ライフサイエンスコーパス: kallidin

1 0, releasing the decapeptide Lys-bradykinin (kallidin).

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

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

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

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

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

7 naling by B2 receptor agonists bradykinin or kallidin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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