ライフサイエンスコーパス: phenylpyridinium

1 ypical" Oct substrates, including 1-methyl-4-phenylpyridinium.

2 reactive microgliosis elicited by 1-methyl-4-phenylpyridinium.

3 reactive microgliosis elicited by 1-methyl-4-phenylpyridinium.

4 dine while retaining transport of 1-methyl-4-phenylpyridinium.

5 ng 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium.

6 c uptake of the organic cation 3H-1-methyl-4-phenylpyridinium (3H-MPP+) was significantly enhanced (8

7 ubstrates [3H]-histamine and [3H]-N-methyl-4-phenylpyridinium ([3H]-MPP+).

8 sitively charged phenyl radicals 3-dehydro-N-phenylpyridinium (a), N-(3-dehydro-5-chlorophenyl)pyridi

9 we use a fluorescent analogue of 1-methyl-4-phenylpyridinium, a neurotoxic metabolite and known subs

10 synaptic vesicle sequestration of 1-methyl-4-phenylpyridinium, a toxic metabolite of 1-methyl-4-pheny

11 ransports organic cations such as 1-methyl-4-phenylpyridinium and cimetidine.

12 Furthermore, a group of phenylpyridinium and quinolinium compounds were used to

13 ma cells to the PD-toxin, MPP(+) (1-methyl-4-phenylpyridinium) and studied ROS upregulation leading t

14 re conducted using [(3)H] MMP(+) (1-methyl-4-phenylpyridinium) as the marker ligand and various displ

15 cations, including the neurotoxin 1-methyl-4-phenylpyridinium, as substrates.

16 erization showed that the incorporation of a phenylpyridinium component increased the film robustness

17 have found that 3,5-diacyl-1,2,4-trialkyl-6-phenylpyridinium derivatives constitute a novel class of

18 TAT-C24Scr, decreased AMPH-evoked 1-methyl-4-phenylpyridinium efflux.

19 lease of the toxic organic cation 1-methyl-4-phenylpyridinium from astrocytes and protects against 1-

20 nduced release of preloaded N-methyl-4-[(3)H]phenylpyridinium from superfused hDAT cells.

21 gnificant neuroprotection against 1-methyl-4-phenylpyridinium, glutamate, and nitric oxide-induced ne

22 ns were comparably susceptible to 1-methyl-4-phenylpyridinium-, glutamate-, or camptothecin-induced c

23 The affinity for hOCT was higher for 4-phenylpyridiniums > 3-phenylpyridiniums > quinolinium, i

24 hOCT was higher for 4-phenylpyridiniums > 3-phenylpyridiniums > quinolinium, indicating that substra

25 d cations, tetraethylammonium and 1-methyl-4-phenylpyridinium, i.e. the pH value did not have an effe

26 polycytidylic acid)-, HIV-1 Tat-, 1-methyl-4-phenylpyridinium(+)-, IL-1beta-, and IL-12 p40(2)-induce

27 on confers protection by blocking 1-methyl-4-phenylpyridinium-induced CHOP up-regulation, ER Ca(2+) s

28 PC12 and MN9D cells vulnerable to 1-methyl-4-phenylpyridinium-induced cytotoxic cell death by a mecha

29 phenyl-1,2,3,6-tetrahydropyridine/1-methyl-4-phenylpyridinium-induced dopaminergic neurotoxicity both

30 st, significantly reduced LPS- or 1-methyl-4-phenylpyridinium-induced dopaminergic neurotoxicity with

31 hagy and protects neurons against 1-methyl-4-phenylpyridinium-induced oxidative stress in an in vitro

32 2)O(2) and the Parkinsonian toxin 1-methyl-4-phenylpyridinium-induced PKCdelta cleavage, kinase activ

33 otential and NAD(+)/NADH ratio in 1-methyl-4-phenylpyridinium-inhibited cells.

34 e type B)-catalyzed production of 1-methyl-4-phenylpyridinium ion (MPP(+)) and is likely to involve a

35 ted with an exogenous neurotoxin, 1-methyl-4-phenylpyridinium ion (MPP(+)) significantly decreased TR

36 he oxidation of MPTP to the toxic 1-methyl-4-phenylpyridinium ion (MPP(+)), which then targets the do

37 al pharmacokinetics or content of 1-methyl-4-phenylpyridinium ion (MPP+), the active metabolite of MP

38 hallenged with the DA neurotoxin, 1-methyl-4-phenylpyridinium ion (MPP+).

39 I inhibitors such as rotenone and 1-methyl-4-phenylpyridinium ion, known as a metabolite of 1-methyl-

40 e conversion of MPTP to the toxic 1-methyl-4-phenylpyridinium ion.

41 I inhibitor such as rotenone and 1-methyl-4-phenylpyridinium ion.

42 m) = 329 mum), and the neurotoxin 1-methyl-4-phenylpyridinium (K(m) = 33 mum).

43 1-Methyl-4-phenylpyridinium, lipopolysaccharide (LPS), and rotenone

44 the well-established LPS and the 1-methyl-4-phenylpyridinium-mediated models of Parkinson's disease,

45 he role of TTP in PD, an in vitro 1-methyl-4-phenylpyridinium (MPP(+) ) cell model and an in vivo 1-m

46 I) and complex II (CII) by toxins 1-methyl-4-phenylpyridinium (MPP(+)) and 3-nitropropionic acid (3-N

47 ss, and neurotoxicity produced by 1-methyl-4-phenylpyridinium (MPP(+)) and 6-hydroxydopamine (6-OHDA)

48 to compare fluorescent analogs of 1-methyl-4-phenylpyridinium (MPP(+)) as reporters for the human ser

49 ed with the parkinsonian toxicant 1-methyl-4-phenylpyridinium (MPP(+)) as well as in the substantia n

50 mitochondrial complex I inhibitor 1-methyl-4-phenylpyridinium (MPP(+)) dysregulates mitochondrial fis

51 mphetamine-triggered DAT-mediated 1-methyl-4-phenylpyridinium (MPP(+)) efflux.

52 ochondrial calcium in response to 1-methyl-4-phenylpyridinium (MPP(+)) in human neuroblastoma SH-SY5Y

53 and by dopaminergic neurotoxins, 1-methyl-4-phenylpyridinium (MPP(+)) in vitro and in vivo by 1-meth

54 1-Methyl-4-phenylpyridinium (MPP(+)) is a neurotoxin that causes Pa

55 1-Methyl-4-phenylpyridinium (MPP(+)) is selectively toxic to dopami

56 The neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)) produces mitochondria-targeted

57 allenging dopaminergic cells with 1-methyl-4-phenylpyridinium (MPP(+)), a neurotoxin that inhibits co

58 modulate neuronal death caused by 1-methyl-4-phenylpyridinium (MPP(+)), an inhibitor of complex I in

59 lecular mechanisms of toxicity of 1-methyl-4-phenylpyridinium (MPP(+)), an ultimate toxic metabolite

60 the Parkinsonism-inducing toxin, 1-methyl-4-phenylpyridinium (MPP(+)), into dopaminergic terminals i

61 T), and a charged VMAT, substrate 1-methyl-4-phenylpyridinium (MPP(+)), reduced striatal CYAM.

62 ,2,3,6-tetrahydropyridine (MPTP), N-methyl-4-phenylpyridinium (MPP(+)), selectively destroys the dopa

63 ion and transport activity toward 1-methyl-4-phenylpyridinium (MPP(+)), serotonin (5-HT), and dopamin

64 1-Methyl-4-phenylpyridinium (MPP(+)), the active metabolite of the

65 1-Methyl-4-phenylpyridinium (MPP(+)), the toxic metabolite of 1-met

66 cumulation of radiolabeled DA and 1-methyl-4-phenylpyridinium (MPP(+)), was found to directly correla

67 g models of serum deprivation and 1-methyl-4-phenylpyridinium (MPP(+)), we investigated the mechanism

68 rons treated with the neurotoxin, 1-methyl-4-phenylpyridinium (MPP(+)), which induces conversion of e

69 ilar relative effects in blocking 1-methyl-4-phenylpyridinium (MPP(+))-mediated death of dopaminergic

70 te that minocycline inhibits both 1-methyl-4-phenylpyridinium (MPP(+))-mediated iNOS expression and N

71 nes using the mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP(+)).

72 er in complex with the substrates 1-methyl-4-phenylpyridinium (MPP) and metformin and with the inhibi

73 The compound 1-methyl-4-phenylpyridinium (MPP) is a selective inhibitor of mitoc

74 rototypic cationic substrates, 3) 1-methyl-4-phenylpyridinium (MPP), and 4) the novel fluorescent pro

75 Using 1-methyl-4-phenylpyridinium (MPP+) -treated C57 mice primary mesenc

76 exposure to the neurotoxic agents 1-methyl-4-phenylpyridinium (MPP+) and N-methyl-D-aspartate (NMDA).

77 ates the uptake of the neurotoxin 1-methyl-4-phenylpyridinium (MPP+) and the neurotransmitter dopamin

78 ns 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium (MPP+) in a dopaminergic cell line.

79 ahydropyridine and its metabolite 1-methyl-4-phenylpyridinium (MPP+) induce PD symptoms and recapitul

80 ctor (bFGF) could protect against 1-methyl-4-phenylpyridinium (MPP+) induced striatal damage in neona

81 1-Methyl-4-phenylpyridinium (MPP+) levels after MPTP administration

82 3) significantly greater striatal 1-methyl-4-phenylpyridinium (MPP+) levels, as compared to mice dose

83 e involvement of free radicals in N-methyl-4-phenylpyridinium (MPP+) toxicity is less clear.

84 erexpression inhibited endogenous 1-methyl-4-phenylpyridinium (MPP+) uptake activity in HeLa cells.

85 with the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP+), and GM1 ganglioside added after

86 ,2,3,6-tetrahydropyridine (MPTP), 1-methyl-4-phenylpyridinium (MPP+), exerts its lethal effect by inh

87 r to the dopaminergic neurotoxin, 1-methyl-4-phenylpyridinium (MPP+), has been shown to produce PD-li

88 rain neurons treated with 6-OHDA, 1-methyl-4-phenylpyridinium (MPP+), or alpha-synuclein fibrils (alp

89 uced Parkinson's disease involves 1-methyl-4-phenylpyridinium (MPP+), the active metabolite of 1-meth

90 ts by altering striatal levels of 1-methyl-4-phenylpyridinium (MPP+), the active metabolite of MPTP.

91 1-Methyl-4-phenylpyridinium (MPP+), the cytotoxic metabolite of 1-m

92 ith chemical structure similar to 1-methyl-4-phenylpyridinium (MPP+), the MPTP metabolite responsible

93 dsRNA (poly IC)-, HIV-1 Tat-, and 1-methyl-4-phenylpyridinium (MPP+)-, but not IFN-gamma-, induced mi

94 eurons to the complex I inhibitor 1-methyl-4-phenylpyridinium (MPP+).

95 ns 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium (MPP+).

96 rotransmitters and the neurotoxin 1-methyl-4-phenylpyridinium (MPP+).

97 1 behaved like PMAT, transporting 1-methyl-4-phenylpyridinium (MPP+, an organic cation) but not uridi

98 and transport of model substrate 1-methyl-4-phenylpyridinium(+) (MPP(+)) by cell-free-expressed fusi

99 on to dopaminergic loss following 1-methyl-4-phenylpyridinium/MPTP treatment, in vitro and in vivo.

100 with the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium, N27 cells (dopaminergic neuron cell li

101 omplex I inhibitors (rotenone and 1-methyl-4-phenylpyridinium or MPP(+)) on striatal and cortical neu

102 The neurotoxin MPP+ (1-methyl-4-phenylpyridinium), oxidative stress, or impairment of ce

103 N-methyl-4-phenylpyridinium, phenylethylamine, amphetamine, and met

104 he reaction of cytosine with the 3-dehydro-N-phenylpyridinium radical cation.

105 with tyramine and the neurotoxin 1-methyl-4-phenylpyridinium suggest that the flexibility of the sid

106 , and quinidine, but not by MPP+ (1-methyl-4-phenylpyridinium), TEA (tetraethylammonium), decynium-22

107 im, and induces apoptosis only in 1-methyl-4-phenylpyridinium-treated cells.

108 This binding is lost following 1-methyl-4-phenylpyridinium treatment.

109 of monoamines and the neurotoxin 1-methyl-4-phenylpyridinium was significantly reduced in CP tissues

110 xposed to the mitochondrial toxin 1-methyl-4-phenylpyridinium were also partially protected by lactof

111 rkinson's disease-relevant toxin, 1-methyl-4-phenylpyridinium, whereas downregulation of orthodenticl