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1                                              PCPA alone significantly increased nose poke latency com
2                                              PCPA and TP+PCPA significantly decreased locomotor activ
3                                              PCPA significantly and substantially depleted 5-HT and 5
4 abels into the inactivator, [2,3-(13)C(2)]-1-PCPA, followed by analysis using on-line liquid chromato
5 d between the flavin cofactor of MAO N and 1-PCPA are similar to those reported for the irreversible
6                  1-Phenylcyclopropylamine (1-PCPA) is shown to be an inactivator of the fungal flavoe
7 idence supports covalent attachment of the 1-PCPA inactivator to the cofactor as N(5)-3-oxo-3-phenylp
8 eversible inactivation product formed with 1-PCPA and mammalian mitochondrial monoamine oxidase B.
9                                            2-PCPA shows limited selectivity for human MAOs versus LSD
10 files of LSD1 activity and inactivation by 2-PCPA as a function of pH are consistent with a mechanism
11 AD as the site of covalent modification by 2-PCPA.
12 ating that trans-2-phenylcyclopropylamine (2-PCPA, tranylcypromine, Parnate) was the most potent with
13                          Here we show that 2-PCPA is a time-dependent, mechanism-based irreversible i
14                                         Both PCPA and TP+PCPA significantly and substantially deplete
15 etic parameters of the inhibition of LSD1 by PCPA and determined the crystal structure of LSD1-CoREST
16 otonin depleting drug p-chlorophenylalanine (PCPA) or with the serotonin reuptake inhibitor fluoxetin
17  of 5-HT stores using p-chlorophenylalanine (PCPA), a 5-HT-synthesis inhibitor, abolished luminal fac
18 tional experiments suggest cotranscriptional PCPA counteracted by U1 association with nascent transcr
19 also reveals that the phenyl ring of the FAD-PCPA adduct in LSD1 does not form extensive interactions
20 th FAD in LSD1 that is distinct from the FAD-PCPA adduct of MAO B.
21 roup of mice pretreated with AMPT 100 mg/kg, PCPA 100 mg/kg or PRAZ 1 mg/kg, the effect of D1 was att
22 ally expressed transcripts (HIDE-seq) mapped PCPA sites genome wide in divergent organisms.
23  structure of LSD1-CoREST in the presence of PCPA.
24  contain substitutions on the phenyl ring of PCPA to fully engage neighboring residues.
25 droxylase inhibitor parachlorophenylalanine (PCPA; 100 mg/kg, s.c.).
26 stnatal day 26 with parachlorophenylalanine (PCPA 100 mg/kg, every other day); controls received sali
27 y pretreatment with parachlorophenylalanine (PCPA), completely prevented the anticonvulsant action of
28 ostnatal day 26 using parachlorophylalanine (PCPA).
29 e in the presence of p-chloro-phenylalanine (PCPA), a tryptophan hydroxylase inhibitor, the serotonin
30 tidepressant trans-2-phenylcyclopropylamine (PCPA; tranylcypromine; Parnate), are also capable of inh
31 termination by cleavage and polyadenylation (PCPA) at cryptic polyadenylation signals (PASs) in intro
32                       Following provocation, PCPA and TP+PCPA significantly increased aggression towa
33 o inhibit splicing, dose-dependently shifted PCPA downstream and elicited mRNA 3' UTR shortening and
34      The most striking effect of combining T+PCPA was a significant increase in attack frequency as w
35 rain areas, but to a much lesser extent than PCPA.
36                   At puberty (P40), half the PCPA-treated rats and half the saline-treated rats began
37                              Freezing in the PCPA group was significantly elevated compared to TP and
38                          Chronic exposure to PCPA alone significantly decreased locomotor activity an
39                                           TP+PCPA males were also significantly more aggressive in th
40 significantly elevated compared to TP and TP+PCPA groups, but not compared to controls.
41                             Both PCPA and TP+PCPA significantly and substantially depleted 5-HT and 5
42                                  PCPA and TP+PCPA significantly decreased locomotor activity.
43           Following provocation, PCPA and TP+PCPA significantly increased aggression toward smaller n
44                 Following withdrawal from TP+PCPA, most behavioral and neurochemical measures returne
45 P significantly increased aggression whereas PCPA did not, suggesting that in a high-threat context,
46 ss spectrometry analyses are consistent with PCPA forming a covalent adduct with FAD in LSD1 that is

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