ライフサイエンスコーパス: NPR-A

1 NPR-A mediates the vasorelaxant effect of ANP in pulmona

2 Guanylyl cyclase-A (NPR-A; GC-A) is the major and possibly the only receptor

3 Natriuretic peptide receptor A (NPR-A) and natriuretic peptide receptor B (NPR-B) are tr

4 Natriuretic peptide receptor A (NPR-A) is an essential cardiovascular regulator that is

5 Natriuretic peptide receptor A (NPR-A) is the biological receptor for atrial natriuretic

6 Natriuretic peptide receptor A (NPR-A/GC-A) and B (NPR-B/GC-B) are members of the transm

7 ation of the natriuretic peptide receptor-A (NPR-A) is hypothesized to mediate its desensitization in

8 NP) binds to natriuretic peptide receptor-A (NPR-A), a membrane guanylyl cyclase, and to natriuretic

9 yclic guanosine monophosphate production and NPR-A gene expression in cultured rat aortic smooth musc

10 for NPR-A, whereas one was as potent as any NPR-A activator known.

11 on of guanylyl cyclase (GC)-A, also known as NPR-A or NPR1, by cardiac natriuretic peptides (NPs).

12 NPR-C as a local decoy receptor attenuating NPR-A effects in the kidney, where these receptors are c

13 inked natriuretic peptide receptors A and B (NPR-A and -B), respectively, stimulates increases in int

14 In contrast with NPR-B, NPR-A appears to be expressed largely in restricted cell

15 In contrast, NPR-A gene expression was undetectable in neural tissues

16 Intervention strategies aimed at controlling NPR-A expression are limited by the paucity of studies i

17 Here, we characterize two distinct NPR-A phosphatase activities.

18 -A promoter regulation, virtually eliminates NPR-A promoter activity in RASM cells.

19 Mice in which the gene encoding NPR-A, a guanylyl cyclase-linked natriuretic peptide rec

20 Messenger RNA encoding NPR-A was identified in left ventricle and coronary arte

21 he medium after 293T cells stably expressing NPR-A were warmed from 4 degrees to 37 degrees C.

22 eased affinity and full agonist activity for NPR-A, whereas one was as potent as any NPR-A activator

23 y reports indicate that ATP is essential for NPR-A and NPR-B activation.

24 es revealed differential gene expression for NPR-A/B/C in NG108 and Neuro2a cells.

25 To further increase the potency of CD-NP for NPR-A, we converted two different triplet sequences with

26 Strong Pro-Q Diamond signals for NPR-A and NPR-B were obtained when receptors were isolat

27 tified six in vivo phosphorylation sites for NPR-A and five sites for NPR-B and demonstrated that the

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

29 Improved NPR-A specificity could provide more effective natriuret

30 eductions were not explained by decreases in NPR-A protein levels, as indicated by immunoblot analysi

31 The increase in NPR-A expression was associated with an increase in NPR-

32 be linked mechanistically to the increase in NPR-A gene expression.

33 xpression was associated with an increase in NPR-A gene promoter activity that was critically depende

34 is was associated with a twofold increase in NPR-A mRNA levels in the inner medulla.

35 Sp1 sites previously shown to be involved in NPR-A promoter regulation, virtually eliminates NPR-A pr

36 hypercalcemic analogue RO-25-6760, increased NPR-A-dependent cyclic guanosine monophosphate productio

37 dual labeling immunocytochemistry localized NPR-A protein to cardiomyocytes, endocardial endothelial

38 in situ hybridization histochemistry to map NPR-A and NPR-B mRNA-expressing cell populations.

39 biotinylation assays indicated that neither NPR-A nor NPR-B was internalized or degraded in response

40 Significant levels of neuronal NPR-A mRNA expression were observed only in the mitral c

41 Labeling for NPR-B but not NPR-A mRNA was observed in pituicytes in the neural lobe

42 explained through binding and activation of NPR-A or NPR-B.

43 idase to abolish ANP-dependent activation of NPR-A.

44 required for hormone-dependent activation of NPR-A.

45 In contrast, the activity of NPR-A-6E was more linear with time and was unaffected by

46 ate content and guanylyl cyclase activity of NPR-A.

47 Amplification of NPR-A activity represents a plausible mechanism to accou

48 significant downregulation in the density of NPR-A in heart and coronary artery of patients with isch

49 egrees C stimulated the dephosphorylation of NPR-A, and microcystin blocked the temperature-dependent

50 further stimulated the dephosphorylation of NPR-A, and microcystin failed to inhibit this process.

51 ains the ligand-dependent desensitization of NPR-A and NPR-B and characterized their trafficking prop

52 egulation account for the desensitization of NPR-A and NPR-B that occurs in response to various physi

53 icrocystin, inhibited the desensitization of NPR-A in membrane guanylyl cyclase assays in the absence

54 lly, we observed that the desensitization of NPR-A in membranes from mouse kidneys and NIH3T3 cells w

55 Finally, the desensitization of NPR-A-6E in whole cells was markedly blunted compared wi

56 n sites within the kinase homology domain of NPR-A and determined that the conversion of these residu

57 Expression of NPR-A mRNA was observed in forebrain white matter tracts

58 In an attempt to generate a form of NPR-A that mimics a fully phosphorylated receptor but th

59 The level of NPR-A Pro-Q staining was also high in kidney but was muc

60 e ligand-dependent trafficking properties of NPR-A remain controversial, whereas nothing is known abo

61 els of IDE profoundly alters the response of NPR-A and NPR-B to the stimulation of ANP, BNP, and CNP

62 ired changes in the phosphorylation state of NPR-A because the guanylyl cyclase activity of a recepto

63 cyclase activity or phosphorylation state of NPR-A.

64 d IDE expression enhances the stimulation of NPR-A and NPR-B by ANP and CNP, respectively.

65 he p38 MAPK-dependent osmotic stimulation of NPR-A gene expression noted previously.

66 Rat ANP (rANP) mutants that bind rat NPR-A selectively over rat NPR-C were isolated from rand

67 stimulating cGMP production from cloned rat NPR-A (ED50 = 1.8 nM) and was reduced in NPR-C binding b

68 was only a slightly better activator of rat NPR-A due to the promiscuous nature of CNP in this speci

69 to the type A natriuretic peptide receptor (NPR-A) expressed on the surface of vascular cells.

70 creased type A natriuretic peptide receptor (NPR-A) expression through a p38 MAPKbeta pathway in inne

71 on, the type A natriuretic peptide receptor (NPR-A) plays a major role in determining urinary sodium

72 of the type A natriuretic peptide receptor (NPR-A), a receptor that signals reductions in BP and sup

73 of the type A natriuretic peptide receptor (NPR-A), and dehydration natriuresis.

74 rmones inhibit natriuretic peptide receptors NPR-A or NPR-B in a variety of different cell types.

75 riuretic peptide (CNP)] and their receptors (NPR-A, NPR-B, NPR-C) at several early stages in the embr

76 guanylate cyclase (GC)-coupled NP receptors, NPR-A and NPR-B, whereas the third NP receptor, NPR-C, l

77 vely activate natriuretic peptide receptors, NPR-A and NPR-B, raising the cyclic GMP (cGMP) levels.

78 and Sp1 act synergistically to reconstitute NPR-A promoter activity.

79 tor but was equally as potent in stimulating NPR-A-6E, suggesting that ATP is required to keep the wi

80 , for phosphorylated residues, we found that NPR-A-6E was activated 10-fold by ANP and ATP.

81 Together, these data indicate that NPR-A is regulated by two distinct phosphatases, possibl

82 Finally, we show that NPR-A and NPR-B are desensitized in cells in which they

83 Together, these studies show that NPR-A promoter activity is dominantly regulated through

84 R subtypes have been described in brain: the NPR-A selectively binds ANP, whereas NPR-B exhibits high

85 These data implicate the NPR-A in autoregulation of ANP neurons and central regis

86 ination of the VD-dependent induction of the NPR-A gene promoter but did not affect osmotic stimulati

87 Activation of the NPR-A guanylyl cyclase requires ANP binding to the extra

88 ggests that Sgk1-dependent activation of the NPR-A pathway may contribute to this response.

89 on-dependent decrease in the activity of the NPR-A promoter in RASM cells confirming that endogenous

90 sequence CCAAT between -141 and -137 of the NPR-A promoter that, when mutated, reduces promoter acti

91 Ligand binding to NPR-A rapidly activates its guanylyl cyclase domain, but

92 gested binding of [125I]-DNP was specific to NPR-A.

93 ge can lead to hyperactivation of BNP toward NPR-A.

94 euroblastoma cell proliferation through type NPR-A/B (GC) receptors.

95 However, unlike NPR-A, the dephosphorylated receptor was not completely

96 orylation, we engineered a receptor variant (NPR-A-6E) containing glutamate substitutions at all six

97 510, and T513) which are phosphorylated when NPR-A is expressed in HEK 293 cells.