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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 epleting 5-HT with para-chlorophenylalanine (PCPA) mimicked seizure-induced hypoventilation, partiall
19 tional experiments suggest cotranscriptional PCPA counteracted by U1 association with nascent transcr
20 also reveals that the phenyl ring of the FAD-PCPA adduct in LSD1 does not form extensive interactions
21 th FAD in LSD1 that is distinct from the FAD-PCPA adduct of MAO B.
22 roup of mice pretreated with AMPT 100 mg/kg, PCPA 100 mg/kg or PRAZ 1 mg/kg, the effect of D1 was att
23 ally expressed transcripts (HIDE-seq) mapped PCPA sites genome wide in divergent organisms.
24  structure of LSD1-CoREST in the presence of PCPA.
25  contain substitutions on the phenyl ring of PCPA to fully engage neighboring residues.
26 droxylase inhibitor parachlorophenylalanine (PCPA; 100 mg/kg, s.c.).
27 stnatal day 26 with parachlorophenylalanine (PCPA 100 mg/kg, every other day); controls received sali
28 y pretreatment with parachlorophenylalanine (PCPA), completely prevented the anticonvulsant action of
29 ostnatal day 26 using parachlorophylalanine (PCPA).
30 e in the presence of p-chloro-phenylalanine (PCPA), a tryptophan hydroxylase inhibitor, the serotonin
31 tidepressant trans-2-phenylcyclopropylamine (PCPA; tranylcypromine; Parnate), are also capable of inh
32 cing premature cleavage and polyadenylation (PCPA) and loss of expression of long (>45 kb) genes, a s
33 termination by cleavage and polyadenylation (PCPA) at cryptic polyadenylation signals (PASs) in intro
34 emature 3' end cleavage and polyadenylation (PCPA) from cryptic polyadenylation signals (PASs) in int
35                       Following provocation, PCPA and TP+PCPA significantly increased aggression towa
36 ocessing factors, including those regulating PCPA.
37 o inhibit splicing, dose-dependently shifted PCPA downstream and elicited mRNA 3' UTR shortening and
38 Fs), that binds intronic PASs and suppresses PCPA.
39      The most striking effect of combining T+PCPA was a significant increase in attack frequency as w
40 rain areas, but to a much lesser extent than PCPA.
41                   At puberty (P40), half the PCPA-treated rats and half the saline-treated rats began
42                              Freezing in the PCPA group was significantly elevated compared to TP and
43                          Chronic exposure to PCPA alone significantly decreased locomotor activity an
44                                           TP+PCPA males were also significantly more aggressive in th
45 significantly elevated compared to TP and TP+PCPA groups, but not compared to controls.
46                             Both PCPA and TP+PCPA significantly and substantially depleted 5-HT and 5
47                                  PCPA and TP+PCPA significantly decreased locomotor activity.
48           Following provocation, PCPA and TP+PCPA significantly increased aggression toward smaller n
49                 Following withdrawal from TP+PCPA, most behavioral and neurochemical measures returne
50 tisense oligonucleotide (U1 AMO), triggering PCPA.
51 P significantly increased aggression whereas PCPA did not, suggesting that in a high-threat context,
52 ss spectrometry analyses are consistent with PCPA forming a covalent adduct with FAD in LSD1 that is