ライフサイエンスコーパス: NPR-C

1 NPR-C activation by C2238-alphaANP inhibited the protein

2 NPR-C can be coimmunoprecipitated with Galpha(i), and C-

3 NPR-C may represent a new target for the prevention of A

4 NPR-C mRNA levels increased four- to eightfold within 6

5 NPR-C targeting represents a potential strategy to reduc

6 NPR-C(-/-) mice had markedly smaller WAT and BAT depots

7 In addition, NPR-C can couple to specific Galpha(i)-Gbetagamma-mediat

8 edly reduced intracellular cAMP levels in an NPR-C-dependent manner.

9 we have learned of the potential role of an NPR-C (natriuretic peptide receptor-C) in atrial fibrosi

10 CNP molecule is bound in the interface of an NPR-C dimer, resulting in asymmetric interactions betwee

11 tracellular FLAG-tagged versions of GC-A and NPR-C independently of each other and ligand for the fir

12 Here, we evaluated GC-A and NPR-C internalization using traditional and novel approa

13 Internalization of GC-A and NPR-C is poorly understood, in part, because previous st

14 nd wtANP bound and activated human NPR-A and NPR-C similarly, whereas fsANP had a slightly increased

15 In the PNS, NPR-B and NPR-C transcripts were highly expressed in dorsal root s

16 atriuretic peptide receptor (NPR)-B(-/-) and NPR-C(-/-) animals, and human umbilical vein endothelial

17 regulation of the coronary circulation, and NPR-C activation underlies the vasorelaxant activity of

18 tic or pharmacological inhibition of CNP and NPR-C, but not NPR-B, reduces the angiogenic potential o

19 in vivo in endothelium-specific CNP(-/-) and NPR-C(-/-), but not NPR-B(-/-), mice; the detrimental ph

20 ormed to assess angiogenesis development and NPR-C localization.

21 e performed to assess plaque development and NPR-C localization.

22 This study used wild-type and NPR-C knockout (NPR-C(-/)(-)) mice to investigate the ef

23 ration, and ICa,L similarly in wild-type and NPR-C(-/-) myocytes.

24 ream to desensitize the receptors (VPAC2 and NPR-C), inhibit adenylyl and guanylyl cyclase activities

25 g the possibility that past studies ascribed NPR-C-mediated processes to GC-A.

26 de (CNP)] and their receptors (NPR-A, NPR-B, NPR-C) at several early stages in the embryonic mouse ne

27 l (NT)-proBNP, which is not believed to bind NPR-C, would not be associated with BMI and (2) that low

28 However, none of the chimeric peptides bound NPR-C with significantly higher affinity than endogenous

29 vasorelaxation ex vivo, which was rescued by NPR-C pharmacological inhibition.

30 h agonism of natriuretic peptide receptor C (NPR-C), and loss of this signaling has been associated w

31 ctivation of natriuretic peptide receptor C (NPR-C), which plays a pivotal role in the regulation of

32 e identified natriuretic peptide receptor-C (NPR-C) as the cognate receptor that primarily underlies

33 lase, and to natriuretic peptide receptor-C (NPR-C), which plays a role in peptide clearance.

34 A (GC-A) and natriuretic peptide receptor-C (NPR-C).

35 to PMA (0.1 microM) decreased mesangial cell NPR-C mRNA levels by more than 50% within 3 h and 125I-a

36 ing after ischemia or vessel injury, and CNP/NPR-C expression and localization in tissue from patient

37 ly, we identified an association between CNP/NPR-C expression and obesity in patient samples.

38 The proangiogenic effect of CNP/NPR-C is dependent on activation of G(i), ERK1/2, and ph

39 nsion by demonstrating the importance of CNP/NPR-C signaling in preserving vascular homoeostasis.

40 We tested the hypothesis that CNP/NPR-C signaling is a novel regulatory pathway governing

41 thermore, these results suggest that the CNP/NPR-C pathway has potential as a disease-modifying thera

42 d with reduced levels of CNP and its cognate NPR-C.

43 Immunohistochemistry confirmed NPR-C upregulation in the angiogenic lesion with colocal

44 ding and cross-linking studies only detected NPR-C, raising the possibility that past studies ascribe

45 This study shows that PDGF and PMA diminish NPR-C mRNA abundance and that PMA does so by acceleratin

46 Either NPR-C inhibition by antisense oligonucleotide or NPR-C g

47 urified from medium bathing cells expressing NPR-C, a receptor known to internalize natriuretic pepti

48 For FLAG-NPR-C, neither ANP, BNP, nor CNP increased its internali

49 internalized slowly (0.5%/min), whereas FLAG-NPR-C was internalized rapidly (2.5%/min) in HeLa cells.

50 ]-ANP(4-23)-NH(2) (desANP(4-23)) (analog for NPR-C receptor) exerted antiproliferative actions in thr

51 Gene expression for NPR-C, which recognizes all natriuretic peptides, was pr

52 These data are consistent with a role for NPR-C as a local decoy receptor attenuating NPR-A effect

53 rity over the CANF peptide alone for imaging NPR-C receptor in angiogenesis.

54 -specific-activity nanoprobe for PET imaging NPR-C receptor in a mouse model of hind limb ischemia-in

55 and these effects were completely absent in NPR-C(-/-) myocytes.

56 rat NPR-A (ED50 = 1.8 nM) and was reduced in NPR-C binding by approximately 200-fold.

57 cts through specific NP receptors, including NPR-C (natriuretic peptide receptor-C), are cardioprotec

58 Treatment with cycloheximide induces NPR-C mRNA, but downregulation of this mRNA by either PD

59 duction, which was shown to be linked to its NPR-C activity.

60 his study used wild-type and NPR-C knockout (NPR-C(-/)(-)) mice to investigate the effects of Ang II

61 or natriuretic peptide receptor C knockout (NPR-C(-/-)) mice.

62 e animals that is diminished in mice lacking NPR-C.

63 ctive functions and developed small-molecule NPR-C agonists to target this pathway.

64 genetic deletion of endothelial CNP, but not NPR-C, can be rescued by pharmacological administration

65 The C-type NPR (NPR-C) is responsible for clearance of NP hormones from

66 rationale for pharmacological activation of NPR-C as an innovative approach to treating peripheral a

67 Administration of NPR-C agonists promotes a vasorelaxation of isolated res

68 d the crystal structures of the complexes of NPR-C with atrial natriuretic peptide (ANP), and with br

69 mycin D inhibited the rapid disappearance of NPR-C mRNA with PMA.

70 Disappearance of NPR-C transcripts after PMA treatment was more than twic

71 middle regions of the cytoplasmic domain of NPR-C to identify the G protein-activating sequence.

72 B (10 ng/ml) also produced downregulation of NPR-C mRNA, but the rate of transcript disappearance was

73 ith PMA or PDGF still decreased the level of NPR-C mRNA despite the presence of cycloheximide.

74 ntegrated nanoprobe to prove the presence of NPR-C and offer sensitive detection with PET during deve

75 binding specificity and cross-reactivity of NPR-C with NP hormones, we have determined the crystal s

76 of natriuretic peptide receptor-3 (NPR3) or NPR-C is in the clearance of natriuretic peptides that p

77 C inhibition by antisense oligonucleotide or NPR-C gene silencing by small interfering RNA rescued su

78 nts that bind rat NPR-A selectively over rat NPR-C were isolated from randomized libraries of rANP-di

79 Natriuretic peptide C receptor (NPR-C) expression in rat mesangial cells is downregulate

80 the natriuretic peptide clearance receptor (NPR-C) in adipose tissue.

81 n of natriuretic peptide clearance receptor (NPR-C) with PET on atherosclerosis-like lesions in an an

82 the natriuretic peptide clearance receptor (NPR-C).

83 domain of the unliganded human NP receptor (NPR-C) and its complex with CNP, a 22-amino acid NP.

84 ane, natriuretic peptide clearance receptor, NPR-C, which is devoid of kinase and guanylyl cyclase ac

85 -A and NPR-B, whereas the third NP receptor, NPR-C, lacks the GC kinase domain and acts as the NP cle

86 One variant was identified with reduced NPR-C binding; rANP (G16R, A17E, Q18A) [rANP(REA18)].

87 raction, in similar fashion to the selective NPR-C ligand, cANP4-23.

88 istry and immunofluorescence staining showed NPR-C near the luminal surface of the plaque and in VSMC

89 As such, NPR-C is a novel therapeutic target to treat cardiovascu

90 We further deduce that NPR-C is internalized faster than GC-A and that increase

91 We found that NPR-C is coexpressed in transient receptor potential van

92 These results indicate that NPR-C expression is rapidly regulated by changes in the

93 cture of the NPR-C/CNP complex, reveals that NPR-C uses a conformationally inflexible surface to bind

94 type mice were cotreated with Ang II and the NPR-C agonist cANF (0.07-0.14 mg/kg per day) for 3 weeks

95 otreating wild-type mice with Ang II and the NPR-C agonist cANF dose dependently reduced AF inducibil

96 ide association studies that have linked the NPR-C (Npr3) locus with hypertension by demonstrating th

97 omplexes, with the previous structure of the NPR-C/CNP complex, reveals that NPR-C uses a conformatio

98 val and impairs endothelial function through NPR-C signaling.

99 P affects endothelial cell integrity through NPR-C-dependent inhibition of the cAMP/protein kinase A/

100 8-alphaANP showed higher affinity binding to NPR-C, than T2238-alphaANP.

101 the specificity of the targeted nanoprobe to NPR-C receptor.

102 ia in wild-type mice, whereas Ang II-treated NPR-C(-/-) mice exhibited substantially higher fibrosis

103 in left atrial myocytes from Ang II-treated NPR-C(-/-) mice.

104 e effects were exacerbated in Ang II-treated NPR-C(-/-) mice.

105 riven by enhanced BNP clearance mediated via NPR-C.

106 However, it is unknown whether NPR-C is present and overexpressed during angiogenesis.

107 and cranial ganglia beginning at E10.5, with NPR-C signal also prominent in adjoining nerves, consist

108 tained in human aortic endothelial cell with NPR-C knockdown.