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 mRNA levels increased four- to eightfold within 6

4 NPR-C targeting represents a potential strategy to reduc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 8-alphaANP showed higher affinity binding to NPR-C, than T2238-alphaANP.

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

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

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

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

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