ライフサイエンスコーパス: NMS

1 NMS were rated using the Movement Disorder Society Unifi

2 NMS-P118 proved to be a potent, orally available, and hi

3 Human MPNST cell lines (Mash-1, YST-1, NMS-2 and NMS-2PC cells) similarly coexpress multiple NR

4 constants of 30minus sign100 nM for the M(2) NMS-liganded and unliganded receptor, respectively.

5 es in the submillimolar range, inhibited [3H]NMS dissociation, and showed various patterns of positiv

6 holine (ACh) 3- to 5-fold for inhibiting [3H]NMS binding to M4 receptors but has no effect on ACh aff

7 In contrast, it inhibits [3H]NMS dissociation from M1 to M4 receptors at submillimola

8 effects of THRX-160209 on retardation of [3H]NMS dissociation were competitively inhibited by obidoxi

9 m binding of l-[3H]N-methyl scopolamine ([3H]NMS) to the five human muscarinic receptor subtypes (M1-

10 neutral, and negative cooperativity with [3H]NMS and acetylcholine, but there was no predictive relat

11 approximately neutral cooperativity with [3H]NMS at M1 to M4 and possibly M5 receptors.

12 ) was determined by the displacement of [3H]-NMS binding using membranes from transfected Chinese ham

13 715 and compared the binding modes of Cpd-5, NMS-P715, and reversine.

14 Comparison between unfolding of an NMS construct and that of truncated G-quadruplex constru

15 n MPNST cell lines (Mash-1, YST-1, NMS-2 and NMS-2PC cells) similarly coexpress multiple NRG-1 isofor

16 f the Mps1 kinase mutants bound to Cpd-5 and NMS-P715 and compared the binding modes of Cpd-5, NMS-P7

17 Individually, CSS and NMS have no effect.

18 ed motif, GAAG/CTTC, present in both CSS and NMS, is responsible for repression as the mutation in th

19 recombinant plasmids indicated that CSS- and NMS-mediated repression of transcription is position- an

20 four p97 inhibitors (DBeQ, ML240, ML241, and NMS-873) have differential responses to Walker A and B m

21 rom the action of the orthosteric antagonist NMS.

22 ed resistance to the MPS1 inhibitors AZ3146, NMS-P715, and CCT251455, identifying five point mutation

23 n the multivariate analysis, higher baseline NMS score was associated with female sex (p=0.008), high

24 We found that HI activity was enhanced by NMS depending on the Ab's fine specificity (antigenic re

25 oxo-2,3-dihydro-1H-isoind ole-4-carboxamide (NMS-P118, 20by).

26 resistance to two closely related compounds, NMS-P715 and its derivative Cpd-5, but not to the well c

27 diction, as only one of the markers displays NMS (one-sided events).

28 with PD are treated with antidepressants for NMSs, and the effect of the combination of PD medication

29 [(3)H]NMS ([(3)H]N-methylscopolamine) binding experiments conf

30 m2-Toxin fully blocked the binding of [(3)H]NMS and [(3)H]oxotremorine-M to M2 receptors with Hill c

31 Experimental data on [(3)H]NMS and [(3)H]QNB association and dissociation perfectly

32 egative, or neutral cooperativity with [(3)H]NMS and ACh, depending on the receptor subtype and natur

33 n the membranes were preincubated with [(3)H]NMS and then exposed to benzilylcholine mustard (covalen

34 amine failed to fully inhibit specific [(3)H]NMS binding in a manner that was quantitatively describe

35 t brain showed that m2-toxin decreased [(3)H]NMS binding in regions rich in M2 receptors and increase

36 ity to inhibit or modulate orthosteric [(3)H]NMS binding revealed that para-LRB-AC42 shared several p

37 ass: 7471 Da; irreversible blockade of [(3)H]NMS binding to cloned M(1) receptors at 25 degrees C; no

38 ed the nature of [(3)H]pirenzepine and [(3)H]NMS binding to human cortex and showed total [(3)H]piren

39 n M4 receptors, but slightly increased [(3)H]NMS binding to M1 receptors, an allosteric effect.

40 Surprisingly, there was no change in [(3)H]NMS binding to the cortex from this subset or those with

41 Zn(2+), acetylcholine displacement of [(3)H]NMS binding was enhanced by Mg(2+) and Zn(2+), acetylcho

42 and showed total [(3)H]pirenzepine and [(3)H]NMS binding was reduced by Zn(2+), acetylcholine displac

43 M(2)-M(5) receptors; 6-fold slowing of [(3)H]NMS dissociation at 37 degrees C).

44 ine significantly retarded the rate of [(3)H]NMS dissociation from CHO-hM(1) cell membranes, conclusi

45 n PG987 and other allosteric agents on [(3)H]NMS dissociation from M(3) receptors indicate that PG987

46 IN 62,577 and WIN 51,708 do not affect [(3)H]NMS dissociation from M(3) receptors.

47 (covalently binding specific ligand), [(3)H]NMS dissociation was blocked in wild-type receptors, but

48 87), has the unique effect of speeding [(3)H]NMS dissociation; its largest effect, 2.5-fold, is at M(

49 Dissociation kinetic studies using [(3)H]NMS further support that LY2119620 binds allosterically

50 ed 77% of the binding sites for 0.1 nM [(3)H]NMS in the rat brainstem (K(i) = 11 nM).

51 alogs with [(3)H]N-methyl scopolamine ([(3)H]NMS) and unlabeled acetylcholine (ACh) at M(1)-M(4) musc

52 obtained in [(3)H]N-methylscopolamine ([(3)H]NMS) binding studies, in that both AC-42 and the prototy

53 to inhibit [(3)H]N-methylscopolamine ([(3)H]NMS) binding to M1, left-shifting the ACh Ki approximate

54 ociation of [(3)H]N-methylscopolamine ([(3)H]NMS) from these receptors.

55 ations with N-[(3)H]methylscopolamine ([(3)H]NMS) or R(-)-[(3)H]quinuclidinyl benzilate ([(3)H]QNB),

56 binding of [(3)H]N-methylscopolamine ([(3)H]NMS) to cloned M2 receptors.

57 ced by Zn(2+), whereas BQCA effects on [(3)H]NMS, but not [(3)H]pirenzepine, binding was enhanced by

58 substantially more binding sites than [(3)H]NMS.

59 Longitudinal increase in NMS severity was associated with the older age (0.008) a

60 iation of a greater longitudinal increase in NMS with lower baseline Abeta1-42 level is an important

61 We evaluated the change in NMSs in patients taking an antidepressant and rasagiline

62 t a role for dopamine-enhancing therapies in NMSs in early PD and encourage further study and confirm

63 ues of brucine with [3H]N-methylscopolamine (NMS) and unlabeled acetylcholine at m1-m5 muscarinic rec

64 line and the antagonist N-methylscopolamine (NMS) at M(1)minus signM(4) receptors have been analyzed

65 nyl benzilate (QNB) and N-methylscopolamine (NMS) bind to the binding pocket of the muscarinic acetyl

66 adiolabeled antagonists N-methylscopolamine (NMS) in the presence of methoctramine and its precursors

67 nce of noninactivated serum from naive mice (NMS).

68 The affinity of NMS at the allosteric site is in the micromolar range fo

69 amino acids to alanine decreased affinity of NMS for the allosteric binding site confirming results o

70 r loop are involved in allosteric binding of NMS.

71 ctramine physically prevents dissociation of NMS from the orthosteric binding site.

72 binding site on the extracellular domain of NMS-occupied M(2) receptors by interacting primarily wit

73 Understanding of interactions of NMS at the allosteric binding site is essential for corr

74 /Trp(604) and the trifluoromethoxy moiety of NMS-P715, the methoxy moiety of Cpd-5, and complete abse

75 The allosteric binding site of NMS overlaps with the binding site of some allosteric, e

76 This study of NMS in early PD identified clinical and biological varia

77 ug may be a useful agent in the treatment of NMS.

78 ociated with reduced worsening of a range of NMSs in preliminary analyses.

79 eptors, but reversibly and without effect on NMS dissociation.

80 ine neurotransmission and antidepressants on NMSs has not been studied.

81 ow that high concentrations of either QNB or NMS slow down dissociation of their radiolabeled species

82 iously characterized patients with recurrent NMS (five females and three males; 34+/-2 yr) were recru

83 be better tolerated than the closely related NMS-P715.

84 ns expressing the neuropeptide neuromedin S (NMS) plays an essential role in the generation of daily

85 n the proprietary Nerviano Medical Sciences (NMS) chemical collection, followed by SAR optimization,

86 ed dissociation of [3H]N-methyl scopolamine (NMS).

87 is named as native mechanical segmentation (NMS).

88 be detectable as non-Mendelian segregations (NMS).

89 d a downstream negative modulatory sequence (NMS), which function in concert with each other, are req

90 ence of purified IgM and normal mouse serum (NMS), but not serum from Rag-2(-/-) mice, implicating a

91 o unliganded M(1) receptors but did not slow NMS dissociation.

92 ongitudinal evolution in non-motor symptoms (NMS) in a prospective cohort of, at baseline, patients w

93 ive impairment, and other nonmotor symptoms (NMSs) are common early in Parkinson disease (PD) and may

94 nts with presumed neurally mediated syncope (NMS) and documented asystole but syncope still recurred

95 at Paxil prevents neurally mediated syncope (NMS) by attenuating the sympathoinhibition and vagotonia

96 he development of neurally mediated syncope (NMS) by manipulating overall sympathetic outflow in subj

97 ubjects completed the study, whereas all the NMS patients developed syncope.

98 n three out of eight controls and in all the NMS patients.

99 The NMSs were assessed by Movement Disorder Society-sponsore

100 surgery-like precisions, we anticipate this NMS approach offers unprecedented perspective to deciphe

101 ndependent of the concentration of unlabeled NMS or QNB added to reveal dissociation.

102 (MDS-UPDRS) Part I score and other validated NMS scales at baseline and after 2 years.

103 ompounds exhibit positive cooperativity with NMS, particularly at M(2) and M(4) receptors.

104 ncement of sympathetic tone in patients with NMS improves orthostatic tolerance and raises the possib