PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
7777221-3	1995	The present experiment tested whether the MAO inhibitor antidepressant phenelzine shares this common effect of anxiolytics and imipramine on hippocampal RSA.	Phenelzine	71-81	monoamine oxidase A	Rattus norvegicus	42-45
7931216-1	1994	The MAO inhibitor phenelzine (2-phenylethylhydrazine; PLZ) is used widely in psychiatry for the treatment of depression and panic disorder.	Phenelzine	18-28	monoamine oxidase A	Rattus norvegicus	4-7
8584653-1	1995	Phenelzine (PLZ), a frequently prescribed monoamine oxidase (MAO) inhibitor, is used as an antidepressant/antipanic drug and has been shown to cause marked increases in rat brain levels of the amino acids gamma-aminobutyric acid (GABA) and alanine.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	42-59
8584653-1	1995	Phenelzine (PLZ), a frequently prescribed monoamine oxidase (MAO) inhibitor, is used as an antidepressant/antipanic drug and has been shown to cause marked increases in rat brain levels of the amino acids gamma-aminobutyric acid (GABA) and alanine.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	61-64
8584653-1	1995	Phenelzine (PLZ), a frequently prescribed monoamine oxidase (MAO) inhibitor, is used as an antidepressant/antipanic drug and has been shown to cause marked increases in rat brain levels of the amino acids gamma-aminobutyric acid (GABA) and alanine.	Phenelzine	12-15	monoamine oxidase A	Rattus norvegicus	42-59
8584653-1	1995	Phenelzine (PLZ), a frequently prescribed monoamine oxidase (MAO) inhibitor, is used as an antidepressant/antipanic drug and has been shown to cause marked increases in rat brain levels of the amino acids gamma-aminobutyric acid (GABA) and alanine.	Phenelzine	12-15	monoamine oxidase A	Rattus norvegicus	61-64
8584653-6	1995	The effects of PLZ on GLN and GABA were blocked by prior treatment of the rats with tranylcypromine, a MAO inhibitor that had been shown previously to have no direct effect itself on GABA levels in rat brain.	Phenelzine	15-18	monoamine oxidase A	Rattus norvegicus	103-106
8584653-7	1995	Since PLZ is known to be a substrate (as well as an inhibitor) of MAO, the studies with tranylcypromine pretreatment suggest that the effects on GLN and GABA are caused, at least in part, by a metabolite of PLZ.	Phenelzine	6-9	monoamine oxidase A	Rattus norvegicus	66-69
8584653-7	1995	Since PLZ is known to be a substrate (as well as an inhibitor) of MAO, the studies with tranylcypromine pretreatment suggest that the effects on GLN and GABA are caused, at least in part, by a metabolite of PLZ.	Phenelzine	207-210	monoamine oxidase A	Rattus norvegicus	66-69
8584654-6	1995	The metabolism of agmatine by DAO was inhibited by aminoguanidine (IC50 14.9 nM) and by the antidepressant, phenelzine (IC50 1.95 microM).	Phenelzine	108-118	amine oxidase, copper containing 1	Rattus norvegicus	30-33
8151003-1	1994	A case report of a hypertensive crisis resulting from the ingestion of tap beer in a patient on an irreversible monamine oxidase inhibitor (MAOI; phenelzine) stimulated the investigation of different kinds of beer for tyramine concentration.	Phenelzine	146-156	nuclear RNA export factor 1	Homo sapiens	71-74
7931216-1	1994	The MAO inhibitor phenelzine (2-phenylethylhydrazine; PLZ) is used widely in psychiatry for the treatment of depression and panic disorder.	Phenelzine	30-52	monoamine oxidase A	Rattus norvegicus	4-7
1282522-6	1992	The results support other reports of comparable antidepressant efficacy for brofaromine and phenelzine, both inhibitors of MAO-A in humans.	Phenelzine	92-102	monoamine oxidase A	Homo sapiens	123-128
8093834-3	1993	Phenelzine, an inhibitor of both type A and type B monoamine oxidase (MAO), reduced the binding of 3H-idazoxan in the locus coeruleus and in several areas with noradrenergic innervation from tegmental cell bodies.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	70-73
1610412-1	1992	The effects of long-term (28-day) administration of several antidepressant/antipanic drugs [imipramine, desipramine, tranylcypromine and phenelzine (PLZ)] on gamma-aminobutyric acid-tranaminase (GABA-T) activity and GABA levels were investigated in rat frontal cortex.	Phenelzine	137-147	4-aminobutyrate aminotransferase	Rattus norvegicus	158-193
1483111-6	1992	Porcine SSAO was inhibited both by semicarbazide and phenelzine while deprenyl or clorgyline were without any effect on enzyme activity.	Phenelzine	53-63	amine oxidase copper containing 2	Homo sapiens	8-12
1358403-7	1992	On the other hand, a complete shift to the low-affinity binding state was observed after a 24 h in vivo treatment with inhibitors of monoamine oxidase A (phenelzine or clorgyline) but not of monoamine oxidase B (deprenyl).	Phenelzine	154-164	monoamine oxidase A	Rattus norvegicus	133-152
1610412-0	1992	Effects of the antidepressant/antipanic drug phenelzine on GABA concentrations and GABA-transaminase activity in rat brain.	Phenelzine	45-55	4-aminobutyrate aminotransferase	Rattus norvegicus	83-100
1610412-4	1992	Time-response studies on inhibition of GABA-T in whole brain demonstrated that at a dose of PLZ of 15 mg/kg i.p.	Phenelzine	92-95	4-aminobutyrate aminotransferase	Rattus norvegicus	39-45
2025379-8	1991	Repeated administration of clorgyline, phenelzine, tranylcypromine, citalopram, or sertraline produced an attenuation of the hypothermic response of rats to acute subcutaneous injection of the 5-HT1A-receptor-agonist DPAT.	Phenelzine	39-49	5-hydroxytryptamine receptor 1A	Rattus norvegicus	193-199
1351783-0	1992	The antidepressants fluoxetine, idazoxan and phenelzine alter corticotropin-releasing hormone and tyrosine hydroxylase mRNA levels in rat brain: therapeutic implications.	Phenelzine	45-55	corticotropin releasing hormone	Rattus norvegicus	62-93
1852266-5	1991	5-Fluoro-alpha-methyltryptamine markedly protected only MAOA against inhibition by phenelzine, without protecting MAOB.	Phenelzine	83-93	monoamine oxidase A	Mus musculus	56-60
2059905-4	1991	Metyrapone, alpha-naphthoflavone, phenelzine, mercuric chloride, and nitrogen significantly inhibited the reaction indicating the involvement of the cytochrome P-450 monooxygenase.	Phenelzine	34-44	cytochrome P450, family 2, subfamily j, polypeptide 3	Rattus norvegicus	149-179
2248058-4	1990	Phenelzine, isocarboxazid and tranylcypromine were nonspecific, inhibiting MAO-A and MAO-B to about the same extent.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	75-80
1871333-0	1991	Enzymatic N-methylation of phenelzine catalyzed by phenylethanolamine N-methyltransferase.	Phenelzine	27-37	phenylethanolamine N-methyltransferase	Bos taurus	51-89
2248058-4	1990	Phenelzine, isocarboxazid and tranylcypromine were nonspecific, inhibiting MAO-A and MAO-B to about the same extent.	Phenelzine	0-10	monoamine oxidase B	Rattus norvegicus	85-90
1982447-0	1990	Recent studies on the MAO inhibitor phenelzine and its possible metabolites.	Phenelzine	36-46	monoamine oxidase A	Rattus norvegicus	22-25
35199904-7	2022	Here, an uncharacterized enzyme, essential for bacterial growth, was assigned as PLP-dependent cysteine desulfurase and confirmed to be inhibited by the marketed drug phenelzine.	Phenelzine	167-177	proteolipid protein 1	Homo sapiens	81-84
33815485-4	2021	We then calculated in vitro kinetic parameters of four NAT2 alleles (NAT2*4, *5, *6, and *7) for N-acetylation of aminoglutethimide, diaminodiphenyl sulfone, hydralazine, isoniazid, phenelzine, procaineamide, sulfamethazine (SMZ), and sulfapyrizine.	Phenelzine	182-192	N-acetyltransferase 2	Homo sapiens	55-59
33815485-4	2021	We then calculated in vitro kinetic parameters of four NAT2 alleles (NAT2*4, *5, *6, and *7) for N-acetylation of aminoglutethimide, diaminodiphenyl sulfone, hydralazine, isoniazid, phenelzine, procaineamide, sulfamethazine (SMZ), and sulfapyrizine.	Phenelzine	182-192	N-acetyltransferase 2	Homo sapiens	69-73
2597196-2	1989	The present study compares the inhibition of rat liver mitochondrial MAO by phenelzine and 1,1-dideuterated phenelzine and the metabolism of these drugs by that enzyme.	Phenelzine	76-86	monoamine oxidase A	Rattus norvegicus	69-72
2597196-0	1989	Deuterium isotope effect of phenelzine on the inhibition of rat liver mitochondrial monoamine oxidase activity.	Phenelzine	28-38	monoamine oxidase A	Rattus norvegicus	84-101
2597196-1	1989	Phenelzine is a suicide monoamine oxidase (MAO) inhibitor with antidepressant properties.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	24-41
2597196-1	1989	Phenelzine is a suicide monoamine oxidase (MAO) inhibitor with antidepressant properties.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	43-46
2597196-3	1989	Phenylacetaldehyde, which was measured by a high performance liquid chromatographic procedure, was found to be the major metabolite of phenelzine after incubation with MAO.	Phenelzine	135-145	monoamine oxidase A	Rattus norvegicus	168-171
2597196-9	1989	These results support the notion that the irreversible inhibition of MAO activity by phenelzine proceeds via a phenylethyldiazene intermediate, which reacts with the enzyme to form a covalent adduct.	Phenelzine	85-95	monoamine oxidase A	Rattus norvegicus	69-72
2460774-3	1988	This was performed by measuring the protection of MAO by the test compound against the irreversible inhibition produced by phenelzine.	Phenelzine	123-133	monoamine oxidase A	Rattus norvegicus	50-53
2622983-9	1989	In phenelzine- and isocarboxazid-treated rats the disruption of FR-40 responses by LSD and 8-OHDPAT were significantly reduced during Period 1, Period 2 and Washout Period.	Phenelzine	3-13	period circadian regulator 1	Rattus norvegicus	134-142
2920501-8	1989	The data suggest that the selective reversible MAO-A inhibitor brofaromine has a larger therapeutic safety than phenelzine.	Phenelzine	112-122	monoamine oxidase A	Homo sapiens	47-52
3861206-2	1985	This was recorded as the protection against the irreversible inhibition of MAO produced by phenelzine by determining the remaining deaminating activity in the absence and presence of citalopram using a low (0.1 microM) concentration of [14C]-5-hydroxytryptamine (5-HT) as substrate.	Phenelzine	91-101	monoamine oxidase A	Rattus norvegicus	75-78
3346672-7	1988	antagonized, in a dose-dependent fashion, the irreversible inhibition of brain and liver MAO-A induced by phenelzine.	Phenelzine	106-116	monoamine oxidase A	Rattus norvegicus	89-94
2885004-5	1987	Phenelzine, an MAO inhibitor, inhibited liver TAT, but other MAO inhibitors (tranylcypromine and isocarboxazid) did not.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	15-18
2885004-5	1987	Phenelzine, an MAO inhibitor, inhibited liver TAT, but other MAO inhibitors (tranylcypromine and isocarboxazid) did not.	Phenelzine	0-10	tyrosine aminotransferase	Rattus norvegicus	46-49
3005903-2	1986	This was achieved by measuring their ability to protect MAO from irreversible inhibition by phenelzine, determined by the deaminating activity of synaptosomal preparations in the absence and presence of maprotiline, a selective inhibitor of the uptake of noradrenaline, or of amfonelic acid, a potent inhibitor of the uptake of dopamine, with small (0.25 microM) concentrations of [14C]noradrenaline or [14C]dopamine as substrate.	Phenelzine	92-102	monoamine oxidase A	Rattus norvegicus	56-59
3393230-6	1988	Rat cerebral MAO activity was inhibited dose-dependently by phenelzine and by deuterated phenelzine.	Phenelzine	60-70	monoamine oxidase A	Rattus norvegicus	13-16
3393230-8	1988	The present study shows that the efficacy of phenelzine was increased about 5-fold by deuteration, that deuterated phenelzine increased tryptamine, m-tyramine and p-tyramine levels much more than it did the other monoamines, that phenylethylamine levels were least affected by the drug treatments, and that deuterated phenelzine inhibited MAO more than did phenelzine.	Phenelzine	45-55	monoamine oxidase A	Rattus norvegicus	339-342
3393230-8	1988	The present study shows that the efficacy of phenelzine was increased about 5-fold by deuteration, that deuterated phenelzine increased tryptamine, m-tyramine and p-tyramine levels much more than it did the other monoamines, that phenylethylamine levels were least affected by the drug treatments, and that deuterated phenelzine inhibited MAO more than did phenelzine.	Phenelzine	115-125	monoamine oxidase A	Rattus norvegicus	339-342
3362290-1	1988	The MAO inhibitor phenelzine (PLZ) at a dose of 25 mg/kg does not affect the behavior of rats.	Phenelzine	18-28	monoamine oxidase A	Rattus norvegicus	4-7
3362290-1	1988	The MAO inhibitor phenelzine (PLZ) at a dose of 25 mg/kg does not affect the behavior of rats.	Phenelzine	30-33	monoamine oxidase A	Rattus norvegicus	4-7
2871132-0	1986	Inhibition of aromatic L-amino acid decarboxylase and tyrosine aminotransferase by the monoamine oxidase inhibitor phenelzine.	Phenelzine	115-125	monoamine oxidase A	Rattus norvegicus	87-104
2871132-8	1986	It is suggested that the multiple enzyme inhibition caused by administration of high doses of phenelzine accounts for its unusual effects on striatal p-tyramine levels compared with other MAO inhibitors, i.e., its initial lack of effect on p-tyramine levels followed later by very large increases in p-tyramine levels.	Phenelzine	94-104	monoamine oxidase A	Rattus norvegicus	188-191
6531439-1	1984	Phenelzine (2-phenylethylhydrazine, PZ, Nardil) a clinically important antidepressant, inhibits several enzyme systems including monoamine oxidase (MAO).	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	129-146
6477643-9	1984	A large difference between the neuronal and the extraneuronal protection against the phenelzine-induced irreversible MAO inhibition in the hypothalamus was found after both acute and repeated treatment.	Phenelzine	85-95	monoamine oxidase A	Rattus norvegicus	117-120
6747915-0	1984	Interactions of a non-selective monoamine oxidase inhibitor, phenelzine, with inhibitors of 5-hydroxytryptamine, dopamine or noradrenaline re-uptake.	Phenelzine	61-71	monoamine oxidase A	Rattus norvegicus	32-49
6747915-8	1984	Following phenelzine, brain monoamine oxidase (MAO) A inhibition was 99% and that of MAO B, 88%; 5-HT concentration was significantly elevated in the cortex and hypothalamus, as was hypothalamic noradrenaline.	Phenelzine	10-20	monoamine oxidase A	Rattus norvegicus	28-45
6747915-8	1984	Following phenelzine, brain monoamine oxidase (MAO) A inhibition was 99% and that of MAO B, 88%; 5-HT concentration was significantly elevated in the cortex and hypothalamus, as was hypothalamic noradrenaline.	Phenelzine	10-20	monoamine oxidase A	Rattus norvegicus	47-50
6531439-1	1984	Phenelzine (2-phenylethylhydrazine, PZ, Nardil) a clinically important antidepressant, inhibits several enzyme systems including monoamine oxidase (MAO).	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	148-151
6531439-1	1984	Phenelzine (2-phenylethylhydrazine, PZ, Nardil) a clinically important antidepressant, inhibits several enzyme systems including monoamine oxidase (MAO).	Phenelzine	12-34	monoamine oxidase A	Rattus norvegicus	129-146
6531439-1	1984	Phenelzine (2-phenylethylhydrazine, PZ, Nardil) a clinically important antidepressant, inhibits several enzyme systems including monoamine oxidase (MAO).	Phenelzine	12-34	monoamine oxidase A	Rattus norvegicus	148-151
6531439-1	1984	Phenelzine (2-phenylethylhydrazine, PZ, Nardil) a clinically important antidepressant, inhibits several enzyme systems including monoamine oxidase (MAO).	Phenelzine	40-46	monoamine oxidase A	Rattus norvegicus	129-146
6531439-1	1984	Phenelzine (2-phenylethylhydrazine, PZ, Nardil) a clinically important antidepressant, inhibits several enzyme systems including monoamine oxidase (MAO).	Phenelzine	40-46	monoamine oxidase A	Rattus norvegicus	148-151
6646243-3	1983	Thus, with this technique the protection of MAO by the reversible inhibitors administered orally 1 h prior to the subcutaneous injection of phenelzine against the phenelzine effect could be determined inside and outside the specific aminergic neurons.	Phenelzine	140-150	monoamine oxidase A	Rattus norvegicus	44-47
6646243-3	1983	Thus, with this technique the protection of MAO by the reversible inhibitors administered orally 1 h prior to the subcutaneous injection of phenelzine against the phenelzine effect could be determined inside and outside the specific aminergic neurons.	Phenelzine	163-173	monoamine oxidase A	Rattus norvegicus	44-47
7082351-1	1982	The selectivity of benserazide and phenelzine toward inhibition of benzylamine oxidase (BzAO) and monoamine oxidases (MAO-A and MAO-B) was studied in homogenates of rat skull and lung.	Phenelzine	35-45	monoamine oxidase A	Rattus norvegicus	118-123
6305994-2	1983	A carbon radical is formed during the oxidative metabolism of phenelzine that reacts with the prosthetic heme of cytochrome P-450 and irreversibly inactivates the enzyme.	Phenelzine	62-72	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	113-129
6305994-5	1983	The metabolism of phenelzine, an alkyl hydrazine, thus yields a carbon radical that inactivates cytochrome P-450, is converted to a hydrocarbon by hydrogen atom abstraction, and reacts with spin traps or (presumably) alternative cellular targets.	Phenelzine	18-28	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	96-112
7082351-1	1982	The selectivity of benserazide and phenelzine toward inhibition of benzylamine oxidase (BzAO) and monoamine oxidases (MAO-A and MAO-B) was studied in homogenates of rat skull and lung.	Phenelzine	35-45	monoamine oxidase B	Rattus norvegicus	128-133
7082351-3	1982	Both drugs inhibited BzAO but only phenelzine inhibited MAO, whether tested in vitro or in vivo.	Phenelzine	35-45	monoamine oxidase A	Rattus norvegicus	56-59
7082351-7	1982	A reversible component in phenelzine-induced inhibition of MAO-A and -B is also suggested from in vivo studies.	Phenelzine	26-36	monoamine oxidase A	Rattus norvegicus	59-71
6161382-4	1980	The antilipolytic effect of insulin on adrenaline and 1-methyl-3-isobutyl xanthine stimulated lipolysis, is suppressed in the presence of inhibitors of prostaglandin synthetase i.e. indomethacin or phenelzine.	Phenelzine	198-208	insulin	Homo sapiens	28-35
6124090-7	1982	The occasional increase in serum PRL levels found in patients treated with lithium or the MAO inhibitor phenelzine are suggestive of important interindividual differences which may be revealed by neuroendocrine studies, differences which could be valuable in understanding the mechanism of action of these agents - e.g., does lithium decrease DA receptor sensitivity?	Phenelzine	104-114	prolactin	Homo sapiens	33-36
7288604-3	1981	In vitro, the addition of phenelzine produced immediate decrease in cytochrome P-450.	Phenelzine	26-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	68-84
7288604-4	1981	This initial decrease was found to be due to the direct binding of phenelzine to the ferrous heme of cytochrome P-450.	Phenelzine	67-77	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	101-117
7288604-5	1981	Further decrease in cytochrome P-450 occurred upon incubation of microsomes with phenelzine in the presence of NADPH.	Phenelzine	81-91	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	20-36
7288604-7	1981	The decrease in cytochrome P-450 with concomitant loss of heme can be partially inhibited by a substrate (aminopyrine) or by an inhibitor (metyrapone) of the microsomal enzymes, indicating the possible involvement of the metabolism of phenelzine to a reactive intermediate.	Phenelzine	235-245	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	16-32
7288604-8	1981	The comparison of the effect of phenelzine to that of phenylhydrazine strengthened the possibility that a reactive metabolic intermediate of phenelzine can cause heme destruction in cytochrome P-450.	Phenelzine	32-42	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	182-198
7288604-8	1981	The comparison of the effect of phenelzine to that of phenylhydrazine strengthened the possibility that a reactive metabolic intermediate of phenelzine can cause heme destruction in cytochrome P-450.	Phenelzine	141-151	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	182-198
7288604-9	1981	Thus, phenelzine exerts its inhibitory action on microsomal drug metabolism most likely by decreasing the cytochrome P-450 content largely through heme destruction.	Phenelzine	6-16	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	106-122
153184-0	1978	[Effect of an MAO inhibitor, phenelzine, on acetylation of isoniazid by isolated perfused rat liver].	Phenelzine	29-39	monoamine oxidase A	Rattus norvegicus	14-17
5801348-0	1969	Low serum pseudocholinesterase levels complicating treatment with phenelzine.	Phenelzine	66-76	butyrylcholinesterase	Homo sapiens	10-30
1187753-2	1975	The administration of NE, DOPA, amphetamine, phenelzine, desipramine and clonidine induced the reappearance of the CAR.	Phenelzine	45-55	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	115-118
5801348-1	1969	Four patients undergoing treatment with phenelzine developed low serum pseudocholinesterase levels.	Phenelzine	40-50	butyrylcholinesterase	Homo sapiens	71-91
5801348-3	1969	In three cases investigations showed that the serum pseudocholinesterase levels returned to normal after withdrawal of phenelzine.	Phenelzine	119-129	butyrylcholinesterase	Homo sapiens	52-72
31249575-3	2019	The LSD1 inhibitor phenelzine targeted both the flavin adenine dinucleotide (FAD) and CoREST binding domains of LSD1, unlike the LSD1 inhibitor GSK2879552, which only targeted the FAD domain.	Phenelzine	19-29	lysine (K)-specific demethylase 1A	Mus musculus	4-8
31270215-15	2019	SSAO, MAO, PEPCK and SREBP1c are involved in the metabolic effects of phenelzine.	Phenelzine	70-80	amine oxidase, copper containing 3	Mus musculus	0-4
31270215-15	2019	SSAO, MAO, PEPCK and SREBP1c are involved in the metabolic effects of phenelzine.	Phenelzine	70-80	phosphoenolpyruvate carboxykinase 1, cytosolic	Mus musculus	11-16
31270215-15	2019	SSAO, MAO, PEPCK and SREBP1c are involved in the metabolic effects of phenelzine.	Phenelzine	70-80	sterol regulatory element binding transcription factor 1	Mus musculus	21-28
33839994-4	2022	Also discussed are the encouraging findings of the effects of PLZ in animal models of stroke, spinal cord injury, traumatic brain injury, and multiple sclerosis, as well other actions such as reduction of nitrative stress, reduction of the effects of a toxin on dopaminergic neurons, potential anticonvulsant actions, and effects on brain-derived neurotrophic factor, neural cell adhesion molecules, an anti-apoptotic factor, and brain levels of ornithine and N-acetylamino acids.	Phenelzine	62-65	brain derived neurotrophic factor	Homo sapiens	333-366
32483206-4	2020	Targeting MAO-A with phenelzine or clorgyline, the FDA-approved drugs for antidepression, resensitize the Enz resistant (EnzR) cells to Enz treatment and further suppress EnzR cell growth in vitro and in vivo.	Phenelzine	21-31	monoamine oxidase A	Homo sapiens	10-15
32483206-6	2020	Together, our results show that targeting the Enz/ARv7/MAO-A signaling with the antidepressants phenelzine or clorgyline can restore Enz sensitivity to suppress EnzR cell growth, which may indicate that these antidepression drugs can overcome the Enz resistance to further suppress the EnzR CRPC.	Phenelzine	96-106	monoamine oxidase A	Homo sapiens	55-60
32203303-0	2020	MAOA inhibitor phenelzine efficacious in recurrent prostate cancer.	Phenelzine	15-25	monoamine oxidase A	Homo sapiens	0-4
31249575-3	2019	The LSD1 inhibitor phenelzine targeted both the flavin adenine dinucleotide (FAD) and CoREST binding domains of LSD1, unlike the LSD1 inhibitor GSK2879552, which only targeted the FAD domain.	Phenelzine	19-29	REST corepressor 2	Mus musculus	86-92
31249575-3	2019	The LSD1 inhibitor phenelzine targeted both the flavin adenine dinucleotide (FAD) and CoREST binding domains of LSD1, unlike the LSD1 inhibitor GSK2879552, which only targeted the FAD domain.	Phenelzine	19-29	lysine (K)-specific demethylase 1A	Mus musculus	112-116
31249575-3	2019	The LSD1 inhibitor phenelzine targeted both the flavin adenine dinucleotide (FAD) and CoREST binding domains of LSD1, unlike the LSD1 inhibitor GSK2879552, which only targeted the FAD domain.	Phenelzine	19-29	lysine (K)-specific demethylase 1A	Mus musculus	112-116
31249575-5	2019	Overall, the LSD1 inhibitors phenelzine and GSK2879552 are useful tools for dissecting the contribution of LSD1 demethylase activity and the nuclear LSD1-CoREST complex to switching macrophage polarization programs.	Phenelzine	29-39	lysine (K)-specific demethylase 1A	Mus musculus	13-17
31249575-5	2019	Overall, the LSD1 inhibitors phenelzine and GSK2879552 are useful tools for dissecting the contribution of LSD1 demethylase activity and the nuclear LSD1-CoREST complex to switching macrophage polarization programs.	Phenelzine	29-39	lysine (K)-specific demethylase 1A	Mus musculus	107-111
31249575-5	2019	Overall, the LSD1 inhibitors phenelzine and GSK2879552 are useful tools for dissecting the contribution of LSD1 demethylase activity and the nuclear LSD1-CoREST complex to switching macrophage polarization programs.	Phenelzine	29-39	lysine (K)-specific demethylase 1A	Mus musculus	107-111
31249575-5	2019	Overall, the LSD1 inhibitors phenelzine and GSK2879552 are useful tools for dissecting the contribution of LSD1 demethylase activity and the nuclear LSD1-CoREST complex to switching macrophage polarization programs.	Phenelzine	29-39	REST corepressor 2	Mus musculus	154-160
30650583-6	2019	Phenelzine, which inhibits MAO and AOC, limits adipogenesis in cultured preadipocytes and impairs lipogenesis in mature adipocytes.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	27-30
30709838-4	2019	Inactivation of CYP2C8 by amiodarone (100 muM), clopidogrel acyl-beta-d-glucuronide (100 muM), gemfibrozil 1-O-beta-glucuronide (100 muM), and phenelzine (100 muM) was investigated in HLMs and three recombinant human CYP2C8 preparations (Supersomes, Bactosomes, and EasyCYP Bactosomes) using amodiaquine N-deethylation as the marker reaction.	Phenelzine	143-153	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	16-22
30709838-9	2019	Phenelzine caused strong inactivation of CYP2C8 in one Supersome lot (91% inhibition) but not in HLMs or other recombinant CYP2C8 preparations.	Phenelzine	0-10	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	41-47
30857888-0	2019	Attenuation of the effects of oxidative stress by the MAO-inhibiting antidepressant and carbonyl scavenger phenelzine.	Phenelzine	107-117	monoamine oxidase A	Rattus norvegicus	54-57
30857888-1	2019	Phenelzine (beta-phenylethylhydrazine) is a monoamine oxidase (MAO)-inhibiting antidepressant with anxiolytic properties.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	44-61
30857888-1	2019	Phenelzine (beta-phenylethylhydrazine) is a monoamine oxidase (MAO)-inhibiting antidepressant with anxiolytic properties.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	63-66
30857888-1	2019	Phenelzine (beta-phenylethylhydrazine) is a monoamine oxidase (MAO)-inhibiting antidepressant with anxiolytic properties.	Phenelzine	12-37	monoamine oxidase A	Rattus norvegicus	44-61
30857888-1	2019	Phenelzine (beta-phenylethylhydrazine) is a monoamine oxidase (MAO)-inhibiting antidepressant with anxiolytic properties.	Phenelzine	12-37	monoamine oxidase A	Rattus norvegicus	63-66
30857888-5	2019	Phenelzine is unusual in that it is both an inhibitor of and a substrate for MAO, the latter action producing at least one active metabolite, beta-phenylethylidenehydrazine (PEH).	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	77-80
30857888-7	2019	Phenelzine may ameliorate the effects of oxidative stress by reducing formation of reactive metabolites (aldehydes, hydrogen peroxide, ammonia/ammonia derivatives) produced by the interaction of MAO with biogenic amines, by sequestering various other reactive aldehydes and by inhibiting primary amine oxidase.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	195-198
30693539-8	2019	RESULTS: We observed that MAOAIs, particularly clorgyline and phenelzine, were effective at decreasing MAOA activity in human prostate cancer cells.	Phenelzine	62-72	monoamine oxidase A	Homo sapiens	26-30
30739825-1	2019	Phenelzine was first employed to design new aryl hydrazine-based LSD1 inhibitors based on the experience-based discovery (EBD) strategy.	Phenelzine	0-10	lysine demethylase 1A	Homo sapiens	65-69
29256041-8	2018	The monoamine oxidase (MAO) and potential CoREST inhibitor, phenelzine, which is brain penetrant, was able to stimulate HIV production in human microglial cell lines and human glial cells recovered from the brains of HIV-infected humanized mice.	Phenelzine	60-70	REST corepressor 1	Homo sapiens	42-48
29802870-6	2018	Phenelzine treatment up-regulated the expression and proteolysis of L1.1 (a homolog of the mammalian recognition molecule L1) and phosphorylation of Erk in the spinal cord caudal to lesion site.	Phenelzine	0-10	immunoglobulin kappa variable 1-6	Homo sapiens	68-72
29802870-6	2018	Phenelzine treatment up-regulated the expression and proteolysis of L1.1 (a homolog of the mammalian recognition molecule L1) and phosphorylation of Erk in the spinal cord caudal to lesion site.	Phenelzine	0-10	L1 cell adhesion molecule	Homo sapiens	68-70
29802870-6	2018	Phenelzine treatment up-regulated the expression and proteolysis of L1.1 (a homolog of the mammalian recognition molecule L1) and phosphorylation of Erk in the spinal cord caudal to lesion site.	Phenelzine	0-10	mitogen-activated protein kinase 1	Homo sapiens	149-152
30242487-2	2018	The monoamine oxidases A and B (MAOA/MAOB) are prime candidates for the investigation into the role of DNA methylation in mental disorders, given their pivotal role in the metabolism of monoamines and as pharmacological targets of potent antidepressant drugs such as tranylcypromine, phenelzine or moclobemide.	Phenelzine	284-294	monoamine oxidase A	Homo sapiens	32-36
30242487-2	2018	The monoamine oxidases A and B (MAOA/MAOB) are prime candidates for the investigation into the role of DNA methylation in mental disorders, given their pivotal role in the metabolism of monoamines and as pharmacological targets of potent antidepressant drugs such as tranylcypromine, phenelzine or moclobemide.	Phenelzine	284-294	monoamine oxidase B	Homo sapiens	37-41
29852243-7	2018	Interestingly, known aldehyde scavenger phenelzine can significantly alleviate post-I/R SCI hypersensitivity, reduce acrolein, suppress TPRA1 upregulation, and improve motor neuron survival.	Phenelzine	40-50	transmembrane protein adipocyte associated 1	Homo sapiens	136-141
28823263-5	2017	RESULTS: Phenelzine inhibited proliferation and promoted apoptosis of Jeko-1 cells in a dose-dependent way by increasing the expression of apoptosis related protein BAX, Caspase-3 and p21, while decreasing anti-apoptotic protein BCL-2.	Phenelzine	9-19	BCL2 associated X, apoptosis regulator	Homo sapiens	165-168
29889084-7	2018	Phenelzine-treated mice showed decreased levels of pro-inflammatory cytokines, such as interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha in the injured spinal cord during the acute phase of inflammation.	Phenelzine	0-10	interleukin 1 beta	Mus musculus	87-104
29889084-7	2018	Phenelzine-treated mice showed decreased levels of pro-inflammatory cytokines, such as interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha in the injured spinal cord during the acute phase of inflammation.	Phenelzine	0-10	interleukin 6	Mus musculus	106-152
28823263-5	2017	RESULTS: Phenelzine inhibited proliferation and promoted apoptosis of Jeko-1 cells in a dose-dependent way by increasing the expression of apoptosis related protein BAX, Caspase-3 and p21, while decreasing anti-apoptotic protein BCL-2.	Phenelzine	9-19	caspase 3	Homo sapiens	170-179
28823263-5	2017	RESULTS: Phenelzine inhibited proliferation and promoted apoptosis of Jeko-1 cells in a dose-dependent way by increasing the expression of apoptosis related protein BAX, Caspase-3 and p21, while decreasing anti-apoptotic protein BCL-2.	Phenelzine	9-19	H3 histone pseudogene 16	Homo sapiens	184-187
28823263-5	2017	RESULTS: Phenelzine inhibited proliferation and promoted apoptosis of Jeko-1 cells in a dose-dependent way by increasing the expression of apoptosis related protein BAX, Caspase-3 and p21, while decreasing anti-apoptotic protein BCL-2.	Phenelzine	9-19	BCL2 apoptosis regulator	Homo sapiens	229-234
28823263-7	2017	Moreover, phosphorylation of GSF-3beta, beta-catenin, c-myc and cyclinD1 decreased after exposure to phenelzine for 24 hours.	Phenelzine	101-111	catenin beta 1	Homo sapiens	40-52
28823263-7	2017	Moreover, phosphorylation of GSF-3beta, beta-catenin, c-myc and cyclinD1 decreased after exposure to phenelzine for 24 hours.	Phenelzine	101-111	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	54-59
28823263-7	2017	Moreover, phosphorylation of GSF-3beta, beta-catenin, c-myc and cyclinD1 decreased after exposure to phenelzine for 24 hours.	Phenelzine	101-111	cyclin D1	Homo sapiens	64-72
28823263-8	2017	CONCLUSION: Phenelzine can inhibit Jeko-1 cell proliferation and induce apoptosis by regulating methylation and acetylation of histone and suppressing Wnt/beta-catenin signal pathway, suggesting its therapeutic benefit for mantle cell lymophma.	Phenelzine	12-22	catenin beta 1	Homo sapiens	155-167
26316187-0	2015	Monoamine Oxidase-A Occupancy by Moclobemide and Phenelzine: Implications for the Development of Monoamine Oxidase Inhibitors.	Phenelzine	49-59	monoamine oxidase A	Homo sapiens	0-19
27750484-4	2017	Phenelzine (PZ) is a U.S. Food and Drug Administration-approved monoamine oxidase (MAO) inhibitor (MAO-I) used for treatment of refractory depression that possesses a hydrazine functional group recently discovered by other investigators to scavenge reactive carbonyls.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	64-81
27750484-4	2017	Phenelzine (PZ) is a U.S. Food and Drug Administration-approved monoamine oxidase (MAO) inhibitor (MAO-I) used for treatment of refractory depression that possesses a hydrazine functional group recently discovered by other investigators to scavenge reactive carbonyls.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	83-86
27750484-4	2017	Phenelzine (PZ) is a U.S. Food and Drug Administration-approved monoamine oxidase (MAO) inhibitor (MAO-I) used for treatment of refractory depression that possesses a hydrazine functional group recently discovered by other investigators to scavenge reactive carbonyls.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	99-102
27259485-8	2016	The MAO-A/B inhibitor phenelzine decreased FADD (up to 33 %) and increased p-FADD (up to 65 %) and p-FADD/FADD (up to 2.4-fold).	Phenelzine	22-32	monoamine oxidase A	Rattus norvegicus	4-11
27014985-8	2016	(4) Phenelzine could upregulate the expression of Bax, caspase-3, p21, and downregulate Bcl-2 expression.	Phenelzine	4-14	BCL2 associated X, apoptosis regulator	Homo sapiens	50-53
27014985-8	2016	(4) Phenelzine could upregulate the expression of Bax, caspase-3, p21, and downregulate Bcl-2 expression.	Phenelzine	4-14	caspase 3	Homo sapiens	55-64
27014985-8	2016	(4) Phenelzine could upregulate the expression of Bax, caspase-3, p21, and downregulate Bcl-2 expression.	Phenelzine	4-14	H3 histone pseudogene 16	Homo sapiens	66-69
27014985-8	2016	(4) Phenelzine could upregulate the expression of Bax, caspase-3, p21, and downregulate Bcl-2 expression.	Phenelzine	4-14	BCL2 apoptosis regulator	Homo sapiens	88-93
27014985-10	2016	(5) Phenelzine inhibited DNMT1 expression and promoted p15 expression.	Phenelzine	4-14	DNA methyltransferase 1	Homo sapiens	25-30
27014985-10	2016	(5) Phenelzine inhibited DNMT1 expression and promoted p15 expression.	Phenelzine	4-14	cyclin dependent kinase inhibitor 2B	Homo sapiens	55-58
27014985-11	2016	CONCLUSIONS: Phenelzine increased the methylation of histone H3K4me1, H3K4me2, acetylation of histone H3 and p21, and decreased the expression of DNMT1 and p15, and ultimately inhibited the proliferation and apoptosis of Molt-4 cells.	Phenelzine	13-23	H3 histone pseudogene 16	Homo sapiens	109-112
27014985-11	2016	CONCLUSIONS: Phenelzine increased the methylation of histone H3K4me1, H3K4me2, acetylation of histone H3 and p21, and decreased the expression of DNMT1 and p15, and ultimately inhibited the proliferation and apoptosis of Molt-4 cells.	Phenelzine	13-23	DNA methyltransferase 1	Homo sapiens	146-151
27014985-11	2016	CONCLUSIONS: Phenelzine increased the methylation of histone H3K4me1, H3K4me2, acetylation of histone H3 and p21, and decreased the expression of DNMT1 and p15, and ultimately inhibited the proliferation and apoptosis of Molt-4 cells.	Phenelzine	13-23	cyclin dependent kinase inhibitor 2B	Homo sapiens	156-159
25656918-3	2015	The results from single point time dependent inhibition and shift assays suggest that clorgyline, pargyline, phenelzine, and selegiline were metabolism based inhibitors of CYP2B6.	Phenelzine	109-119	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	172-178
25656918-4	2015	In IC50 shift assays, clorgyline, pargyline, phenelzine and selegiline are metabolism based inhibitors of CYP2B6 with fold shit of 3.0-, 3.7-, 2.9-, and 11.4-fold respectively.	Phenelzine	45-55	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	106-112
25656918-6	2015	Phenelzine inactivated CYP2B6 with KI and k(inact) values of 44.9 +- 6.9 muM and 0.085 +- 0.003 min(-1) respectively.	Phenelzine	0-10	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	23-29
25656918-13	2015	Caution is required while co-administering phenelzine with substrates that are exclusively metabolized by CYP2B6 enzyme and substrates that have narrow therapeutic index.	Phenelzine	43-53	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	106-112
24607770-1	2014	Phenelzine, a non-selective irreversible inhibitor of monoamine oxidase (MAO), has been used in the treatment of depression and anxiety disorders for several decades.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	54-71
24607770-1	2014	Phenelzine, a non-selective irreversible inhibitor of monoamine oxidase (MAO), has been used in the treatment of depression and anxiety disorders for several decades.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	73-76
24607770-4	2014	Administration of either phenelzine or PEH to rats has been reported to produce dramatic increases in rat brain levels of GABA and alanine while reducing levels of glutamine; these effects are abolished for phenelzine, but not for PEH, when the animals are pre-treated with another MAO inhibitor, suggesting that they are mediated by the MAO-catalyzed formation of PEH from phenelzine.	Phenelzine	25-35	monoamine oxidase A	Rattus norvegicus	282-285
24607770-4	2014	Administration of either phenelzine or PEH to rats has been reported to produce dramatic increases in rat brain levels of GABA and alanine while reducing levels of glutamine; these effects are abolished for phenelzine, but not for PEH, when the animals are pre-treated with another MAO inhibitor, suggesting that they are mediated by the MAO-catalyzed formation of PEH from phenelzine.	Phenelzine	25-35	monoamine oxidase A	Rattus norvegicus	338-341
24707965-0	2014	A selective phenelzine analogue inhibitor of histone demethylase LSD1.	Phenelzine	12-22	lysine demethylase 1A	Homo sapiens	65-69
24707965-2	2014	This study describes the design and synthesis of analogues of a monoamine oxidase antidepressant, phenelzine, and their LSD1 inhibitory properties.	Phenelzine	98-108	lysine demethylase 1A	Homo sapiens	120-124
24707965-3	2014	A novel phenelzine analogue (bizine) containing a phenyl-butyrylamide appendage was shown to be a potent LSD1 inhibitor in vitro and was selective versus monoamine oxidases A/B and the LSD1 homologue, LSD2.	Phenelzine	8-18	lysine demethylase 1A	Homo sapiens	105-109
24707965-3	2014	A novel phenelzine analogue (bizine) containing a phenyl-butyrylamide appendage was shown to be a potent LSD1 inhibitor in vitro and was selective versus monoamine oxidases A/B and the LSD1 homologue, LSD2.	Phenelzine	8-18	lysine demethylase 1A	Homo sapiens	185-189
24707965-3	2014	A novel phenelzine analogue (bizine) containing a phenyl-butyrylamide appendage was shown to be a potent LSD1 inhibitor in vitro and was selective versus monoamine oxidases A/B and the LSD1 homologue, LSD2.	Phenelzine	8-18	lysine demethylase 1B	Homo sapiens	201-205
23392617-1	2013	Phenelzine is a monoamine oxidase (MAO) inhibitor used in treatment of depression and anxiety disorders.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	16-33
24972362-10	2014	With nortriptyline, 1/10 (10%) remitted with nortriptyline+lithium, and 1/5 (20%) when phenelzine was added.	Phenelzine	87-97	WD repeat and HMG-box DNA binding protein 1	Homo sapiens	68-75
23242743-1	2013	The antidepressant phenelzine is a monoamine oxidase inhibitor known to inhibit various other enzymes, among them semicarbazide-sensitive amine oxidase (currently named primary amine oxidase: SSAO/PrAO), absent from neurones but abundant in adipocytes.	Phenelzine	19-29	amine oxidase, copper containing 3	Mus musculus	192-196
23392617-1	2013	Phenelzine is a monoamine oxidase (MAO) inhibitor used in treatment of depression and anxiety disorders.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	35-38
23392617-3	2013	Phenelzine is not only an inhibitor of, but also a substrate for, MAO and it has been suggested that an active metabolite, namely beta-phenylethylidenehydrazine (PEH), is responsible for phenelzine"s effects on amino acids.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	66-69
20148560-9	2010	We re-explored MAO antidepressant agent phenelzine (phenethylhydrazine), previously reported to be a weak LSD1 inhibitor, and found that it is far more potent than previously appreciated.	Phenelzine	40-50	lysine demethylase 1A	Homo sapiens	106-110
22763802-3	2012	The purpose of this study was to determine if phenelzine affects the production of NO and tumor necrosis factor-alpha (TNF-alpha) in activated microglia cells.	Phenelzine	46-56	tumor necrosis factor	Mus musculus	90-117
22763802-3	2012	The purpose of this study was to determine if phenelzine affects the production of NO and tumor necrosis factor-alpha (TNF-alpha) in activated microglia cells.	Phenelzine	46-56	tumor necrosis factor	Mus musculus	119-128
22763802-5	2012	Phenelzine increased the lipopolysaccharide (LPS)-induced expression of inducible nitric oxide synthase (iNOS), as well as the release of TNF-alpha and IL-6 in BV-2 microglia cells.	Phenelzine	0-10	nitric oxide synthase 2, inducible	Mus musculus	72-103
22763802-5	2012	Phenelzine increased the lipopolysaccharide (LPS)-induced expression of inducible nitric oxide synthase (iNOS), as well as the release of TNF-alpha and IL-6 in BV-2 microglia cells.	Phenelzine	0-10	nitric oxide synthase 2, inducible	Mus musculus	105-109
22763802-5	2012	Phenelzine increased the lipopolysaccharide (LPS)-induced expression of inducible nitric oxide synthase (iNOS), as well as the release of TNF-alpha and IL-6 in BV-2 microglia cells.	Phenelzine	0-10	tumor necrosis factor	Mus musculus	138-147
22763802-5	2012	Phenelzine increased the lipopolysaccharide (LPS)-induced expression of inducible nitric oxide synthase (iNOS), as well as the release of TNF-alpha and IL-6 in BV-2 microglia cells.	Phenelzine	0-10	interleukin 6	Mus musculus	152-156
22763802-6	2012	It is also confirmed that phenelzine increased the levels of NO, TNF-alpha and IL-6 in LPS-activated primary microglia cells.	Phenelzine	26-36	tumor necrosis factor	Mus musculus	65-74
22763802-6	2012	It is also confirmed that phenelzine increased the levels of NO, TNF-alpha and IL-6 in LPS-activated primary microglia cells.	Phenelzine	26-36	interleukin 6	Mus musculus	79-83
22763802-7	2012	Phenelzine increased nuclear translocation of NF-kappaB by phosphorylation of IkappaB-alpha in LPS-activated microglia cells.	Phenelzine	0-10	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	78-91
22763802-8	2012	These findings suggest that high doses of phenelzine could aggravate inflammatory responses in microglia cells that are mediated by NO and TNF-alpha.	Phenelzine	42-52	tumor necrosis factor	Mus musculus	139-148
21876670-8	2011	In addition, small hairpin RNAs directed against LSD1/KDM1 or inhibition of its activity with the monoamine oxidase inhibitor phenelzine suppresses the activation of HIV transcription in latently infected T cells.Our data support the model that a LSD1/KDM1/CoREST complex, normally known as a transcriptional suppressor, acts as a novel activator of HIV transcription through demethylation of K51 in Tat.	Phenelzine	126-136	lysine demethylase 1A	Homo sapiens	247-251
21876670-8	2011	In addition, small hairpin RNAs directed against LSD1/KDM1 or inhibition of its activity with the monoamine oxidase inhibitor phenelzine suppresses the activation of HIV transcription in latently infected T cells.Our data support the model that a LSD1/KDM1/CoREST complex, normally known as a transcriptional suppressor, acts as a novel activator of HIV transcription through demethylation of K51 in Tat.	Phenelzine	126-136	lysine demethylase 1A	Homo sapiens	252-256
21876670-8	2011	In addition, small hairpin RNAs directed against LSD1/KDM1 or inhibition of its activity with the monoamine oxidase inhibitor phenelzine suppresses the activation of HIV transcription in latently infected T cells.Our data support the model that a LSD1/KDM1/CoREST complex, normally known as a transcriptional suppressor, acts as a novel activator of HIV transcription through demethylation of K51 in Tat.	Phenelzine	126-136	REST corepressor 1	Homo sapiens	257-263
21876670-8	2011	In addition, small hairpin RNAs directed against LSD1/KDM1 or inhibition of its activity with the monoamine oxidase inhibitor phenelzine suppresses the activation of HIV transcription in latently infected T cells.Our data support the model that a LSD1/KDM1/CoREST complex, normally known as a transcriptional suppressor, acts as a novel activator of HIV transcription through demethylation of K51 in Tat.	Phenelzine	126-136	tyrosine aminotransferase	Homo sapiens	400-403
22535688-7	2012	Three of these were the monoamine oxidase inhibitors nialamide, isocarboxazid, and phenelzine with average IC(50) values for inhibiting GUS of 71, 128, and 2300 nM, respectively.	Phenelzine	83-93	glucuronidase beta	Homo sapiens	136-139
20148560-9	2010	We re-explored MAO antidepressant agent phenelzine (phenethylhydrazine), previously reported to be a weak LSD1 inhibitor, and found that it is far more potent than previously appreciated.	Phenelzine	52-70	lysine demethylase 1A	Homo sapiens	106-110
19201819-9	2009	By contrast, the reduction in both cell triglycerides and sterol regulatory element-binding protein-1c (SREBP-1c) was detectable at lower phenelzine concentrations (1-10 microM).	Phenelzine	138-148	sterol regulatory element binding transcription factor 1	Homo sapiens	58-102
19201819-9	2009	By contrast, the reduction in both cell triglycerides and sterol regulatory element-binding protein-1c (SREBP-1c) was detectable at lower phenelzine concentrations (1-10 microM).	Phenelzine	138-148	sterol regulatory element binding transcription factor 1	Homo sapiens	104-112
19201819-10	2009	Phenelzine effect on triglyceride content was prevented by providing free fatty acids to the cells and was partially reversed by overexpression of a dominant-positive form of SREBP-1c, showing the privileged targeting of the lipogenic pathway.	Phenelzine	0-10	sterol regulatory element binding transcription factor 1	Homo sapiens	175-183
19203467-0	2008	Neurochemical effects of the monoamine oxidase inhibitor phenelzine on brain GABA and alanine: A comparison with vigabatrin.	Phenelzine	57-67	monoamine oxidase A	Rattus norvegicus	29-46
18761333-6	2008	Imipramine typically increased and phenelzine decreased GR expression in other feedback-related brain regions such as the paraventricular hypothalamus and prefrontal cortex.	Phenelzine	35-45	nuclear receptor subfamily 3, group C, member 1	Mus musculus	56-58
18761333-7	2008	Imipramine effects were limited to feedback-related regions, whereas phenelzine had additional effects to decrease accumbens GR and central amygdala MR expression.	Phenelzine	69-79	nuclear receptor subfamily 3, group C, member 1	Mus musculus	125-127
18539478-7	2008	Phenelzine clearly inhibited both MAO and SSAO when tested on adipocytes.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	34-37
18539478-7	2008	Phenelzine clearly inhibited both MAO and SSAO when tested on adipocytes.	Phenelzine	0-10	amine oxidase, copper containing 3	Rattus norvegicus	42-46
18426226-4	2008	Phenylethylhydrazine stoichiometrically reduces the covalent FAD moieties of MAO A and of MAO B.	Phenelzine	0-20	BRCA2 DNA repair associated	Homo sapiens	61-64
18426226-4	2008	Phenylethylhydrazine stoichiometrically reduces the covalent FAD moieties of MAO A and of MAO B.	Phenelzine	0-20	monoamine oxidase A	Homo sapiens	77-82
18426226-4	2008	Phenylethylhydrazine stoichiometrically reduces the covalent FAD moieties of MAO A and of MAO B.	Phenelzine	0-20	monoamine oxidase B	Homo sapiens	90-95
18426226-5	2008	Molecular oxygen is required for the inhibition reactions, and the level of O2 consumption for phenylethylhydrazine is 6-7-fold higher with either MAO A or MAO B than for the corresponding reactions with benzylhydrazine or phenylhydrazine.	Phenelzine	95-115	monoamine oxidase A	Homo sapiens	147-152
18426226-5	2008	Molecular oxygen is required for the inhibition reactions, and the level of O2 consumption for phenylethylhydrazine is 6-7-fold higher with either MAO A or MAO B than for the corresponding reactions with benzylhydrazine or phenylhydrazine.	Phenelzine	95-115	monoamine oxidase B	Homo sapiens	156-161
18426226-8	2008	The three-dimensional (2.3 A) structures of phenylethylhydrazine- and benzylhydrazine-inhibited MAO B show that alkylation occurs at the N(5) position on the re face of the covalent flavin with loss of the hydrazyl nitrogens.	Phenelzine	44-64	monoamine oxidase B	Homo sapiens	96-101
18923402-6	2009	Treatment for 14 days with 70 mg/kg per day venlafaxine, which inhibits both the NET and SERT, or 10 mg/kg per day phenelzine, a monoamine oxidase inhibitor, produced antidepressant-like effects on behavior without altering NET or SERT expression.	Phenelzine	115-125	solute carrier family 6 member 4	Rattus norvegicus	231-235
19203467-7	2008	CONCLUSIONS: At the doses studied, PLZ was as effective as VIG at elevating brain GABA levels, but, unlike VIG, also inhibited MAO and ALA-T (and increased brain ALA levels).	Phenelzine	35-38	monoamine oxidase A	Rattus norvegicus	127-130
19203467-7	2008	CONCLUSIONS: At the doses studied, PLZ was as effective as VIG at elevating brain GABA levels, but, unlike VIG, also inhibited MAO and ALA-T (and increased brain ALA levels).	Phenelzine	35-38	glutamic--pyruvic transaminase	Rattus norvegicus	135-140
19203467-8	2008	Pretreatment of rats with the MAO inhibitor tranylcypromine prevented the increase in brain GABA and ALA levels with PLZ, but did not block the effect of VIG on GABA.	Phenelzine	117-120	monoamine oxidase A	Rattus norvegicus	30-33
19203467-1	2008	PURPOSE: To compare phenelzine (PLZ), an antidepressant drug with anxiolytic properties which inhibits monoamine oxidase (MAO) but also elevates rat brain levels of the amino acids ?-aminobutyric acid (GABA) and alanine (ALA), with vigabatrin (VIG), an anticonvulsant which elevates brain GABA by inhibition of GABA transaminase (GABA-T), with regard to their actions on brain levels of GABA and ALA and on activities of MAO, GABA-T and ALA transaminase (ALA-T).	Phenelzine	20-30	monoamine oxidase A	Rattus norvegicus	122-125
19203467-1	2008	PURPOSE: To compare phenelzine (PLZ), an antidepressant drug with anxiolytic properties which inhibits monoamine oxidase (MAO) but also elevates rat brain levels of the amino acids ?-aminobutyric acid (GABA) and alanine (ALA), with vigabatrin (VIG), an anticonvulsant which elevates brain GABA by inhibition of GABA transaminase (GABA-T), with regard to their actions on brain levels of GABA and ALA and on activities of MAO, GABA-T and ALA transaminase (ALA-T).	Phenelzine	32-35	monoamine oxidase A	Rattus norvegicus	103-120
19203467-1	2008	PURPOSE: To compare phenelzine (PLZ), an antidepressant drug with anxiolytic properties which inhibits monoamine oxidase (MAO) but also elevates rat brain levels of the amino acids ?-aminobutyric acid (GABA) and alanine (ALA), with vigabatrin (VIG), an anticonvulsant which elevates brain GABA by inhibition of GABA transaminase (GABA-T), with regard to their actions on brain levels of GABA and ALA and on activities of MAO, GABA-T and ALA transaminase (ALA-T).	Phenelzine	32-35	monoamine oxidase A	Rattus norvegicus	122-125
17768678-0	2008	Phenelzine causes an increase in brain ornithine that is prevented by prior monoamine oxidase inhibition.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	76-93
17768678-1	2008	Phenelzine (PLZ), a nonselective irreversible inhibitor of monoamine oxidase (MAO), also inhibits GABA-transaminase (GABA-T), markedly increasing brain GABA levels.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	59-76
17768678-1	2008	Phenelzine (PLZ), a nonselective irreversible inhibitor of monoamine oxidase (MAO), also inhibits GABA-transaminase (GABA-T), markedly increasing brain GABA levels.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	78-81
17768678-1	2008	Phenelzine (PLZ), a nonselective irreversible inhibitor of monoamine oxidase (MAO), also inhibits GABA-transaminase (GABA-T), markedly increasing brain GABA levels.	Phenelzine	0-10	4-aminobutyrate aminotransferase	Rattus norvegicus	98-115
17768678-1	2008	Phenelzine (PLZ), a nonselective irreversible inhibitor of monoamine oxidase (MAO), also inhibits GABA-transaminase (GABA-T), markedly increasing brain GABA levels.	Phenelzine	0-10	4-aminobutyrate aminotransferase	Rattus norvegicus	117-123
17768678-1	2008	Phenelzine (PLZ), a nonselective irreversible inhibitor of monoamine oxidase (MAO), also inhibits GABA-transaminase (GABA-T), markedly increasing brain GABA levels.	Phenelzine	12-15	monoamine oxidase A	Rattus norvegicus	59-76
17768678-1	2008	Phenelzine (PLZ), a nonselective irreversible inhibitor of monoamine oxidase (MAO), also inhibits GABA-transaminase (GABA-T), markedly increasing brain GABA levels.	Phenelzine	12-15	monoamine oxidase A	Rattus norvegicus	78-81
17768678-1	2008	Phenelzine (PLZ), a nonselective irreversible inhibitor of monoamine oxidase (MAO), also inhibits GABA-transaminase (GABA-T), markedly increasing brain GABA levels.	Phenelzine	12-15	4-aminobutyrate aminotransferase	Rattus norvegicus	98-115
17768678-1	2008	Phenelzine (PLZ), a nonselective irreversible inhibitor of monoamine oxidase (MAO), also inhibits GABA-transaminase (GABA-T), markedly increasing brain GABA levels.	Phenelzine	12-15	4-aminobutyrate aminotransferase	Rattus norvegicus	117-123
17768678-8	2008	To determine whether a metabolite formed by the action of MAO on PLZ may be responsible for the elevation in brain ORN observed, animals were pretreated with vehicle or the MAO inhibitor tranylcypromine (TCP) before vehicle or PLZ (15 mg/kg), and brains collected 3 h later.	Phenelzine	65-68	monoamine oxidase A	Rattus norvegicus	58-61
17768678-9	2008	ORN levels (measured by an HPLC procedure) were dose- and time-dependently increased in PLZ-treated animals, with levels reaching approximately 650% of control at 6 and 12 h. Pretreatment with TCP completely abolished the PLZ-induced increase in brain ORN, suggesting, as with GABA, that a metabolite of PLZ formed by the action of MAO is responsible for the elevation of brain ORN observed.	Phenelzine	88-91	monoamine oxidase A	Rattus norvegicus	332-335
17768678-9	2008	ORN levels (measured by an HPLC procedure) were dose- and time-dependently increased in PLZ-treated animals, with levels reaching approximately 650% of control at 6 and 12 h. Pretreatment with TCP completely abolished the PLZ-induced increase in brain ORN, suggesting, as with GABA, that a metabolite of PLZ formed by the action of MAO is responsible for the elevation of brain ORN observed.	Phenelzine	222-225	monoamine oxidase A	Rattus norvegicus	332-335
17768678-9	2008	ORN levels (measured by an HPLC procedure) were dose- and time-dependently increased in PLZ-treated animals, with levels reaching approximately 650% of control at 6 and 12 h. Pretreatment with TCP completely abolished the PLZ-induced increase in brain ORN, suggesting, as with GABA, that a metabolite of PLZ formed by the action of MAO is responsible for the elevation of brain ORN observed.	Phenelzine	222-225	monoamine oxidase A	Rattus norvegicus	332-335
15564336-6	2005	Phenelzine significantly increased circadian nadir and postrestraint plasma corticosterone levels in sham-operated mice, an effect that correlated with increased adrenocortical sensitivity to ACTH.	Phenelzine	0-10	pro-opiomelanocortin-alpha	Mus musculus	192-196
17912044-0	2007	The monoamine oxidase inhibitor phenelzine enhances the discriminative stimulus effect of nicotine in rats.	Phenelzine	32-42	monoamine oxidase A	Rattus norvegicus	4-21
17912044-3	2007	This study examined the effects of three MAOIs (phenelzine, clorgyline and pargyline) with varying selectivity for MAOA and MAOB in the nicotine drug discrimination procedure in rats.	Phenelzine	48-58	monoamine oxidase A	Rattus norvegicus	115-119
16500030-8	2006	Given to normal rats, fluoxetine increased total brain-derived neurotrophic factor mRNA only in hippocampus, whereas desipramine or phenelzine increased brain-derived neurotrophic factor mRNA in both frontal cortex and hippocampus.	Phenelzine	132-142	brain-derived neurotrophic factor	Rattus norvegicus	153-186
16500030-12	2006	Treatment with desipramine or phenelzine of corticosterone pellet-implanted rats reversed the corticosterone-induced decrease in total brain-derived neurotrophic factor expression in both brain areas; however, fluoxetine reversed the decrease only partially in hippocampus.	Phenelzine	30-40	brain-derived neurotrophic factor	Rattus norvegicus	135-168
17348765-3	2007	The first-generation MAOIs such as phenelzine and isocarboxazid were largely nonselective inhibitors of both subtypes of MAO, MAO(A) and MAO(B).	Phenelzine	35-45	monoamine oxidase A	Homo sapiens	126-132
17348765-3	2007	The first-generation MAOIs such as phenelzine and isocarboxazid were largely nonselective inhibitors of both subtypes of MAO, MAO(A) and MAO(B).	Phenelzine	35-45	monoamine oxidase B	Homo sapiens	137-143
16669850-6	2006	Phenelzine and isoniazid inactivated all CYP but were most potent toward CYP3A and CYP2C19.	Phenelzine	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	73-78
16669850-6	2006	Phenelzine and isoniazid inactivated all CYP but were most potent toward CYP3A and CYP2C19.	Phenelzine	0-10	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	83-90
16669850-10	2006	With the exception of phenelzine-mediated CYP3A inactivation, glutathione and superoxide dismutase failed to protect CYP from inactivation by isoniazid and phenelzine.	Phenelzine	22-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-47
15564336-8	2005	Consistent with the latter possibility, phenelzine significantly increased plasma ACTH and paraventricular hypothalamus CRH mRNA in ADX, corticosterone-replaced mice.	Phenelzine	40-50	pro-opiomelanocortin-alpha	Mus musculus	82-86
15564336-8	2005	Consistent with the latter possibility, phenelzine significantly increased plasma ACTH and paraventricular hypothalamus CRH mRNA in ADX, corticosterone-replaced mice.	Phenelzine	40-50	corticotropin releasing hormone	Mus musculus	120-123
15564336-10	2005	We conclude that chronic phenelzine treatment induces sustained increases in glucocorticoids by impairing glucocorticoid feedback, increasing adrenocortical responsiveness to ACTH, and increasing glucocorticoid-independent stimulation of hypothalamic-pituitary activity.	Phenelzine	25-35	pro-opiomelanocortin-alpha	Mus musculus	175-179
11510881-3	2001	The present study was performed using anaesthetized rats to compare the importance of MAO and COMT in DA-mediated natriuresis by use of the MAO inhibitor phenelzine.	Phenelzine	154-164	monoamine oxidase A	Rattus norvegicus	140-143
15207360-1	2004	Phenylethylidenehydrazine (PEH), an analog of the monoamine oxidase inhibitor, beta-phenylethylhydrazine (phenelzine), inhibits the gamma-aminobutyric acid (GABA) catabolic enzyme GABA-transaminase and increases brain levels of GABA.	Phenelzine	79-104	4-aminobutyrate aminotransferase	Rattus norvegicus	180-197
15207360-1	2004	Phenylethylidenehydrazine (PEH), an analog of the monoamine oxidase inhibitor, beta-phenylethylhydrazine (phenelzine), inhibits the gamma-aminobutyric acid (GABA) catabolic enzyme GABA-transaminase and increases brain levels of GABA.	Phenelzine	106-116	4-aminobutyrate aminotransferase	Rattus norvegicus	180-197
15663788-0	2005	Brainstem levels of transcription factor AP-2 in rat are changed after treatment with phenelzine, but not with citalopram.	Phenelzine	86-96	fatty acid binding protein 4	Rattus norvegicus	41-45
15663788-5	2005	In addition, previous studies have shown that the levels of AP-2alpha and AP-2beta in rat whole brain were decreased after 10 days of treatment with citalopram (SSRI) and imipramine (TCA), and were increased with phenelzine (MAO-I).	Phenelzine	213-223	transcription factor AP-2 alpha	Rattus norvegicus	60-69
15663788-7	2005	However, after treatment with phenelzine for 1, 7 or 21 days the levels of AP-2alpha and AP-2beta had increased after 7 days, but had returned to control levels at day 21.	Phenelzine	30-40	transcription factor AP-2 alpha	Rattus norvegicus	75-84
15663788-9	2005	The present data suggest that the increase in AP-2 levels previously seen in rat whole brain after subchronic treatment with phenelzine is located in the brainstem.	Phenelzine	125-135	fatty acid binding protein 4	Rattus norvegicus	46-50
15304522-7	2004	Simultaneous inactivation of CYP2C8 and CYP3A4 (paclitaxel 3"-phenyl-hydroxylation) was observed using amiodarone, isoniazid, and phenelzine with the efficiency of inactivation greater for the CYP3A4 pathway.	Phenelzine	130-140	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	29-35
15304522-7	2004	Simultaneous inactivation of CYP2C8 and CYP3A4 (paclitaxel 3"-phenyl-hydroxylation) was observed using amiodarone, isoniazid, and phenelzine with the efficiency of inactivation greater for the CYP3A4 pathway.	Phenelzine	130-140	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	40-46
15304522-7	2004	Simultaneous inactivation of CYP2C8 and CYP3A4 (paclitaxel 3"-phenyl-hydroxylation) was observed using amiodarone, isoniazid, and phenelzine with the efficiency of inactivation greater for the CYP3A4 pathway.	Phenelzine	130-140	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	193-199
12943557-0	2003	Phenelzine treatment increases transcription factor AP-2 levels in rat brain.	Phenelzine	0-10	fatty acid binding protein 4	Rattus norvegicus	52-56
12943557-7	2003	RESULTS: Subchronic administration (10 days) of phenelzine (PLZ) increased the levels of AP-2alpha, AP-2beta and the DNA binding activity of AP-2 in nuclear extracts prepared from rat whole brain when compared with sham treated animals.	Phenelzine	48-58	transcription factor AP-2 alpha	Rattus norvegicus	89-98
12943557-7	2003	RESULTS: Subchronic administration (10 days) of phenelzine (PLZ) increased the levels of AP-2alpha, AP-2beta and the DNA binding activity of AP-2 in nuclear extracts prepared from rat whole brain when compared with sham treated animals.	Phenelzine	48-58	fatty acid binding protein 4	Rattus norvegicus	89-93
12943557-7	2003	RESULTS: Subchronic administration (10 days) of phenelzine (PLZ) increased the levels of AP-2alpha, AP-2beta and the DNA binding activity of AP-2 in nuclear extracts prepared from rat whole brain when compared with sham treated animals.	Phenelzine	60-63	transcription factor AP-2 alpha	Rattus norvegicus	89-98
12943557-7	2003	RESULTS: Subchronic administration (10 days) of phenelzine (PLZ) increased the levels of AP-2alpha, AP-2beta and the DNA binding activity of AP-2 in nuclear extracts prepared from rat whole brain when compared with sham treated animals.	Phenelzine	60-63	fatty acid binding protein 4	Rattus norvegicus	89-93
11702019-1	2001	We investigated the regulatory effect of the dopaminergic agent L-dopa, the mood stabilizer lithium and the nonselective monoamine oxidase inhibitor phenelzine on brain vesicular monoamine transporter (VMAT2) expression.	Phenelzine	149-159	solute carrier family 18 member A2	Rattus norvegicus	202-207
11702019-7	2001	Phenelzine did not modulate VMAT2 gene expression but reduced the synaptophysin mRNA level (19%, p < 0.05).	Phenelzine	0-10	synaptophysin	Rattus norvegicus	66-79
10781703-0	2000	Comparison of neurochemical effects of the monoamine oxidase inhibitors phenelzine, moclobemide and brofaromine in the rat after short- and long-term administration.	Phenelzine	72-82	monoamine oxidase A	Rattus norvegicus	43-60
10736426-0	2000	Time-dependent changes in brain monoamine oxidase activity and in brain levels of monoamines and amino acids following acute administration of the antidepressant/antipanic drug phenelzine.	Phenelzine	177-187	monoamine oxidase A	Rattus norvegicus	32-49
10736426-1	2000	Phenelzine (PLZ) is a non-selective monoamine oxidase (MAO) inhibitor commonly used to treat depression and panic disorder.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	36-53
10736426-1	2000	Phenelzine (PLZ) is a non-selective monoamine oxidase (MAO) inhibitor commonly used to treat depression and panic disorder.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	55-58
10736426-1	2000	Phenelzine (PLZ) is a non-selective monoamine oxidase (MAO) inhibitor commonly used to treat depression and panic disorder.	Phenelzine	12-15	monoamine oxidase A	Rattus norvegicus	36-53
10736426-1	2000	Phenelzine (PLZ) is a non-selective monoamine oxidase (MAO) inhibitor commonly used to treat depression and panic disorder.	Phenelzine	12-15	monoamine oxidase A	Rattus norvegicus	55-58
10736426-7	2000	In contrast, the effects of PLZ on MAO activity and monoamines were longer-lasting.	Phenelzine	28-31	monoamine oxidase A	Rattus norvegicus	35-38
10736426-8	2000	For example, PLZ-induced increases in dopamine and 5-HT were observed 1 week after injection, and PLZ-induced inhibition of MAO activity persisted for 2 weeks.	Phenelzine	98-101	monoamine oxidase A	Rattus norvegicus	124-127
10736426-9	2000	Thus, in addition to demonstrating that the effects of PLZ on MAO activity and monoamines were long-lasting, these results indicate that the effects of PLZ on MAO activity and on brain levels of monoamines and amino acids are temporally dissociated.	Phenelzine	55-58	monoamine oxidase A	Rattus norvegicus	62-65
10736426-9	2000	Thus, in addition to demonstrating that the effects of PLZ on MAO activity and monoamines were long-lasting, these results indicate that the effects of PLZ on MAO activity and on brain levels of monoamines and amino acids are temporally dissociated.	Phenelzine	152-155	monoamine oxidase A	Rattus norvegicus	159-162
10781703-4	2000	RESULTS: After 30 days of administration, moclobemide and brofaromine selectively inhibited brain MAO-A activity and phenelzine inhibited MAO-A and -B to equal extents.	Phenelzine	117-127	monoamine oxidase A	Rattus norvegicus	138-150
10575045-5	1999	SERT density in the CA3 region of the hippocampus of the same rats, assessed by quantitative autoradiography with tritiated cyanoimipramine ([(3)H]CN-IMI), was decreased by 80-90% in SSRI-treated rats but not in those treated with phenelzine or DMI.	Phenelzine	231-241	solute carrier family 6 member 4	Rattus norvegicus	0-4
10693959-3	2000	Desipramine, phenelzine, and fluoxetine all increased the intensities of the PDE4A bands in hippocampal preparations; trazodone did not.	Phenelzine	13-23	phosphodiesterase 4A	Rattus norvegicus	77-82
10693959-4	2000	In preparations of cerebral cortex, the intensities of the PDE4A bands were increased following desipramine treatment, not changed following phenelzine or fluoxetine treatment, and decreased following trazodone treatment.	Phenelzine	141-151	phosphodiesterase 4A	Rattus norvegicus	59-64
9776388-0	1998	Behavioral effects of phenelzine in an experimental model for screening anxiolytic and anti-panic drugs: correlation with changes in monoamine-oxidase activity and monoamine levels.	Phenelzine	22-32	monoamine oxidase A	Rattus norvegicus	133-150
10208320-1	1999	Phenelzine (PLZ) is a non-selective monoamine oxidase (MAO) inhibitor commonly used to treat depression and panic disorder.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	36-53
10208320-1	1999	Phenelzine (PLZ) is a non-selective monoamine oxidase (MAO) inhibitor commonly used to treat depression and panic disorder.	Phenelzine	0-10	monoamine oxidase A	Rattus norvegicus	55-58
10208320-1	1999	Phenelzine (PLZ) is a non-selective monoamine oxidase (MAO) inhibitor commonly used to treat depression and panic disorder.	Phenelzine	12-15	monoamine oxidase A	Rattus norvegicus	36-53
10208320-1	1999	Phenelzine (PLZ) is a non-selective monoamine oxidase (MAO) inhibitor commonly used to treat depression and panic disorder.	Phenelzine	12-15	monoamine oxidase A	Rattus norvegicus	55-58
9829163-3	1998	While the classical, nonselective and nonreversible MAOIs, such as phenelzine and tranylcypromine, are characterised by the risk of inducing a hypertensive crisis when dietary tyramine is ingested, the selective monoamine oxidase-B (MAO-B) inhibitor selegiline (deprenyl) and, even more so, the selective and reversible monoamine oxidase-A (MAO-A) inhibitor moclobemide, are free from this potential interaction.	Phenelzine	67-77	monoamine oxidase B	Homo sapiens	212-231
9829163-3	1998	While the classical, nonselective and nonreversible MAOIs, such as phenelzine and tranylcypromine, are characterised by the risk of inducing a hypertensive crisis when dietary tyramine is ingested, the selective monoamine oxidase-B (MAO-B) inhibitor selegiline (deprenyl) and, even more so, the selective and reversible monoamine oxidase-A (MAO-A) inhibitor moclobemide, are free from this potential interaction.	Phenelzine	67-77	monoamine oxidase B	Homo sapiens	233-238
9829163-3	1998	While the classical, nonselective and nonreversible MAOIs, such as phenelzine and tranylcypromine, are characterised by the risk of inducing a hypertensive crisis when dietary tyramine is ingested, the selective monoamine oxidase-B (MAO-B) inhibitor selegiline (deprenyl) and, even more so, the selective and reversible monoamine oxidase-A (MAO-A) inhibitor moclobemide, are free from this potential interaction.	Phenelzine	67-77	monoamine oxidase A	Homo sapiens	320-339
9829163-3	1998	While the classical, nonselective and nonreversible MAOIs, such as phenelzine and tranylcypromine, are characterised by the risk of inducing a hypertensive crisis when dietary tyramine is ingested, the selective monoamine oxidase-B (MAO-B) inhibitor selegiline (deprenyl) and, even more so, the selective and reversible monoamine oxidase-A (MAO-A) inhibitor moclobemide, are free from this potential interaction.	Phenelzine	67-77	monoamine oxidase A	Homo sapiens	341-346
9776388-2	1998	injection for 14 days) treatments with the non-selective irreversible monoamine-oxidase (MAO) inhibitor phenelzine (10 and 30 mg/kg) on defensive behaviors of Swiss mice in the mouse defense test battery (MDTB) which has been designed for screening anxiolytic and anti-panic drugs.	Phenelzine	104-114	monoamine oxidase A	Rattus norvegicus	70-87
9776388-2	1998	injection for 14 days) treatments with the non-selective irreversible monoamine-oxidase (MAO) inhibitor phenelzine (10 and 30 mg/kg) on defensive behaviors of Swiss mice in the mouse defense test battery (MDTB) which has been designed for screening anxiolytic and anti-panic drugs.	Phenelzine	104-114	monoamine oxidase A	Rattus norvegicus	89-92
9776388-12	1998	Measurements of MAO activity revealed substantial reductions in both type A and B forms with a full inhibition of both forms being observed only after chronic treatment with phenelzine.	Phenelzine	174-184	monoamine oxidase A	Rattus norvegicus	16-19
9776388-13	1998	These results suggest that the effects of phenelzine may be due mainly to its effects on the 5-HT system and presumably related to the full inhibition of MAO-A and/or MAO-B.	Phenelzine	42-52	monoamine oxidase A	Rattus norvegicus	154-159
9776388-13	1998	These results suggest that the effects of phenelzine may be due mainly to its effects on the 5-HT system and presumably related to the full inhibition of MAO-A and/or MAO-B.	Phenelzine	42-52	monoamine oxidase B	Rattus norvegicus	167-172
9459570-5	1998	The steady-state levels of GAT-1 mRNA were increased significantly (23%) after long-term, but not by short-term, treatment with phenelzine.	Phenelzine	128-138	solute carrier family 6 member 12	Rattus norvegicus	27-32
9610944-7	1998	Comparison of rats treated with the monoamine oxidase (MAO) inhibitor, phenelzine [3 mg/kg, s.c., daily for 2-6 weeks] to the saline-treated groups revealed a failure to habituate to the chronic handling, as the baseline withdrawal (after injection of artificial CSF) by the phenelzine-treated animals was not different from the baseline withdrawal by unhandled rats.	Phenelzine	71-81	monoamine oxidase A	Rattus norvegicus	36-53
9610944-7	1998	Comparison of rats treated with the monoamine oxidase (MAO) inhibitor, phenelzine [3 mg/kg, s.c., daily for 2-6 weeks] to the saline-treated groups revealed a failure to habituate to the chronic handling, as the baseline withdrawal (after injection of artificial CSF) by the phenelzine-treated animals was not different from the baseline withdrawal by unhandled rats.	Phenelzine	71-81	monoamine oxidase A	Rattus norvegicus	55-58
8818569-10	1996	Northern blot analysis revealed that the observed increases in renal CYP2E1 protein levels after treatment with hydrazine or phenelzine were not accompanied by concomitant increases in CYP2E1 mRNA.	Phenelzine	125-135	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	69-75
9324239-4	1997	"Anticonvulsant" dose of isatin (80 mg/kg) reduced phenelzine-dependent inhibition of MAO B but not MAO A.	Phenelzine	51-61	monoamine oxidase B	Rattus norvegicus	86-91
9228188-7	1997	[3H]2-BFI binding sites (Bmax = 72 fmol/mg protein) in brain were differentially modulated by treatment (7 days) with cirazoline (up-regulation: 25%) and the MAO inhibitor phenelzine (down-regulation: 31%), indicating that these I2-sites are regulated in vivo, as is the case for those labelled by [3H]idazoxan.	Phenelzine	172-182	monoamine oxidase A	Rattus norvegicus	158-161
9324239-2	1997	The influence of isatin on the degree of irreversible MAO inhibition by phenelzine and pargyline has been studied in vitro and in vivo experiments.	Phenelzine	72-82	monoamine oxidase A	Rattus norvegicus	54-57
9258353-6	1997	This is in contrast to a large blood pressure rise in rats pretreated with phenelzine followed by tyramine, and in accord with the belief that an inhibitor selective for MAO A which is reversibly bound to the enzyme and therefore displaced by any ingested tyramine will not lead to the "cheese effect" (hypertension during treatment with MAO inhibitors usually caused by ingestion of foods containing tyramine).	Phenelzine	75-85	monoamine oxidase A	Rattus norvegicus	170-175
9258353-6	1997	This is in contrast to a large blood pressure rise in rats pretreated with phenelzine followed by tyramine, and in accord with the belief that an inhibitor selective for MAO A which is reversibly bound to the enzyme and therefore displaced by any ingested tyramine will not lead to the "cheese effect" (hypertension during treatment with MAO inhibitors usually caused by ingestion of foods containing tyramine).	Phenelzine	75-85	monoamine oxidase A	Rattus norvegicus	170-173
9025956-7	1997	Inhibition of MAO in rat liver homogenates was also measured following administration of the antidepressant, phenelzine.	Phenelzine	109-119	monoamine oxidase A	Rattus norvegicus	14-17
8864539-11	1996	Chronic treatment (7 days) with the monoamine oxidase (MAO) inhibitors clorgyline (10 mg kg-1) and phenelzine (10 mg kg-1) decreased the immunoreactivity of the 29/30-kDa (17-24%), 45-kDa (19%) and 66-kDa (23-31%) imidazoline receptor proteins.	Phenelzine	99-109	monoamine oxidase A	Rattus norvegicus	36-53
8864539-11	1996	Chronic treatment (7 days) with the monoamine oxidase (MAO) inhibitors clorgyline (10 mg kg-1) and phenelzine (10 mg kg-1) decreased the immunoreactivity of the 29/30-kDa (17-24%), 45-kDa (19%) and 66-kDa (23-31%) imidazoline receptor proteins.	Phenelzine	99-109	monoamine oxidase A	Rattus norvegicus	55-58
8818569-3	1996	Therefore, the effects of treatment with hydrazine or one of the therapeutic hydrazines phenelzine and hydralazine on rat hepatic and renal CYP2E1 and GST-alpha expression were investigated.	Phenelzine	88-98	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	140-146
8818569-7	1996	In addition, hydrazine and phenelzine treatment produced substantial elevations (approximately 464% and 566%, respectively) in renal CYP2E1 protein, whereas hydralazine administration did not alter renal CYP2E1 expression.	Phenelzine	27-37	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	133-139
8749840-1	1995	The antidepressant/antipanic drug phenelzine (PLZ) is both an inhibitor of, and a substrate for, monoamine oxidase (MAO).	Phenelzine	34-44	monoamine oxidase A	Rattus norvegicus	97-114
8749840-1	1995	The antidepressant/antipanic drug phenelzine (PLZ) is both an inhibitor of, and a substrate for, monoamine oxidase (MAO).	Phenelzine	34-44	monoamine oxidase A	Rattus norvegicus	116-119
8749840-1	1995	The antidepressant/antipanic drug phenelzine (PLZ) is both an inhibitor of, and a substrate for, monoamine oxidase (MAO).	Phenelzine	46-49	monoamine oxidase A	Rattus norvegicus	97-114
8749840-1	1995	The antidepressant/antipanic drug phenelzine (PLZ) is both an inhibitor of, and a substrate for, monoamine oxidase (MAO).	Phenelzine	46-49	monoamine oxidase A	Rattus norvegicus	116-119
8736433-6	1996	Unlike after imipramine, Arc NPY and POMC mRNA levels are increased significantly to 134-172% of control following 56-day treatment with the antidepressant drugs fluoxetine, phenelzine, or idazoxan.	Phenelzine	174-184	neuropeptide Y	Rattus norvegicus	29-32
8736433-6	1996	Unlike after imipramine, Arc NPY and POMC mRNA levels are increased significantly to 134-172% of control following 56-day treatment with the antidepressant drugs fluoxetine, phenelzine, or idazoxan.	Phenelzine	174-184	proopiomelanocortin	Rattus norvegicus	37-41
8749840-4	1995	Both TCP and (-)-deprenyl caused a greater reduction in the GABA-elevating action of PLZ than did clorgyline, suggesting that MAO-B is more important than MAO-A in the formation of the active metabolite of PLZ.	Phenelzine	85-88	monoamine oxidase B	Rattus norvegicus	126-131
8749840-4	1995	Both TCP and (-)-deprenyl caused a greater reduction in the GABA-elevating action of PLZ than did clorgyline, suggesting that MAO-B is more important than MAO-A in the formation of the active metabolite of PLZ.	Phenelzine	85-88	monoamine oxidase A	Rattus norvegicus	155-160
8749840-4	1995	Both TCP and (-)-deprenyl caused a greater reduction in the GABA-elevating action of PLZ than did clorgyline, suggesting that MAO-B is more important than MAO-A in the formation of the active metabolite of PLZ.	Phenelzine	206-209	monoamine oxidase B	Rattus norvegicus	126-131