ライフサイエンスコーパス: kallidin

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1 onse observed at 4 h with 100 nM des-Arg(10)-kallidin.

2 he B1 receptor antagonist des-Arg(10),Leu(9)-kallidin.

3 nse observed at 20 h with 100 nM des-Arg(10)-kallidin.

4 inding of the B1-selective agonist des-Arg10-kallidin.

5 subtype-selective agonists BK and des-Arg10-kallidin.

6 naling by B2 receptor agonists bradykinin or kallidin.

7 gonists des-Arg(9)-bradykinin or des-Arg(10)-kallidin.

8 Both desArg(10)-kallidin and ACE inhibitors enhance arginine uptake and

9 ation of their respective ligands, des-Arg10-kallidin and bradykinin (BK), both wild type receptors,

10 HEK293 cells using the agonist [3H]des-Arg10-kallidin and the antagonist [3H]NPC17731.

11 Ca(2+) exchanger is required for des-Arg(10)-kallidin- and TGF-beta1-stimulated fibrogenesis and part

12 IDE specifically degrades bradykinin and kallidin at the Pro/Phe site.

13 of B1R signaling to its agonist, des-Arg(10)-kallidin (DAKD).

14 -known BR ligands, BK, [des-Arg(10), Leu(9)]-kallidin (DALKD), and HOE140 showed different binding pr

15 luated the feasibility of using radiolabeled kallidin derivatives to visualize B1R expression in a pr

16 In addition, unlike desArg(10)-kallidin, enalaprilat can also release NO independent of

17 DesArg(10)-kallidin enhances inositol-phosphate generation and elev

18 ever, nardilysin does not release desArg(10) kallidin from the physiological precursor low molecular

19 nalaprilat and the peptide ligand desArg(10)-kallidin (in nanomolar concentrations) release NO by act

20 ition, B1 receptor activation by des-Arg(10)-kallidin induced a rise in cytosolic Ca(2+) that is cons

21 cycloheximide did not block the des-Arg(10)-kallidin-induced increase in CTGF mRNA.

22 d formation of bradykinin (BK) and Lys-BK or kallidin (KD) and their carboxypeptidase metabolites des

23 d endogenous BR ligands, bradykinin (BK) and kallidin (KD), this interaction could not be predicted,

24 LMKRPPGFSPFRSSRI-NH(2), releasing desArg(10) kallidin (KRPPGFSPF).

25 Bradykinin (BK) and kallidin (Lys-BK), liberated from kininogens by kallikre

26 es at two monobasic sites M-K and F-R of the kallidin model peptide Abz-MISLMKRPPGFSPFRSSRI-NH(2), re

27 +)](i) in cells stimulated with B2R agonists kallidin or bradykinin.

28 of BK, a B2 receptor-selective peptide, and kallidin or Lys-BK, a less receptor-selective peptide, f

29 at radiolabeled peptides based on the native kallidin sequence were ineffective at visualizing B1R-po

30 inding of the less subtype-selective agonist kallidin showed little sensitivity to TM-VI exchange.

31 engagement of the B1 receptor by des-Arg(10)-kallidin stabilized connective tissue growth factor (CTG

32 ing growth factor (TGF)-beta and des-Arg(10)-kallidin stimulate the expression of connective tissue g

33 on of the kinin B1 receptor with des-Arg(10)-kallidin stimulated a rise in cytosolic Ca(2+) that was

34 with kinetics distinct from the des-Arg(10)-kallidin-stimulated Ca(2+) response.

35 RNA expression in TGF-beta1- and des-Arg(10)-kallidin-stimulated human lung myofibroblasts.

36 Our results show that the des-Arg(10)-kallidin-stimulated increase in alpha1(I) collagen mRNA

37 The des-Arg(10)-kallidin-stimulated increase of cytosolic Ca(2+) was blo

38 vity, blocked the TGF-beta1- and des-Arg(10)-kallidin-stimulated increases of CTGF mRNA.

39 In contrast to BK and des-Arg10-kallidin, the binding of the less subtype-selective agon

40 via CPM-mediated conversion of bradykinin or kallidin to des-Arg kinin B1R agonists.

41 contrast, incubation of 3H-labeled des-Arg10-kallidin with cells expressing B1KR resulted in a modest

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