ライフサイエンスコーパス: NPR-B

1 NPR-B isolated from resting 3T3-NPR-B cells was phosphor

2 NPR-B protects against AF by preventing enhanced atrial

3 NPR-B(+/-) mice displayed larger increases in action pot

4 NIH3T3 fibroblasts overexpressing NPR-B (3T3-NPR-B) to CNP resulted in time-dependent decreases in bo

5 In vitro dephosphorylation of crude 3T3-NPR-B membranes with purified protein phosphatase 2A was

6 NPR-B isolated from resting 3T3-NPR-B cells was phosphorylated on serine and threonine r

7 c peptide (CNP)] and their receptors (NPR-A, NPR-B, NPR-C) at several early stages in the embryonic m

8 -A while maintaining the ability to activate NPR-B.

9 We conclude that, although NPR-B is expressed in a number of tissues, its major rol

10 indicate that ATP is essential for NPR-A and NPR-B activation.

11 igand-dependent desensitization of NPR-A and NPR-B and characterized their trafficking properties usi

12 Finally, we show that NPR-A and NPR-B are desensitized in cells in which they are not in

13 ession enhances the stimulation of NPR-A and NPR-B by ANP and CNP, respectively.

14 ybridization histochemistry to map NPR-A and NPR-B mRNA-expressing cell populations.

15 account for the desensitization of NPR-A and NPR-B that occurs in response to various physiological a

16 profoundly alters the response of NPR-A and NPR-B to the stimulation of ANP, BNP, and CNP in culture

17 Strong Pro-Q Diamond signals for NPR-A and NPR-B were obtained when receptors were isolated from lu

18 ate natriuretic peptide receptors, NPR-A and NPR-B, raising the cyclic GMP (cGMP) levels.

19 cyclase (GC)-coupled NP receptors, NPR-A and NPR-B, whereas the third NP receptor, NPR-C, lacks the G

20 levels were reduced in patients with AF, and NPR-B(+/-) mice were more susceptible to AF.

21 with AF or sinus rhythm and in wild-type and NPR-B-deficient (NPR-B(+/-)) mice.

22 Atrial NPR-B protein levels were reduced in patients with AF, a

23 retic peptide receptor A (NPR-A/GC-A) and B (NPR-B/GC-B) are members of the transmembrane guanylyl cy

24 ane receptor natriuretic peptide receptor B (NPR-B [also known as guanylate cyclase B, GC-B, and GUC2

25 clase-linked natriuretic peptide receptor B (NPR-B) and stimulates marked elevations of the intracell

26 (NPR-A) and natriuretic peptide receptor B (NPR-B) are transmembrane guanylyl cyclases that catalyze

27 ide, whereas natriuretic peptide receptor B (NPR-B) stimulates long bone growth in a C-type natriuret

28 Natriuretic peptide receptor-B (NPR-B) is the primary signaling molecule for CNP.

29 e binding to natriuretic peptide receptor-B (NPR-B) stimulates cGMP synthesis, which regulates vasore

30 In contrast, NPR-B mRNA was widely expressed throughout the neuraxis.

31 dicated that acute hyperosmolarity decreased NPR-B activity in a reversible, concentration- and time-

32 rhythm and in wild-type and NPR-B-deficient (NPR-B(+/-)) mice.

33 Labeling for NPR-B but not NPR-A mRNA was observed in pituicytes in t

34 orylation sites for NPR-A and five sites for NPR-B and demonstrated that the phosphorylation of these

35 had a slightly increased efficacy for human NPR-B.

36 e events and delayed afterdepolarizations in NPR-B(+/-) atrial myocytes.

37 receptor) and phospholamban was increased in NPR-B(+/-) atria in the presence of isoproterenol compar

38 hosphodiesterase 2) activity were reduced in NPR-B(+/-) mice leading to larger increases in atrial cA

39 Lysophosphatidic acid also inhibited NPR-B in a calcium- and phosphorylation-dependent proces

40 Intense NPR-B mRNA hybridization was observed in preoptic-hypoth

41 tor with glutamates substituted at all known NPR-B phosphorylation sites is unresponsive to hyperosmo

42 tification and characterization of the major NPR-B phosphorylation sites.

43 tion assays indicated that neither NPR-A nor NPR-B was internalized or degraded in response to natriu

44 um-specific CNP(-/-) and NPR-C(-/-), but not NPR-B(-/-), mice; the detrimental phenotype caused by ge

45 logical inhibition of CNP and NPR-C, but not NPR-B, reduces the angiogenic potential of pulmonary mic

46 electrophysiology through the activation of NPR-B (natriuretic peptide receptor B) and cGMP-dependen

47 data indicate that the catalytic activity of NPR-B is tightly coupled to its phosphorylation state an

48 Recently, the guanylyl cyclase activity of NPR-B was shown to correlate with its phosphorylation st

49 show that PKC-dependent dephosphorylation of NPR-B at Ser(523) provides a possible molecular explanat

50 s block the AVP-dependent desensitization of NPR-B even though both processes block PKC-dependent des

51 rogates the AVP-dependent desensitization of NPR-B, and ionomycin, a calcium ionophore, mimics the AV

52 the dephosphorylation and desensitization of NPR-B.

53 the dephosphorylation and desensitization of NPR-B.

54 Intermediate expression of NPR-B mRNA was observed in brainstem nuclei controlling

55 ysophosphatidic acid-dependent inhibition of NPR-B.

56 ain is a critical event in the regulation of NPR-B.

57 with calcium being a universal regulator of NPR-B.

58 Nevertheless, the role of NPR-B in regulating atrial electrophysiology, Ca(2+) hom

59 as nothing is known about the trafficking of NPR-B.

60 hibit natriuretic peptide receptors NPR-A or NPR-B in a variety of different cell types.

61 d through binding and activation of NPR-A or NPR-B.

62 nylyl cyclase B (GC-B, also known as Npr2 or NPR-B), increase cellular cGMP and cause skeletal overgr

63 xposure of NIH3T3 fibroblasts overexpressing NPR-B (3T3-NPR-B) to CNP resulted in time-dependent decr

64 centration-dependent fashion that paralleled NPR-B desensitization.

65 In the PNS, NPR-B and NPR-C transcripts were highly expressed in dor

66 ith the type B natriuretic peptide receptor (NPR-B).

67 The CNP-specific receptor (NPR-B) gene was expressed in cells just outside the VZ,

68 shes the ability of ANP and BNP to stimulate NPR-B.

69 Hyperosmotic medium stimulated NPR-B dephosphorylation, and the receptor was rapidly re

70 Thus, the data suggest that NPR-B is the primary functional NPR in the TM and CM cel

71 phorylation of approximately one-half of the NPR-B population.

72 while concomitantly driving adipogenesis via NPR-B/protein kinase-G.

73 homology domain that are phosphorylated when NPR-B is expressed in human 293 cells.

74 in: the NPR-A selectively binds ANP, whereas NPR-B exhibits high affinity for CNP.

75 f ANP and BNP by IDE render them active with NPR-B and a reduction of IDE expression diminishes the a

76 In contrast with NPR-B, NPR-A appears to be expressed largely in restrict