ライフサイエンスコーパス: big ET

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1 rsion of exogenously added big endothelin-1 (big ET-1) to ET-1 in subcellular fractions obtained by s

2 ne systemic hemodynamics and plasma ET-1 and big ET-1 concentrations were measured using electrical b

3 , systemic hemodynamics, and plasma ET-1 and big ET-1 concentrations.

4 mately 90%) of vasoconstrictions to ET-1 and big ET-1.

5 only slightly reduced responses to ET-1 and big ET-1.

6 e analyzed for immunoreactivity for ET-1 and big ET-1.

7 uch lesser extent, also cleaved big ET-1 and big ET-2 at Trp(21)-Val(22), yielding ET-1 and ET-2.

8 were used to determine whether big ET-1 and big ET-3 adopt similar secondary and tertiary structures

9 Big ET-1 and big ET-3 are precursor peptides which render endothelin-

10 Differences in affinity between big ET-1 and big ET-3 for ECE-1 thus appear to be due solely to seque

11 de activating protease for both big ET-1 and big ET-3 in vivo, and that the cell-cell communication p

12 by ECE-1 (endothelin-converting enzyme), and big ET-3 is also cleaved but apparently to a significant

13 indicate that there is an increase in ET and big ET-1 associated with fully developed atherosclerotic

14 Levels of endogenous ET and big ET-1 detectable by radioimmunoassay in human aorta c

15 Differences in affinity between big ET-1 and big ET-3 for ECE-1 thus appear to be due so

16 In rats, intravenous 16a blocks big ET pressor responses with 30-fold greater potency th

17 is a bona fide activating protease for both big ET-1 and big ET-3 in vivo, and that the cell-cell co

18 to block the hypertensive effects induced by big ET-1.

19 , and, to a much lesser extent, also cleaved big ET-1 and big ET-2 at Trp(21)-Val(22), yielding ET-1

20 Exogenous big ET-1 was added to permeabilized and nonpermeabilized

21 Immunoreactivity for big ET-1 and ET-1 was ubiquitous in the extracellular sp

22 aled intense immunofluorescence staining for big ET-1 and the 2 isoforms of ECE-1 (ECE-1alpha and ECE

23 except in the C-terminal residues, 34-38 in big ET-1 and 34-41 in big ET-3.

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

25 efficient hydrolysis of the W21-V22 bond in big ET-1 and which have the sequence QTVP in big ET-3.

26 which has a loop for residues 27-30 (HVVP in big ET-1), which have previously been demonstrated to be

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

28 eta resulted in an increase in intracellular big ET-1 and a decrease in SMC from the main artery.

29 tracellular site involved in the cleavage of big ET-1 to the biologically active peptide ET-1 by dete

30 nted cGMP, would inhibit ECE-1 conversion of big ET-1 to active ET-1, thus reducing tissue ET-1 conce

31 At pH 6.9, conversion of big ET-1 was inhibited markedly by 30 micromol/L PD15979

32 caused by intravenous infusion of Ang II or big ET-1 to a greater extent and with longer duration th

33 In anesthetized pigs, big ET-1-stimulated increases in systemic blood pressure

34 ET-1 precursor big ET-1 elicited time-dependent vasoconstriction over 2

35 immunoreactivity for ET-1 and its precursor, big ET-1, within the atheromatous plaque.

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

37 otein is a proteolytic enzyme that processes big ET-3, generating ET-3, a potent bioactive peptide wi

38 vesicles with a possible role in processing big ET-1 while in transit to the cell surface via the co

39 The findings of this study indicate that big ET-1 is processed to the mature vasoactive peptide b

40 -1 production in vivo as demonstrated by the big ET-1-induced pressor response in rats.

41 owed poor functional activity in vivo in the big ET-1 pressor test.

42 logy modeling were used to determine whether big ET-1 and big ET-3 adopt similar secondary and tertia

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