 concentrations in nondiabetic rats and rats with st

32 nd IRL-1620 suggested that although ET-1 and ET-3 displayed similar high affinity, S6c and IRL-1620 w

33 presented by the ET-1/ECE-1/ETA axis and the ET-3/ECE-1/ETB axis are each involved in the development

34 ndothelial cells (LECs), and the role of the ET-3 (endothelin-3)/ETBR (endothelin type B receptor) on

35 mponents [endothelin-1 (ET-1), endothelin-3 (ET-3), endothelin receptor A (EdnrA), EdnrB] were determ

36 t retinal blood flow decrease is mediated by ET-3/ETA action.

37 w remained increased, suggesting an abnormal ET-3/ETA action.

38 tinal blood flow increases indicating normal ET-3/ETB action.

39 rease in nondiabetic rats is mediated by the ET-3/ETB and NOS action.

40 In addition, the ET-3/ETBR axis modulates lymphatic collecting vessel pum

41 To determine the effect of ET-3/ETBR axis on lymphatic vessel contractility, we ana

42 echanism linking the isolevuglandin-mediated ET-3/ETBR axis with LECs and infiltrating dendritic cell

43 levuglandin-adduct formation facilitates the ET-3/ETBR communication between LECs and dendritic cells

44 ET-3/ETBR signaling in lymphatic vessel dynamics is a no

45 dothelin axis component (EdnrA, EdnrB, ET-1, ET-3) expression in developing extramedullary hematopoie

46 erences in affinity between big ET-1 and big ET-3 for ECE-1 thus appear to be due solely to sequence

47 n is a proteolytic enzyme that processes big ET-3, generating ET-3, a potent bioactive peptide with m

48 ype B (ET(B)) - with equal affinity, whereas ET-3 has a lower affinity for ET(A).

49 L-1620 were 20-300-fold weaker than ET-1 and ET-3 in competing for 125I-ET-3 binding to canine spleen

50 lts, and recent studies implicating GDNF and ET-3 in the patterning of the enteric nervous system, su

51 nvolvement of MAP kinase (Erk) activation by ET-3 in the transcription of egr-1, and the molecular de

52 ctivating protease for both big ET-1 and big ET-3 in vivo, and that the cell-cell communication pathw

53 ll phenotype also preferentially process big ET-3, in contrast to Ko (null) cells that do not.

54 In nondiabetic rats, ET-3 induced a dose-dependent rapid increase in retinal

55 Using mobility shift assays, we showed that ET-3 induced the expression of Egr-1 protein which bound

56 The ET-3-induced initial rapid retinal blood flow increase i

57 FR139317 partially attenuated the ET-3-induced lesion when administered 30 min post-occlus

58 ET-3-induced MCA occlusion is therefore amenable to reve

59 Diabetic rats showed comparable ET-3-induced retinal blood flow increases indicating nor

60 Neither ET-1 nor ET-3 induces secretion of CXCL8 in primary human melanoc

61 wed dose-dependent increases 2 minutes after ET-3 injection (P < 0.03), and at later times remained s

62 , P < 0.01) followed 15 and 30 minutes after ET-3 injection by dose-dependent decreases in retinal bl

63 pleen membranes using ETB-selective agonists ET-3, IRL-1620, sarafotoxin 6c (S6c) as well as ETA-sele

64 CE-1 (endothelin-converting enzyme), and big ET-3 is also cleaved but apparently to a significantly l

65 Ocular tissue ET-3 levels were unaffected by diabetes.

66 Its 3 isoforms, ET-1, ET-2, and ET-3, mediate several physiologic actions in several org

67 RNA (ribonuclease protection assay), but not ET-3 mRNA (RT/PCR), abundance was increased in diabetic

68 The effect of ET-3 on retinal blood flow was also investigated in nond

69 oliferation and survival (Ret/Gdnf and EdnrB/Et-3 pathways, Sox10 and Phox2b transcription factors),

70 st-occlusion, but injection 90 min following ET-3 produced a lesion not different to that produced by

71 ET-1 and ET-3 produced large ischemic lesions that were restricte

72 growth factor receptor ligand, endothelin-3 (ET-3), regulate astrocyte proliferation at a very proxim

73 render endothelin-1 (ET-1) and endothelin-3 (ET-3) relatively unreactive and resistant to proteolytic

74 eriments using 125I-ET-3 and unlabeled ET-1, ET-3, S6c, and IRL-1620 suggested that although ET-1 and

75 ET-3 stimulated an increased number of fetal rat diencep

76 he vasoactive peptides endothelin (ET)-1 and ET-3 stimulated the synthesis of VEGF protein 3-4-fold i

77 The ET-3-stimulated decrease in retinal blood flow at later

78 The ET-3-stimulated retinal blood flow increase was inhibite

79 We conclude that the astrocyte mitogen, ET-3, stimulates egr-1 transcription through a MAP kinas

80 fects ET isoform expression (ET-1, ET-2, and ET-3) through capacitative Ca2+ influx.

81 re, we find that ANP inhibits the ability of ET-3 to activate Galpha(q) and Galpha(i) in these cells.

82 Binding of 125I-ET-3 to canine spleen membranes was specific and saturab

83 ely), the maximum binding obtained with 125I-ET-3 was approximately 35% of that obtained with 125I-ET

84 By contrast, the lesion produced by ET-3 was completely inhibited by FR139317 at the 10 min

85 ET-3 was recovered less frequently from San Francisco th

86 A 3-fold induction of egr-CAT expression by ET-3 was significantly reduced by treatment with ANP, or

87 emic damage produced by 100 pmol of ET-1 and ET-3 was similar.

88 affinities obtained with 125I-ET-1 and 125I-ET-3 were comparable (90 and 130 pM, respectively), the

89 Levels of ET-1 and ET-3 were determined by radioimmunoassay in ocular tissu

90 Endothelin-1 (ET-1) and endothelin-3 (ET-3) were injected via a double-injection cannula into

91 ion of endothelin-1 (ET-1) and endothelin-3 (ET-3) were studied in the retinas of diabetic and nondia