ライフサイエンスコーパス: neurophysin

1 tive for oxytocin- or vasopressin-associated neurophysin.

2 on the properties of bovine oxytocin-related neurophysin.

3 gic and/or contains vasopressin- or oxytocin-neurophysins.

4 vasopressin or oxytocin and their respective neurophysins.

5 Native unliganded neurophysin also equilibrated with the disulfide-scrambl

6 dy (PS36) that recognizes both oxytocin (OT)-neurophysin and its prohormone was used to identify oxyt

7 ly sectioned and alternately stained for AVP-neurophysin and OT-neurophysin immunoreactivities.

8 pro regions of the common precursors of the neurophysins and the hormones oxytocin and vasopressin.

9 lar interactions between mature oxytocin and neurophysin, and of the effects of these interactions on

10 Neurophysins are hormone-binding proteins composed of tw

11 Neurophysins are prohormone-derived polypeptides that ar

12 ch have typically served as the paradigm for neurophysin behavior, are metastable in their disulfide-

13 Human growth hormone (hGH) and bovine neurophysin (bNP) DNA reporter fragments were inserted i

14 This textbook perspective on neurophysins changed with the discovery of a gene in the

15 elled PVN neurones were identified as AVP or neurophysin-containing neurones, although all of the cel

16 rtebrate deuterostomes that are derived from neurophysin-containing precursors and that have the sequ

17 The active site of liganded neurophysin contains a salt bridge that involves the sid

18 a) encoding a precursor protein comprising a neurophysin domain in association with NGFFFamide, a myo

19 very of genes encoding proteins comprising a neurophysin domain in association with putative NGFFFami

20 Accordingly, mutations in the neurophysin domain of the human vasopressin gene can cau

21 WYamide precursor does not have a C-terminal neurophysin domain, indicating loss of this character in

22 ropeptide signalling systems occurred when a neurophysin-encoding exon(s) derived from a vasopressin/

23 and of the effects of these interactions on neurophysin folding, raised questions about the intramol

24 effects of ligand peptides on the folding of neurophysin from the reduced state; these peptides serve

25 with autism and genes encoding the oxytocin-neurophysin I preproprotein, the oxytocin receptor, and

26 monomeric state of the H80E mutant of bovine neurophysin-I by (15)N NMR.

27 Bovine neurophysin-I was converted to its des 1-8 derivative, a

28 ptor (OXTR), the structural gene for OT (OXT/neurophysin-I), and CD38.

29 f dimerization on the NMR spectrum of bovine neurophysin-I, and preliminary investigation of the effe

30 the weakly dimerizing H80E mutant of bovine neurophysin-I.

31 d mutations affect the signal peptide or the neurophysin-II carrier protein and are presumed to inter

32 anded state obtained from crystals of bovine neurophysin-II complexes.

33 ith a recently emerging comparison of bovine neurophysin-II derivatives in the liganded and unligande

34 l structure of the unliganded des 1-6 bovine neurophysin-II dimer.

35 Folding of reduced, mononitrated bovine neurophysin-II was monitored by circular dichroism in a

36 ternately stained for AVP-neurophysin and OT-neurophysin immunoreactivities.

37 ices of the lumbar cord showed that oxytocin-neurophysin-immunoreactivity was detected in large numbe

38 intramolecular bonding between oxytocin and neurophysin in the precursor had only a small thermodyna

39 ociated with the refolding of reduced mature neurophysin in the presence of oxytocin was found not to

40 ence of NR2B colocalization with vasopressin-neurophysin in the SON and lateral magnocellular PVN (PV

41 gnificant differences between the two bovine neurophysins in the susceptibility to tryptic cleavage a

42 ructure of the unliganded monomeric state of neurophysin is central to an understanding of the allost

43 n potential allosteric mechanisms underlying neurophysin ligand-facilitated dimerization.

44 s three exons encoding for vasopressin (VP), neurophysin (NP), and glycopeptide (GP).

45 Studies of unliganded porcine neurophysin (oxytocin-associated class) demonstrated tha

46 nding of the allosteric relationship between neurophysin peptide-binding and dimerization.

47 gment of the subunit interface in modulating neurophysin properties and suggest a specific contributi

48 igated the role in folding of the last seven neurophysin residues by comparing the properties of the

49 n several protein properties, the last seven neurophysin residues do not make a significant net therm

50 unnecessary for folding, and the last seven neurophysin residues.

51 t of dimerization in the unliganded state on neurophysin's hormone-binding site, the effect particula

52 necessitates a conformational change in its neurophysin segment and leads to properties of the syste

53 he deletion failed to detect any oxytocin or neurophysin sequences, respectively, confirming that the

54 For oxytocin-neurophysin, the corresponding values were 0.97 and 0.95

55 The results confirmed the ability of neurophysin to fold to a limited extent (20-25% in this

56 tive stabilities of the precursor and mature neurophysin to guanidine denaturation indicated that non

57 rich precursor of oxytocin-associated bovine neurophysin was expressed in Escherichia coli and folded

58 nes encoding NG peptides in association with neurophysin were not found in protostomes, urochordates

59 Bovine neurophysins, which have typically served as the paradig

60 however, is when and how the association of neurophysin with NGFFFamide-like neuropeptides originate

61 s of the 87STOP precursor and its derivative neurophysin with those of the corresponding wild-type pr

62 The association of neurophysins with vasopressin/oxytocin-type peptides dat

63 intramolecular interactions of oxytocin with neurophysin within their common precursor.