ライフサイエンスコーパス: PCPA

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