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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 the dephosphorylation and desensitization of NPR-B.

41 the dephosphorylation and desensitization of NPR-B.

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

43 ysophosphatidic acid-dependent inhibition of NPR-B.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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