PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
8120182-4	1994	Milk production was correlated positively with DMI and water intake within and across parities.	Desipramine	47-50	Weaning weight-maternal milk	Bos taurus	0-4
8120182-7	1994	Rumination and total time spent chewing per unit of DMI were correlated negatively (r = -.58) with milk production within and across parities.	Desipramine	52-55	Weaning weight-maternal milk	Bos taurus	99-103
7734110-2	1994	GPT exerted the same biphasic effect on basal and DA-stimulated enzyme activity in membranes from DMI-treated rats as on saline-treated rats.	Desipramine	98-101	glutamic--pyruvic transaminase	Rattus norvegicus	0-3
7734110-5	1994	D2 inhibition of adenylate cyclase by DA was attenuated by the IAP treatment in both DMI-and saline-treated rats; peak levels of DA plus GTP stimulation shifted from 1 microM to 100 microM GTP.	Desipramine	85-88	Cd47 molecule	Rattus norvegicus	63-66
7734110-6	1994	D1 stimulation of adenylate cyclase by DA was also attenuated by the IAP in the DMI-treated rats.	Desipramine	80-83	Cd47 molecule	Rattus norvegicus	69-72
7734110-7	1994	Since long-term treatment with DMI (15 mg/kg, once a day, for 3 weeks) resulted in suppression of D1 stimulation similar to that seen in the present findings, uncoupling between D2 receptors and Gi due to IAP treatment might accelerate DMI-induced adaptive changes of dual control of adenylate cyclase system by DA.	Desipramine	31-34	Cd47 molecule	Rattus norvegicus	205-208
7734110-7	1994	Since long-term treatment with DMI (15 mg/kg, once a day, for 3 weeks) resulted in suppression of D1 stimulation similar to that seen in the present findings, uncoupling between D2 receptors and Gi due to IAP treatment might accelerate DMI-induced adaptive changes of dual control of adenylate cyclase system by DA.	Desipramine	236-239	Cd47 molecule	Rattus norvegicus	205-208
7969855-4	1994	Chronic desipramine and lithium chloride treatment slightly improved catalase activity in the bulbectomised rats.	Desipramine	8-19	catalase	Rattus norvegicus	69-77
8130740-7	1994	Na+,K(+)-ATPase increase by acute DMI was inhibited when endogenous NA was depleted by the noradrenergic neurotoxin DSP-4 or the NA synthesis inhibitor alpha-methyl-p-tyrosine.	Desipramine	34-37	dual specificity phosphatase 26	Homo sapiens	116-121
8374761-0	1993	Norepinephrine transporter mRNA is elevated in the locus coeruleus following short- and long-term desipramine treatment.	Desipramine	98-109	solute carrier family 6 member 2	Homo sapiens	0-26
8310712-14	1993	CYP2D6 catalyses C-hydroxylation of imipramine to 2-hydroxyimipramine more efficiently than its N-demethylation to desipramine.	Desipramine	115-126	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
8110987-4	1993	Acetylcholinesterase (AChE) was inhibited by CPZ, 3,7,8-trihydroxy-CPZ, acridine orange partially saturated desipramine, imipramine, trans-clopenthixol and tetrahydrocannabidiolic at 10(-4) to 10(-5).	Desipramine	108-119	acetylcholinesterase	Rattus norvegicus	0-20
8110987-4	1993	Acetylcholinesterase (AChE) was inhibited by CPZ, 3,7,8-trihydroxy-CPZ, acridine orange partially saturated desipramine, imipramine, trans-clopenthixol and tetrahydrocannabidiolic at 10(-4) to 10(-5).	Desipramine	108-119	acetylcholinesterase	Rattus norvegicus	22-26
8218295-9	1993	The binding was most potently inhibited by the ligands of the norepinephrine transporter (desipramine and nomifensine).	Desipramine	90-101	solute carrier family 6 member 2	Homo sapiens	62-88
8354888-3	1993	Imipramine and desipramine were structurally modified by the attachment of spacer arms to the aromatic ring which were subsequently attached to bovine serum albumin.	Desipramine	15-26	albumin	Oryctolagus cuniculus	151-164
8374761-1	1993	In situ hybridization for the norepinephrine transporter (NET) mRNA was performed in animals receiving short-term (2 days) and long-term (4 weeks) treatment with desipramine (DMI; 10 mg/kg, intraperitoneal).	Desipramine	162-173	solute carrier family 6 member 2	Homo sapiens	30-56
8374761-1	1993	In situ hybridization for the norepinephrine transporter (NET) mRNA was performed in animals receiving short-term (2 days) and long-term (4 weeks) treatment with desipramine (DMI; 10 mg/kg, intraperitoneal).	Desipramine	162-173	solute carrier family 6 member 2	Homo sapiens	58-61
8374761-1	1993	In situ hybridization for the norepinephrine transporter (NET) mRNA was performed in animals receiving short-term (2 days) and long-term (4 weeks) treatment with desipramine (DMI; 10 mg/kg, intraperitoneal).	Desipramine	175-178	solute carrier family 6 member 2	Homo sapiens	58-61
8374761-2	1993	Following short-term and long-term DMI treatment, a significant (P < 0.05) increase in hybridization of 35S-labeled oligonucleotides to NET mRNA in the locus coeruleus was observed compared to that observed in vehicle-treated animals.	Desipramine	35-38	solute carrier family 6 member 2	Homo sapiens	139-142
8315492-6	1993	MIBG uptake in hNET transfected cells is inhibited by 3 x 10(-6) M norepinephrine (87% inhibition) and by hNET transport inhibitors: 10(-7) M desipramine (94% inhibition) and 10(-7) M mazindol (97% inhibition).	Desipramine	142-153	solute carrier family 6 member 2	Homo sapiens	15-19
8315492-6	1993	MIBG uptake in hNET transfected cells is inhibited by 3 x 10(-6) M norepinephrine (87% inhibition) and by hNET transport inhibitors: 10(-7) M desipramine (94% inhibition) and 10(-7) M mazindol (97% inhibition).	Desipramine	142-153	solute carrier family 6 member 2	Homo sapiens	106-110
8335704-3	1993	In addition, however, the human CYP2D6 isozyme preparation was found to be unequivocally involved in the N-dealkylation of IMI to desmethylimipramine (DMI).	Desipramine	130-149	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-38
8335704-3	1993	In addition, however, the human CYP2D6 isozyme preparation was found to be unequivocally involved in the N-dealkylation of IMI to desmethylimipramine (DMI).	Desipramine	151-154	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-38
1480137-3	1992	Treatment of transgenic animals with the tricyclic antidepressant desipramine increased hypothalamic glucocorticoid receptor mRNA concentration and dexamethasone-binding activity while decreasing plasma adrenocorticotropin hormone concentration and corticosterone levels.	Desipramine	66-77	nuclear receptor subfamily 3, group C, member 1	Mus musculus	101-124
8415816-0	1993	Chronic, combined treatment with desipramine and mianserin: enhanced 5-HT1A receptor function and altered 5-HT1A/5-HT2 receptor interaction in rats.	Desipramine	33-44	5-hydroxytryptamine receptor 1A	Rattus norvegicus	69-75
8415816-0	1993	Chronic, combined treatment with desipramine and mianserin: enhanced 5-HT1A receptor function and altered 5-HT1A/5-HT2 receptor interaction in rats.	Desipramine	33-44	5-hydroxytryptamine receptor 1A	Rattus norvegicus	106-112
8359181-7	1993	There was evidence for linkage between the CYP2D6 gene and the gene regulating the hydroxylation of desipramine and debrisoquine.	Desipramine	100-111	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	43-49
7870896-6	1993	These findings suggest a decrease in the functional response of beta 1, but not beta 2, receptors after treatment with desipramine.	Desipramine	119-130	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	64-70
1362806-0	1992	Semiquantitative analysis of immunoreactivities of tyrosine hydroxylase and aromatic L-amino acid decarboxylase in the locus coeruleus of desipramine-treated mice.	Desipramine	138-149	dopa decarboxylase	Mus musculus	76-111
8415816-3	1993	Pretreatment with desipramine and mianserin in combination induced the most intense 5-HT syndrome and the greatest fall in colonic temperature after injection of the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT).	Desipramine	18-29	5-hydroxytryptamine receptor 1A	Rattus norvegicus	166-172
8336822-7	1993	Several studies have shown a functional upregulation of the 5-HT1A receptor after chronic treatment with DMI.	Desipramine	105-108	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	60-75
8358025-1	1993	Several amphiphilic cations such as mepacrine, desipramine, didodecyldimethylamine, chlorpromazine, oleylamine and W-7 activated the phospholipase D (PLD) activity of cultured LA-N-2 cells.	Desipramine	47-58	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	133-148
8358025-1	1993	Several amphiphilic cations such as mepacrine, desipramine, didodecyldimethylamine, chlorpromazine, oleylamine and W-7 activated the phospholipase D (PLD) activity of cultured LA-N-2 cells.	Desipramine	47-58	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	150-153
8439771-1	1993	The effects of acute and chronic treatment with the tricyclic antidepressant drugs, imipramine, clomipramine and desipramine on levels of neuropeptide Y (NPY) and prepro-NPY-mRNA were studied in different areas of the rat brain.	Desipramine	113-124	neuropeptide Y	Rattus norvegicus	138-152
8439771-1	1993	The effects of acute and chronic treatment with the tricyclic antidepressant drugs, imipramine, clomipramine and desipramine on levels of neuropeptide Y (NPY) and prepro-NPY-mRNA were studied in different areas of the rat brain.	Desipramine	113-124	neuropeptide Y	Rattus norvegicus	154-157
8439771-1	1993	The effects of acute and chronic treatment with the tricyclic antidepressant drugs, imipramine, clomipramine and desipramine on levels of neuropeptide Y (NPY) and prepro-NPY-mRNA were studied in different areas of the rat brain.	Desipramine	113-124	neuropeptide Y	Rattus norvegicus	170-173
8513845-3	1993	This confirms that desipramine is extensively metabolized via the sparteine/debrisoquine oxidation polymorphism i.e. by CYP2D6.	Desipramine	19-30	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	120-126
8513845-5	1993	The 5-fold decrease in clearance in EMs when desipramine was co-administered with paroxetine confirms that paroxetine is a potent inhibitor of CYP2D6.	Desipramine	45-56	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	143-149
8464952-0	1993	Effect of desipramine on cerebrospinal fluid concentrations of corticotropin-releasing factor in human subjects.	Desipramine	10-21	corticotropin releasing hormone	Homo sapiens	63-93
8464952-1	1993	To assess the effect of desipramine (DMI) on corticotropin-releasing-factor (CRF) activity in the central nervous system, we measured cerebrospinal fluid (CSF) concentrations of CRF in healthy volunteers following short-term administration of DMI or placebo.	Desipramine	37-40	corticotropin releasing hormone	Homo sapiens	45-75
1336635-0	1992	The desipramine-induced growth hormone response and the dexamethasone suppression test in obsessive-compulsive disorder.	Desipramine	4-15	growth hormone 1	Homo sapiens	24-38
1359398-0	1992	Long term treatment with desipramine increases the turnover of alpha 2-adrenoceptors in the rat brain.	Desipramine	25-36	adrenoceptor alpha 2A	Rattus norvegicus	63-84
1359398-1	1992	The aim of this study was to quantitate the turnover of alpha 2-adrenoceptors in different regions of the rat brain and its modulation during desipramine (a cyclic antidepressant drug)-induced receptor down-regulation.	Desipramine	142-153	adrenoceptor alpha 2A	Rattus norvegicus	56-77
1359398-5	1992	In the cerebral cortex and other brain regions, desipramine induced a time-dependent modulation of alpha 2-adrenoceptors, with significant decreases in the number of receptors (40-71%; p < 0.01) during the first 7-14 days of treatment and regulation to base-line values by 21-35 days.	Desipramine	48-59	adrenoceptor alpha 2A	Rattus norvegicus	99-120
1387021-10	1992	Rats treated with DMI but not sertraline showed a virtually complete suppression of the growth hormone (GH) secretion elicited by clonidine in controls, while the secretion of corticosterone was augmented.	Desipramine	18-21	gonadotropin releasing hormone receptor	Rattus norvegicus	88-102
1389951-7	1992	CYP2D6 activity was also diminished by the tricyclic antidepressant drugs clomipramine (2.2 microM), desipramine (2.3 microM) and amitriptyline (4.0 microM).	Desipramine	101-112	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
1436127-7	1992	If desipramine (25 mg/kg) was administered before DSP-4 treatment, the DSP-4-induced changes both in noradrenaline uptake and CCK receptor binding were not present, suggesting that both effects were exerted after uptake of the neurotoxin by the nerve terminals.	Desipramine	3-14	cholecystokinin	Rattus norvegicus	126-129
1325288-6	1992	Desimipramine, but not reserpine, easily depleted IFN-gamma-treated LAN-5 cells of their MIBG content.	Desipramine	0-13	interferon gamma	Homo sapiens	50-59
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.	Desipramine	104-115	4-aminobutyrate aminotransferase	Rattus norvegicus	158-193
1614406-1	1992	We have tested the hypothesis that antidepressants affect the expression of the glucocorticoid receptor gene, by looking at glucocorticoid receptor gene promoter activity, glucocorticoid receptor mRNA levels, and glucocorticoid-binding activity after treatment of different cell lines with desipramine.	Desipramine	290-301	nuclear receptor subfamily 3, group C, member 1	Mus musculus	80-103
1614406-2	1992	Treatment of LTK- cells or Neuro 2A cells with desipramine produced a 50-200% increase in chloramphenicol acetyltransferase activity transcribed from a 2.7-kilobase glucocorticoid receptor gene promoter region.	Desipramine	47-58	leukocyte tyrosine kinase	Mus musculus	13-16
1614406-2	1992	Treatment of LTK- cells or Neuro 2A cells with desipramine produced a 50-200% increase in chloramphenicol acetyltransferase activity transcribed from a 2.7-kilobase glucocorticoid receptor gene promoter region.	Desipramine	47-58	nuclear receptor subfamily 3, group C, member 1	Mus musculus	165-188
1614406-3	1992	In cell lines derived from both neuronal and non-neuronal sources, glucocorticoid receptor mRNA concentration doubled after desipramine treatment, and this was associated with a 2-fold higher functional glucocorticoid binding capacity and increased glucocorticoid sensitivity, as measured with the reporter plasmid pMMTVCAT.	Desipramine	124-135	nuclear receptor subfamily 3, group C, member 1	Mus musculus	67-90
1387021-10	1992	Rats treated with DMI but not sertraline showed a virtually complete suppression of the growth hormone (GH) secretion elicited by clonidine in controls, while the secretion of corticosterone was augmented.	Desipramine	18-21	gonadotropin releasing hormone receptor	Rattus norvegicus	104-106
1387021-16	1992	These results show that DMI treatment blunted the sensitivity of post-synaptic alpha 2-adrenoceptors, accompanied by complex interactions manifested as increased responsiveness of alpha 1-adrenoceptors and 5-HT1A receptors.	Desipramine	24-27	5-hydroxytryptamine receptor 1A	Rattus norvegicus	180-212
1346258-0	1992	Analysis of the CYP2D6 gene in relation to debrisoquin and desipramine hydroxylation in a Swedish population.	Desipramine	59-70	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	16-22
1744272-8	1991	Growth hormone-releasing factor increased DMI (23.2 kg/d) over that of controls (21.1 kg/d), whereas bST (21.5 kg/d) did not.	Desipramine	42-45	growth hormone releasing hormone	Bos taurus	0-31
1542151-3	1992	In this study, the influence of changing salt status and angiotensin II activity has been investigated by evaluating the QRS prolonging effects of the sodium channel blocking drug, desmethylimipramine.	Desipramine	181-200	angiotensinogen	Rattus norvegicus	57-71
1542151-10	1992	The QRS response to desmethylimipramine and salt-loaded rats on normal salt diets receiving captopril returned to the control pattern after a subpressor infusion of angiotensin II (3 ng/min), while a higher rate of angiotensin II (10 ng/min) further enhanced the QRS prolonging effect of desmethylimipramine.	Desipramine	20-39	angiotensinogen	Rattus norvegicus	165-179
1542151-11	1992	These data demonstrate that endogenous angiotensin II contributes to the regulation of the cardiac electro-physiological response to DMI.	Desipramine	133-136	angiotensinogen	Rattus norvegicus	39-53
1775194-4	1991	After inhibition of MAO, desipramine caused a further five-fold increase in the basal efflux of dopamine with no change in the basal efflux of DOPAC.	Desipramine	25-36	monoamine oxidase A	Rattus norvegicus	20-23
1839385-0	1991	Similar effects of treatment with desipramine and electroconvulsive shock on 5-hydroxytryptamine1A receptors in rat brain.	Desipramine	34-45	5-hydroxytryptamine receptor 1A	Rattus norvegicus	77-98
1839385-1	1991	The effect of chronic and acute treatment with desipramine (DMI) and electroconvulsive shock (ECS) on 5-hydroxytryptamine1A (5-HT1A) receptors was determined in the cortex and the hippocampus brain regions of rats.	Desipramine	47-58	5-hydroxytryptamine receptor 1A	Rattus norvegicus	102-123
1839385-1	1991	The effect of chronic and acute treatment with desipramine (DMI) and electroconvulsive shock (ECS) on 5-hydroxytryptamine1A (5-HT1A) receptors was determined in the cortex and the hippocampus brain regions of rats.	Desipramine	47-58	5-hydroxytryptamine receptor 1A	Rattus norvegicus	125-131
1839385-1	1991	The effect of chronic and acute treatment with desipramine (DMI) and electroconvulsive shock (ECS) on 5-hydroxytryptamine1A (5-HT1A) receptors was determined in the cortex and the hippocampus brain regions of rats.	Desipramine	60-63	5-hydroxytryptamine receptor 1A	Rattus norvegicus	102-123
1839385-1	1991	The effect of chronic and acute treatment with desipramine (DMI) and electroconvulsive shock (ECS) on 5-hydroxytryptamine1A (5-HT1A) receptors was determined in the cortex and the hippocampus brain regions of rats.	Desipramine	60-63	5-hydroxytryptamine receptor 1A	Rattus norvegicus	125-131
1839385-2	1991	We observed that chronic treatment with both DMI and ECS significantly decreased 5-HT1A receptors, as determined by [3H]8-hydroxy-2-(di-n-propylamino)tetralin [( 3H]8-OH-DPAT) binding, in the cortex but not in the hippocampus.	Desipramine	45-48	5-hydroxytryptamine receptor 1A	Rattus norvegicus	81-87
1912129-1	1991	Twelve patients with DSM-III-R major depressive illness were tested for growth hormone (GH) response to desipramine (DMI), a noradrenergic (NA) reuptake inhibitor.	Desipramine	104-115	growth hormone 1	Homo sapiens	72-86
1912129-1	1991	Twelve patients with DSM-III-R major depressive illness were tested for growth hormone (GH) response to desipramine (DMI), a noradrenergic (NA) reuptake inhibitor.	Desipramine	104-115	growth hormone 1	Homo sapiens	88-90
1912129-1	1991	Twelve patients with DSM-III-R major depressive illness were tested for growth hormone (GH) response to desipramine (DMI), a noradrenergic (NA) reuptake inhibitor.	Desipramine	117-120	growth hormone 1	Homo sapiens	72-86
1912129-1	1991	Twelve patients with DSM-III-R major depressive illness were tested for growth hormone (GH) response to desipramine (DMI), a noradrenergic (NA) reuptake inhibitor.	Desipramine	117-120	growth hormone 1	Homo sapiens	88-90
1912129-6	1991	Patients treated with fluoxetine showed a significant decrease in DMI-mediated GH release irrespective of therapeutic outcome.	Desipramine	66-69	growth hormone 1	Homo sapiens	79-81
1782991-7	1991	Desipramine selectively inhibited the T-current and Cl- efflux for 1 min.	Desipramine	0-11	nuclear receptor subfamily 1, group H, member 5 L homeolog	Xenopus laevis	63-68
1663633-0	1991	Down-regulation of beta receptors by desipramine in vitro involves PKC/phospholipase A2.	Desipramine	37-48	phospholipase A2 group IB	Rattus norvegicus	71-87
1717808-0	1991	Repeated administration of desmethylimipramine blocks the reserpine-induced increase in tyrosine hydroxylase mRNA in locus coeruleus neurons of the rat.	Desipramine	27-46	tyrosine hydroxylase	Rattus norvegicus	88-108
1717808-4	1991	However, coadministration of desmethylimipramine with reserpine blocked the elevation in tyrosine hydroxylase mRNA induced by reserpine alone.	Desipramine	29-48	tyrosine hydroxylase	Rattus norvegicus	89-109
1849767-0	1991	Secretion of growth hormone elicited by intravenous desipramine in the conscious, unrestrained rat.	Desipramine	52-63	gonadotropin releasing hormone receptor	Rattus norvegicus	13-27
1849767-2	1991	Acute intravenous administration of either clonidine (Clon) (50 micrograms kg-1) or desipramine (DMI) (5 mg kg-1) elicited a pulse of growth hormone (GH) and corticosterone secretion in conscious, unrestrained rats.	Desipramine	84-95	gonadotropin releasing hormone receptor	Rattus norvegicus	134-148
1849767-2	1991	Acute intravenous administration of either clonidine (Clon) (50 micrograms kg-1) or desipramine (DMI) (5 mg kg-1) elicited a pulse of growth hormone (GH) and corticosterone secretion in conscious, unrestrained rats.	Desipramine	84-95	gonadotropin releasing hormone receptor	Rattus norvegicus	150-152
1849767-2	1991	Acute intravenous administration of either clonidine (Clon) (50 micrograms kg-1) or desipramine (DMI) (5 mg kg-1) elicited a pulse of growth hormone (GH) and corticosterone secretion in conscious, unrestrained rats.	Desipramine	97-100	gonadotropin releasing hormone receptor	Rattus norvegicus	134-148
1849767-2	1991	Acute intravenous administration of either clonidine (Clon) (50 micrograms kg-1) or desipramine (DMI) (5 mg kg-1) elicited a pulse of growth hormone (GH) and corticosterone secretion in conscious, unrestrained rats.	Desipramine	97-100	gonadotropin releasing hormone receptor	Rattus norvegicus	150-152
1849767-4	1991	The responses to DMI were similar to those with Clon, except that the GH pulse following DMI was delayed and was not dose-dependent.	Desipramine	17-20	gonadotropin releasing hormone receptor	Rattus norvegicus	70-72
1849767-4	1991	The responses to DMI were similar to those with Clon, except that the GH pulse following DMI was delayed and was not dose-dependent.	Desipramine	89-92	gonadotropin releasing hormone receptor	Rattus norvegicus	70-72
1849767-6	1991	The GH response to DMI was inhibited by prior administration of idazoxan (1 mg kg-1) or yohimbine (0.5 mg kg-1), but not by atropine (10 micrograms kg-1), sulpiride (5 mg kg-1) or prazosin (1 mg kg-1).	Desipramine	19-22	gonadotropin releasing hormone receptor	Rattus norvegicus	4-6
1849767-14	1991	DMI caused an activation through indirect mechanisms of alpha 2-adrenoceptors specifically involved in hypothalamic-pituitary regulation of GH release and also a distinct, independent and transient generalized activation of the pituitary-adrenal axis.	Desipramine	0-3	gonadotropin releasing hormone receptor	Rattus norvegicus	140-142
1647239-8	1991	However, the ability of NPY (0.05-0.5 microM) to inhibit forskolin (1 microM) stimulated adenylate cyclase via Y2 NPY-type receptors in rat frontal cortical slices was significantly reduced following chronic desipramine treatment.	Desipramine	208-219	neuropeptide Y	Rattus norvegicus	24-27
1775595-2	1991	We observed that DMI inhibited thrombin-stimulated 3H-inositol bisphosphate (IP2) and 3H-inositol trisphosphate (IP3) but not 3H-inositol monophosphate (IP1) formation in human platelets.	Desipramine	17-20	coagulation factor II, thrombin	Homo sapiens	31-39
1775595-2	1991	We observed that DMI inhibited thrombin-stimulated 3H-inositol bisphosphate (IP2) and 3H-inositol trisphosphate (IP3) but not 3H-inositol monophosphate (IP1) formation in human platelets.	Desipramine	17-20	inhibitor of nuclear factor kappa B kinase regulatory subunit gamma	Homo sapiens	77-80
1775595-2	1991	We observed that DMI inhibited thrombin-stimulated 3H-inositol bisphosphate (IP2) and 3H-inositol trisphosphate (IP3) but not 3H-inositol monophosphate (IP1) formation in human platelets.	Desipramine	17-20	inhibitor of nuclear factor kappa B kinase regulatory subunit gamma	Homo sapiens	153-156
1775595-3	1991	DMI also inhibited norepinephrine (NE) and serotonin (5-HT) stimulated 3H-IP1 formation in rat cerebral cortex.	Desipramine	0-3	inhibitor of nuclear factor kappa B kinase regulatory subunit gamma	Homo sapiens	74-77
1775595-4	1991	DMI increased levels of all three 3H-inositol phospholipids, 3H-phosphatidyl inositol (PI), 3H-PI-4-phosphate (PIP), and 3H-PI 4,5-bisphosphate (PIP2), in both platelets and rat cortex.	Desipramine	0-3	prolactin induced protein	Rattus norvegicus	92-109
1775595-4	1991	DMI increased levels of all three 3H-inositol phospholipids, 3H-phosphatidyl inositol (PI), 3H-PI-4-phosphate (PIP), and 3H-PI 4,5-bisphosphate (PIP2), in both platelets and rat cortex.	Desipramine	0-3	prolactin induced protein	Rattus norvegicus	111-114
1775595-5	1991	The decreased formation of inositol phosphates and increased levels of [3H]-PI, [3H]-PIP, and [3H]-PIP2 by DMI appears to be due to the inhibition of the enzyme phospholipase C rather than its effects on receptors.	Desipramine	107-110	prolactin induced protein	Rattus norvegicus	85-88
1811246-2	1991	Northern blot analysis of Type II GR mRNA showed that treatment of male rats with either desipramine or imipramine increased hypothalamic and hippocampal GR mRNA levels.	Desipramine	89-100	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	34-36
1811246-2	1991	Northern blot analysis of Type II GR mRNA showed that treatment of male rats with either desipramine or imipramine increased hypothalamic and hippocampal GR mRNA levels.	Desipramine	89-100	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	154-156
1811246-6	1991	We conclude that desipramine, imipramine, ketanserin and lithium can modulate GR mRNA in regions of rat brain involved in the control of the HPA axis and may have a common mechanism of action at the level of the GR gene.	Desipramine	17-28	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	78-80
1811246-6	1991	We conclude that desipramine, imipramine, ketanserin and lithium can modulate GR mRNA in regions of rat brain involved in the control of the HPA axis and may have a common mechanism of action at the level of the GR gene.	Desipramine	17-28	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	212-214
1540485-2	1992	The activity of N-sulphotransferase (N-ST) with desipramine (DMI) as substrate was measured in 118 human liver specimens, in platelets obtained from 105 subjects, in 12 specimens of human ileum and colon mucosa and in five specimens of human kidney and lung.	Desipramine	48-59	sulfotransferase family 4A member 1	Homo sapiens	16-35
1540485-2	1992	The activity of N-sulphotransferase (N-ST) with desipramine (DMI) as substrate was measured in 118 human liver specimens, in platelets obtained from 105 subjects, in 12 specimens of human ileum and colon mucosa and in five specimens of human kidney and lung.	Desipramine	48-59	sulfotransferase family 4A member 1	Homo sapiens	37-41
1540485-2	1992	The activity of N-sulphotransferase (N-ST) with desipramine (DMI) as substrate was measured in 118 human liver specimens, in platelets obtained from 105 subjects, in 12 specimens of human ileum and colon mucosa and in five specimens of human kidney and lung.	Desipramine	61-64	sulfotransferase family 4A member 1	Homo sapiens	16-35
1540485-2	1992	The activity of N-sulphotransferase (N-ST) with desipramine (DMI) as substrate was measured in 118 human liver specimens, in platelets obtained from 105 subjects, in 12 specimens of human ileum and colon mucosa and in five specimens of human kidney and lung.	Desipramine	61-64	sulfotransferase family 4A member 1	Homo sapiens	37-41
1647142-1	1991	Seven drug-free patients with bipolar affective disorder, currently in a manic phase, underwent desipramine-induced growth hormone (GH) stimulation, as did seven healthy age- and sex-matched subjects.	Desipramine	96-107	growth hormone 1	Homo sapiens	116-130
1860973-5	1991	Milk to DMI ratio and milk energy to net energy intake ratio were improved by somidobove.	Desipramine	8-11	Weaning weight-maternal milk	Bos taurus	0-4
1672374-3	1991	Desipramine, imipramine, amitriptyline and iprindole inhibited thrombin-stimulated formation of [3H]IP2 and [3H]IP3 in human platelets but had no significant effect on [3H]IP1 formation.	Desipramine	0-11	coagulation factor II, thrombin	Homo sapiens	63-71
1672374-3	1991	Desipramine, imipramine, amitriptyline and iprindole inhibited thrombin-stimulated formation of [3H]IP2 and [3H]IP3 in human platelets but had no significant effect on [3H]IP1 formation.	Desipramine	0-11	inhibitor of nuclear factor kappa B kinase regulatory subunit gamma	Homo sapiens	100-103
1672374-3	1991	Desipramine, imipramine, amitriptyline and iprindole inhibited thrombin-stimulated formation of [3H]IP2 and [3H]IP3 in human platelets but had no significant effect on [3H]IP1 formation.	Desipramine	0-11	inhibitor of nuclear factor kappa B kinase regulatory subunit gamma	Homo sapiens	172-175
1663633-7	1991	Coincubation of C6 cells with either the phospholipase A2 (PLA2) inhibitor mepacrine or the protein kinase C (PKC) inhibitor H7, during chronic treatment with DMI, blocked the down-regulation of beta ARs.	Desipramine	159-162	phospholipase A2 group IB	Rattus norvegicus	41-57
1663633-7	1991	Coincubation of C6 cells with either the phospholipase A2 (PLA2) inhibitor mepacrine or the protein kinase C (PKC) inhibitor H7, during chronic treatment with DMI, blocked the down-regulation of beta ARs.	Desipramine	159-162	phospholipase A2 group IB	Rattus norvegicus	59-63
2076491-2	1990	In tissues previously incubated with [3H]-noradrenaline exposure to cocaine (0.1 to 10 microM) or desmethylimipramine (0.01 to 1 microM) produced a concentration-dependent increase (up to 2 fold) in electrically evoked (3 Hz, 2 ms, 20 mA, 120s every 20 min) fractional overflow of tritium from rat brain cortex slices but not from mouse vas deferens (2.5 Hz, 2 ms, 400 mA, for 90s every 14 min).	Desipramine	98-117	arginine vasopressin	Rattus norvegicus	337-340
19912776-4	1990	The catecholamine uptake blocker desipramine and the alpha(2)-adrenergic receptor agonist clonidine inhibited accumulation of newly synthesized catecholamines, but only after prolonged exposure to drug; NPY synthesis and accumulation were unaltered by these treatments.	Desipramine	33-44	neuropeptide Y	Rattus norvegicus	203-206
2128400-2	1990	Neurotensin was injected into the anterior chamber (AC) at a dose of 30 micrograms to 4 groups of albino rabbits which had previously undergone the following treatment: a) desmethylimipramine IM and, after 30 min, 6-hydroxydopamine IV 7 days prior to the neurotensin administration; b) haloperidol IM for 15 days; c) haloperidol AC 10 minutes before the neurotensin administration.	Desipramine	172-191	neurotensin/neuromedin N	Oryctolagus cuniculus	0-11
1980647-3	1990	The [Ca2+]i response to NMDA was blocked or reversed by selective antagonists such as 2-amino-5-phosphonovalerate (APV), MK801 and ketamine, as well as by desmethylimipramine and dextromethorphan.	Desipramine	155-174	carbonic anhydrase 2	Gallus gallus	5-8
2162547-1	1990	The growth hormone (GH) response to desipramine was measured in ten patients meeting criteria for post-stroke depression (PSD), eight age-matched post-stroke (PS) non-depressed patients and eight healthy controls.	Desipramine	36-47	growth hormone 1	Homo sapiens	4-18
2286698-5	1990	TRIM 4-week totals were significantly associated with total desipramine plus hydroxydesipramine plasma concentrations, r = -0.32, p less than 0.05, but HAM-D and MADS scores were not.	Desipramine	60-71	tripartite motif containing 4	Homo sapiens	0-6
2164943-1	1990	Both 3-day and 15-day desipramine treatments (10 mg/kg, once daily) significantly reduced beta 1- but not beta 2-adrenoceptor and isoproterenol-stimulated adenylyl cyclase activities in rat cortical, hippocampal and amygdaloid membrane preparations.	Desipramine	22-33	adrenoceptor beta 2	Rattus norvegicus	106-125
2095944-0	1990	Responses of growth hormone to desipramine in endogenous and non-endogenous depression.	Desipramine	31-42	growth hormone 1	Homo sapiens	13-27
2095944-1	1990	Desipramine, a monoamine reuptake inhibitor, was used to stimulate release of growth hormone (GH) in 29 DSM-III major depressives and in 10 healthy controls.	Desipramine	0-11	growth hormone 1	Homo sapiens	78-92
2139187-0	1990	Intrathecal administration of thiorphan, bestatin, desipramine and fluoxetine differentially potentiate the antinociceptive effects induced by beta-endorphin and morphine, administered intracerebroventricularly.	Desipramine	51-62	pro-opiomelanocortin-alpha	Mus musculus	143-157
2162547-1	1990	The growth hormone (GH) response to desipramine was measured in ten patients meeting criteria for post-stroke depression (PSD), eight age-matched post-stroke (PS) non-depressed patients and eight healthy controls.	Desipramine	36-47	growth hormone 1	Homo sapiens	20-22
2176515-0	1990	The effect of reserpine, desipramine and thyroid hormone on alpha 1a- and alpha 1b-adrenoceptor binding sites: evidence for a subtype-specific regulation.	Desipramine	25-36	adrenoceptor alpha 1A	Rattus norvegicus	60-95
2207447-6	1990	Intracerebroventricular administration of the beta-2 adrenoceptor agonist salbutamol (1 microgram/rat) to rats pretreated with desipramine for 7 days, 15 min before immobilization, significantly relieved the inhibition by desipramine 5 and 10 min after the initiation of stress but the effect was not demonstrable after 20 and 40 min.	Desipramine	127-138	adrenoceptor beta 2	Rattus norvegicus	46-65
2207447-6	1990	Intracerebroventricular administration of the beta-2 adrenoceptor agonist salbutamol (1 microgram/rat) to rats pretreated with desipramine for 7 days, 15 min before immobilization, significantly relieved the inhibition by desipramine 5 and 10 min after the initiation of stress but the effect was not demonstrable after 20 and 40 min.	Desipramine	222-233	adrenoceptor beta 2	Rattus norvegicus	46-65
2170253-11	1990	Many classical pharmacological agents including guanethidine, clonidine, yohimbine, angiotensin II, nicotine and desipramine influence NPY release.	Desipramine	113-124	neuropeptide Y	Homo sapiens	135-138
1690278-3	1990	The activity of the enzyme marker system, glucose-6-phosphate dehydrogenase covalently conjugated to desipramine, is monitored by colorimetric detection of the rate of NADH formation at 340 nM.	Desipramine	101-112	glucose-6-phosphate dehydrogenase	Homo sapiens	42-75
2172531-1	1990	Desipramine, the monoamine reuptake inhibitor, acts predominantly on noradrenergic neurones, and via alpha-2 receptors brings about the release of growth hormone in normal healthy subjects.	Desipramine	0-11	growth hormone 1	Homo sapiens	147-161
2398522-4	1990	A good correlation between the results of patient serum containing imipramine and desipramine simultaneously analyzed by ADx and gas liquid chromatography (GC) was observed, r2 = 0.964, n = 32.	Desipramine	82-93	ferredoxin 1	Homo sapiens	121-124
2179970-3	1990	Studies with various receptor blockers have shown varying influences on the DMI-induced growth hormone, prolactin, and ACTH/cortisol secretion.	Desipramine	76-79	proopiomelanocortin	Homo sapiens	119-123
2248060-6	1990	This effect was almost completely eliminated by desipramine, suggesting that coadministration of a norepinephrine uptake inhibitor with a reversible MAO inhibitor is likely to reduce the risk of tyramine-induced hypertensive crisis.	Desipramine	48-59	monoamine oxidase A	Rattus norvegicus	149-152
2101962-0	1990	Influence of clenbuterol, a beta-adrenergic agonist, on desipramine induced growth hormone, prolactin and cortisol stimulation.	Desipramine	56-67	amyloid beta precursor protein	Homo sapiens	26-32
2101962-0	1990	Influence of clenbuterol, a beta-adrenergic agonist, on desipramine induced growth hormone, prolactin and cortisol stimulation.	Desipramine	56-67	growth hormone 1	Homo sapiens	76-90
2101962-0	1990	Influence of clenbuterol, a beta-adrenergic agonist, on desipramine induced growth hormone, prolactin and cortisol stimulation.	Desipramine	56-67	prolactin	Homo sapiens	92-101
2101962-1	1990	We report herein the effects of the beta-adrenergic agonist clenbuterol on desipramine (DMI)-induced growth hormone (GH), prolactin (PRL) and cortisol secretion in healthy male subjects.	Desipramine	75-86	growth hormone 1	Homo sapiens	101-115
2101962-1	1990	We report herein the effects of the beta-adrenergic agonist clenbuterol on desipramine (DMI)-induced growth hormone (GH), prolactin (PRL) and cortisol secretion in healthy male subjects.	Desipramine	88-91	growth hormone 1	Homo sapiens	101-115
34597845-3	2021	In this study, we investigated the effects of heat stress and gestational status on ghrelin secretion and its possible associations with DMI in Holstein cattle.	Desipramine	137-140	ghrelin and obestatin prepropeptide	Bos taurus	84-91
2129310-2	1990	Subcutaneous administration of TRH reduced the total immobility time of rats tested in the despair (constrained swim) test and potentiated the anti-immobility effect of intraperitoneally administered desimipramine (DMI).	Desipramine	200-213	thyrotropin releasing hormone	Rattus norvegicus	31-34
2129310-2	1990	Subcutaneous administration of TRH reduced the total immobility time of rats tested in the despair (constrained swim) test and potentiated the anti-immobility effect of intraperitoneally administered desimipramine (DMI).	Desipramine	215-218	thyrotropin releasing hormone	Rattus norvegicus	31-34
2129310-4	1990	Hyperprolactinemia induced by pituitary homografts under the kidney capsule and the intracerebroventricular injection of PRL also potentiated the DMI-induced reduction of total immobility time of rats in the despair test and exerted "antidepressant" effects in aged rats.	Desipramine	146-149	prolactin	Rattus norvegicus	121-124
33945102-9	2021	Imipramine, desipramine, and fluoxetine suppress the production of IL-1beta, CCL2, as well as the expression of ICAM-1.	Desipramine	12-23	interleukin 1 alpha	Homo sapiens	67-75
33945102-9	2021	Imipramine, desipramine, and fluoxetine suppress the production of IL-1beta, CCL2, as well as the expression of ICAM-1.	Desipramine	12-23	C-C motif chemokine ligand 2	Homo sapiens	77-81
33945102-9	2021	Imipramine, desipramine, and fluoxetine suppress the production of IL-1beta, CCL2, as well as the expression of ICAM-1.	Desipramine	12-23	intercellular adhesion molecule 1	Homo sapiens	112-118
34965503-3	2022	Herein, expanding the previous findings on BDNFVal66Met polymorphism, we show that desipramine, a norepinephrine reuptake-inhibitor, rescues behavioral impairments, reduces the arterial thrombosis risk, abolishes pathological coagulation and platelet hyper-reactivity, normalizes leukocyte, platelet, and bone marrow megakaryocyte number and restores physiological norepinephrine levels in homozygous knock-in BDNF Val66Met (BDNFMet/Met) mice.	Desipramine	83-94	brain derived neurotrophic factor	Mus musculus	410-414
34969174-7	2022	The ASMase inhibitor desipramine decreased the level of S1P and the expression of alpha-smooth muscle actin (alpha-SMA) and NLRP3 in SiO2 dust-stained HBE cells, whereas the expression of E-cadherin (E-cad) increased.	Desipramine	21-32	sphingomyelin phosphodiesterase 1	Homo sapiens	4-10
34969174-7	2022	The ASMase inhibitor desipramine decreased the level of S1P and the expression of alpha-smooth muscle actin (alpha-SMA) and NLRP3 in SiO2 dust-stained HBE cells, whereas the expression of E-cadherin (E-cad) increased.	Desipramine	21-32	actin alpha 1, skeletal muscle	Homo sapiens	109-118
34969174-7	2022	The ASMase inhibitor desipramine decreased the level of S1P and the expression of alpha-smooth muscle actin (alpha-SMA) and NLRP3 in SiO2 dust-stained HBE cells, whereas the expression of E-cadherin (E-cad) increased.	Desipramine	21-32	NLR family pyrin domain containing 3	Homo sapiens	124-129
2550266-8	1989	Under our conditions the maximal effect occurred at 1 microM cAMP, revealing increased 32P incorporation in microtubule-associated protein 2 from a crude microtubule preparation obtained from the cerebral cortex of rats treated with desmethylimipramine.	Desipramine	233-252	microtubule-associated protein 2	Rattus norvegicus	108-140
34337165-7	2021	Mechanistically, DMI treatment during reperfusion increased the expression level of the microtubule-associated protein 1A/1B-light chain 3 (LC3) processing enzymes, ATG4B and ATG7.	Desipramine	17-20	annexin A3	Rattus norvegicus	140-143
34337165-7	2021	Mechanistically, DMI treatment during reperfusion increased the expression level of the microtubule-associated protein 1A/1B-light chain 3 (LC3) processing enzymes, ATG4B and ATG7.	Desipramine	17-20	autophagy related 4B, cysteine peptidase	Rattus norvegicus	165-170
34337165-7	2021	Mechanistically, DMI treatment during reperfusion increased the expression level of the microtubule-associated protein 1A/1B-light chain 3 (LC3) processing enzymes, ATG4B and ATG7.	Desipramine	17-20	autophagy related 7	Rattus norvegicus	175-179
34337165-8	2021	Genetic knockdown of ATG4B abolished the cytoprotective effect of DMI.	Desipramine	66-69	autophagy related 4B, cysteine peptidase	Rattus norvegicus	21-26
34337165-9	2021	Together, these results indicate that DMI is a unique agent which enhances LC3 processing in an ATG4B-dependent way.	Desipramine	38-41	annexin A3	Rattus norvegicus	75-78
34337165-9	2021	Together, these results indicate that DMI is a unique agent which enhances LC3 processing in an ATG4B-dependent way.	Desipramine	38-41	autophagy related 4B, cysteine peptidase	Rattus norvegicus	96-101
34232916-13	2021	The elevated expression levels of Leptin, FABP4, SREBP1C, PPARgamma, and C/EBPalpha induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK).	Desipramine	116-119	leptin	Mus musculus	34-40
34232916-13	2021	The elevated expression levels of Leptin, FABP4, SREBP1C, PPARgamma, and C/EBPalpha induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK).	Desipramine	116-119	fatty acid binding protein 4, adipocyte	Mus musculus	42-47
34232916-13	2021	The elevated expression levels of Leptin, FABP4, SREBP1C, PPARgamma, and C/EBPalpha induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK).	Desipramine	116-119	sterol regulatory element binding transcription factor 1	Mus musculus	49-56
34232916-13	2021	The elevated expression levels of Leptin, FABP4, SREBP1C, PPARgamma, and C/EBPalpha induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK).	Desipramine	116-119	peroxisome proliferator activated receptor gamma	Mus musculus	58-67
34232916-13	2021	The elevated expression levels of Leptin, FABP4, SREBP1C, PPARgamma, and C/EBPalpha induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK).	Desipramine	116-119	CCAAT/enhancer binding protein (C/EBP), alpha	Mus musculus	73-83
34232916-29	2021	The elevated expression levels of Leptin, FABP4, SREBP1C, PPARgamma, and C/EBPalpha induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK).	Desipramine	116-119	leptin	Mus musculus	34-40
34232916-29	2021	The elevated expression levels of Leptin, FABP4, SREBP1C, PPARgamma, and C/EBPalpha induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK).	Desipramine	116-119	fatty acid binding protein 4, adipocyte	Mus musculus	42-47
34232916-29	2021	The elevated expression levels of Leptin, FABP4, SREBP1C, PPARgamma, and C/EBPalpha induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK).	Desipramine	116-119	sterol regulatory element binding transcription factor 1	Mus musculus	49-56
34232916-29	2021	The elevated expression levels of Leptin, FABP4, SREBP1C, PPARgamma, and C/EBPalpha induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK).	Desipramine	116-119	peroxisome proliferator activated receptor gamma	Mus musculus	58-67
34232916-29	2021	The elevated expression levels of Leptin, FABP4, SREBP1C, PPARgamma, and C/EBPalpha induced by the stimulation with DMI incubation were dramatically inhibited by the introduction of TSA, accompanied by the upregulation of phosphorylated AMP-activated protein kinase (p-AMPK).	Desipramine	116-119	CCAAT/enhancer binding protein (C/EBP), alpha	Mus musculus	73-83
34062902-7	2021	In contrast to their direct antagonistic effects, prolonged incubation with IMI and DMI increased the maximal response of the alpha1B-AR subtype, and the CIT of both the alpha1A- and the alpha1B-ARs.	Desipramine	84-87	alpha-1-B glycoprotein	Homo sapiens	126-133
34062902-7	2021	In contrast to their direct antagonistic effects, prolonged incubation with IMI and DMI increased the maximal response of the alpha1B-AR subtype, and the CIT of both the alpha1A- and the alpha1B-ARs.	Desipramine	84-87	serpin family A member 1	Homo sapiens	170-177
34062902-7	2021	In contrast to their direct antagonistic effects, prolonged incubation with IMI and DMI increased the maximal response of the alpha1B-AR subtype, and the CIT of both the alpha1A- and the alpha1B-ARs.	Desipramine	84-87	alpha-1-B glycoprotein	Homo sapiens	187-194
35210489-5	2022	Our ex vivo efflux experiments reveal that the NE transporter (NET) blocker desipramine elevates both norepinephrine (NE) and dopamine (DA), but not 5-HT levels, in PFC tissue slices from wild-type (WT) and DAT-KO, but not NET-KO mice.	Desipramine	76-87	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	47-61
35210489-5	2022	Our ex vivo efflux experiments reveal that the NE transporter (NET) blocker desipramine elevates both norepinephrine (NE) and dopamine (DA), but not 5-HT levels, in PFC tissue slices from wild-type (WT) and DAT-KO, but not NET-KO mice.	Desipramine	76-87	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	207-210
35210489-7	2022	Systemic administration of desipramine or fluoxetine inhibits hyperactivity in DAT-KO mice, whereas local PFC infusion of desipramine alone produced this same effect.	Desipramine	27-38	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	79-82
35210489-7	2022	Systemic administration of desipramine or fluoxetine inhibits hyperactivity in DAT-KO mice, whereas local PFC infusion of desipramine alone produced this same effect.	Desipramine	122-133	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	79-82
35015730-6	2022	Combined treatment with desipramine and L-cycloserine (DC) lowered ceramide levels and exerted a protective effect on photoreceptors in AdipoR1-/- mice.	Desipramine	24-35	adiponectin receptor 1	Mus musculus	136-143
35242795-7	2022	Furthermore, DMI, the CLA was significantly greater (P < 0.05) in the CA2 group than the other groups.	Desipramine	13-16	carbonic anhydrase 2	Bos taurus	70-73
2533079-9	1989	It thus appears that 5-HT1 receptors in the VTA, presumably of the 5-HT1B type, act by preventing the anti-immobility effect of DMI.	Desipramine	128-131	5-hydroxytryptamine receptor 1B	Rattus norvegicus	67-73
34599336-9	2021	High allowance increased herbage mass and sites with greater canopy height which allow greater DMI, positively associated with cow BCS at weaning, calf ADG, BWW, and g of calf/kg DMI.	Desipramine	95-98	ADG	Bos taurus	152-155
2529959-4	1989	Analyses of the differences between GMI and DMI indicated that rapid forgetting was more apparent for DAT than for HD patients in the early stages of these disorders.	Desipramine	44-47	solute carrier family 6 member 3	Homo sapiens	102-105
2553044-1	1989	We examined the effects of chronic treatment with antidepressants (imipramine or desipramine) or benzodiazepines (diazepam, alprazolam, or adinazolam) on modulation of corticotropin-releasing-factor (CRF) receptors in discrete areas of rat brain and in anterior pituitary.	Desipramine	81-92	corticotropin releasing hormone	Rattus norvegicus	168-198
2725706-3	1989	When both MAO and COMT were intact, most of the metabolism of 3H-noradrenaline was neuronal (i.e., desipramine-sensitive).	Desipramine	99-110	monoamine oxidase A	Rattus norvegicus	10-13
2725706-3	1989	When both MAO and COMT were intact, most of the metabolism of 3H-noradrenaline was neuronal (i.e., desipramine-sensitive).	Desipramine	99-110	catechol-O-methyltransferase	Rattus norvegicus	18-22
2566928-8	1989	Uptake1 blockade with desipramine (100 nM) or nisoxetine (100 nM) prior to the second stimulation significantly increased noradrenaline overflow and attenuated that of NPY; the attenuation of the stimulation-evoked overflow of NPY was abolished by yohimbine (1 microM).	Desipramine	22-33	pro-neuropeptide Y	Cavia porcellus	168-171
2496890-7	1989	Only rats injected with 6-OHDA without DMI pretreatment showed a significant reduction in ANG II-induced drinking responses.	Desipramine	39-42	angiotensinogen	Rattus norvegicus	90-96
2568728-14	1989	Pretreatment with PBZ significantly increased the SNS-evoked NA and NPY-LI overflow, while DMI enhanced both the functional response and NA release but reduced the NPY-LI overflow.	Desipramine	91-94	neuropeptide Y	Sus scrofa	164-167
2566928-8	1989	Uptake1 blockade with desipramine (100 nM) or nisoxetine (100 nM) prior to the second stimulation significantly increased noradrenaline overflow and attenuated that of NPY; the attenuation of the stimulation-evoked overflow of NPY was abolished by yohimbine (1 microM).	Desipramine	22-33	pro-neuropeptide Y	Cavia porcellus	227-230
3225754-7	1988	These data strongly suggest that the hydroxylation pathways of imipramine and desipramine and the demethylation pathways of imipramine and 2-hydroxyimipramine are each sharing the same species of cytochrome P-450.	Desipramine	78-89	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	196-212
2615927-3	1989	The main findings were (1) sex differences in the growth hormone and cortisol response to desipramine and (2) a significant genetic component of the prolactin and cortisol response to desipramine as indicated by significantly (p less than 0.05) lower within-pair than between-pair variance in the sibling pairs but not random pairs of the experimental subjects.	Desipramine	90-101	growth hormone 1	Homo sapiens	50-64
2615927-3	1989	The main findings were (1) sex differences in the growth hormone and cortisol response to desipramine and (2) a significant genetic component of the prolactin and cortisol response to desipramine as indicated by significantly (p less than 0.05) lower within-pair than between-pair variance in the sibling pairs but not random pairs of the experimental subjects.	Desipramine	184-195	prolactin	Homo sapiens	149-158
2667015-0	1989	Desipramine increases circulating growth hormone in elderly depressed patients: a pilot study.	Desipramine	0-11	growth hormone 1	Homo sapiens	34-48
2975304-0	1988	Growth hormone response to desmethylimipramine in depressed and suicidal adolescents.	Desipramine	27-46	growth hormone 1	Homo sapiens	0-14
3418509-0	1988	Effects of high dose alpha-1-acid glycoprotein on desipramine toxicity in rats.	Desipramine	50-61	orosomucoid 1	Rattus norvegicus	21-46
3418509-9	1988	The serum DMI concentration did not change with albumin infusion but increased 4.7-fold (1.9 +/- 0.7 to 9.0 +/- 1.6 micrograms/ml) after AAG, 2.2 g/kg, and 6.7-fold (2.3 +/- 0.5 to 15.7 +/- 7.0 micrograms/ml) after AAG, 4.4 g/kg.	Desipramine	10-13	orosomucoid 1	Rattus norvegicus	137-140
3418509-9	1988	The serum DMI concentration did not change with albumin infusion but increased 4.7-fold (1.9 +/- 0.7 to 9.0 +/- 1.6 micrograms/ml) after AAG, 2.2 g/kg, and 6.7-fold (2.3 +/- 0.5 to 15.7 +/- 7.0 micrograms/ml) after AAG, 4.4 g/kg.	Desipramine	10-13	orosomucoid 1	Rattus norvegicus	215-218
2828545-11	1988	Decreasing 5-HT2 function by twice-a-day injection of 5 mg/kg of zimeldine or desipramine (DMI) produced 50% (p less than 0.01) and 56% (p less than 0.01), respectively, reductions in head-twitch behaviour.	Desipramine	78-89	hypothermia due to alcohol sensitivity 2	Mus musculus	13-16
3132531-0	1988	Possible involvement of pertussis toxin substrates (Gi, Go) in desipramine-induced refractoriness of adenylate cyclase in cerebral cortices of rats.	Desipramine	63-74	RAS like proto-oncogene B	Rattus norvegicus	52-54
2828545-11	1988	Decreasing 5-HT2 function by twice-a-day injection of 5 mg/kg of zimeldine or desipramine (DMI) produced 50% (p less than 0.01) and 56% (p less than 0.01), respectively, reductions in head-twitch behaviour.	Desipramine	91-94	hypothermia due to alcohol sensitivity 2	Mus musculus	13-16
3427414-0	1987	The modulatory effect of neurotensin on [3H]dopamine release from rat nucleus accumbens slices is enhanced after chronic desipramine treatment.	Desipramine	121-132	neurotensin	Rattus norvegicus	25-36
3427414-4	1987	Superfusion of the DMI-treated rat tissue with buffer-containing neurotensin (100 nM) resulted in an increase in the K+-evoked release of [3H]DA to a level which was higher than that observed with tissue obtained from untreated rats.	Desipramine	19-22	neurotensin	Rattus norvegicus	65-76
3427414-6	1987	These findings are consistent with DMI treatment giving rise to impaired DA release possibly due to DA autoreceptor-mediated inhibition of DA release and cancellation of this effect by neurotensin.	Desipramine	35-38	neurotensin	Rattus norvegicus	185-196
2887701-3	1987	Subchronic infusion of desipramine, a noradrenaline uptake inhibitor, effected a decrease in neocortical and hippocampal beta 1-adrenoceptor density.	Desipramine	23-34	adrenoceptor beta 1	Rattus norvegicus	121-140
3108675-6	1987	Desipramine suppressed the NPY-LI release induced by tyramine apparently by the inhibition of the uptake of tyramine is suggested by the significant positive correlation between the reduction of 14C-tyramine uptake and the inhibition of NPY-LI release induced by desipramine (r = 0.946).	Desipramine	0-11	neuropeptide Y	Rattus norvegicus	27-30
3108675-6	1987	Desipramine suppressed the NPY-LI release induced by tyramine apparently by the inhibition of the uptake of tyramine is suggested by the significant positive correlation between the reduction of 14C-tyramine uptake and the inhibition of NPY-LI release induced by desipramine (r = 0.946).	Desipramine	0-11	neuropeptide Y	Rattus norvegicus	237-240
3108675-6	1987	Desipramine suppressed the NPY-LI release induced by tyramine apparently by the inhibition of the uptake of tyramine is suggested by the significant positive correlation between the reduction of 14C-tyramine uptake and the inhibition of NPY-LI release induced by desipramine (r = 0.946).	Desipramine	263-274	neuropeptide Y	Rattus norvegicus	27-30
3108675-6	1987	Desipramine suppressed the NPY-LI release induced by tyramine apparently by the inhibition of the uptake of tyramine is suggested by the significant positive correlation between the reduction of 14C-tyramine uptake and the inhibition of NPY-LI release induced by desipramine (r = 0.946).	Desipramine	263-274	neuropeptide Y	Rattus norvegicus	237-240
2882523-4	1987	After chronic administration of tricyclic antidepressants (imipramine and desipramine) the number of cortical beta 1 adrenergic receptors decreased without impairing the clenbuterol-induced decrease in spontaneous motor activity.	Desipramine	74-85	hemoglobin, beta adult major chain	Mus musculus	110-116
3666058-0	1987	The influence of desmethylimipramine on the hypothalamic and neurohypophysial vasopressin content in pinealectomized male rats.	Desipramine	17-36	arginine vasopressin	Rattus norvegicus	78-89
3666058-1	1987	The effect of desmethylimipramine (DMI) on the hypothalamic and neurohypophysial vasopressin content was investigated in normal and pinealectomized male rats.	Desipramine	14-33	arginine vasopressin	Rattus norvegicus	81-92
3666058-1	1987	The effect of desmethylimipramine (DMI) on the hypothalamic and neurohypophysial vasopressin content was investigated in normal and pinealectomized male rats.	Desipramine	35-38	arginine vasopressin	Rattus norvegicus	81-92
3666058-4	1987	injection of DMI (20 micrograms; dissolved in 10 microliters of normal saline) decreased vasopressin content in the neurohypophysis of non-operated and sham-operated animals.	Desipramine	13-16	arginine vasopressin	Rattus norvegicus	89-100
3628616-3	1987	Clinical studies have suggested that sleep deprivation could potentiate the therapeutic effects of antidepressants, and there were reports on DMI stimulation of GH.	Desipramine	142-145	growth hormone 1	Homo sapiens	161-163
3628616-5	1987	The GH levels increased substantially (8- to 10-fold) after DMI in both experimental conditions.	Desipramine	60-63	growth hormone 1	Homo sapiens	4-6
3628616-6	1987	Sleep deprivation neither changed GH basal levels nor potentiated the DMI-induced GH increase.	Desipramine	70-73	growth hormone 1	Homo sapiens	82-84
3598027-1	1987	Adverse reactions to the tricyclic antidepressant drugs imipramine and desipramine have been described and include eosinophilia, pulmonary infiltrates with eosinophilia, and elevated total serum IgE levels.	Desipramine	71-82	immunoglobulin heavy constant epsilon	Homo sapiens	195-198
3598027-3	1987	This article describes a patient manifesting bronchospasm, profound eosinophilia, and elevated serum IgE levels after therapy with desipramine that resolved rapidly after withdrawal of the drug.	Desipramine	131-142	immunoglobulin heavy constant epsilon	Homo sapiens	101-104
3595714-4	1987	There was a positive correlation between the inhibitory effect of desipramine on the NPY release and on the uptake of [14C]tyramine into synaptosomes.	Desipramine	66-77	neuropeptide Y	Oryctolagus cuniculus	85-88
3595714-6	1987	These data suggest that tyramine enters into nerve terminals through a desipramine-sensitive mechanism, resulting in the co-release of NE and NPY which can be reduced by guanethidine.	Desipramine	71-82	neuropeptide Y	Oryctolagus cuniculus	142-145
3101979-0	1987	Chronic administration of desipramine or nialamide decreases wet-dog shakes in rats produced by the TRH-analog MK-771.	Desipramine	26-37	thyrotropin releasing hormone	Rattus norvegicus	100-103
3101979-1	1987	The effect of chronic administration of the tricyclic antidepressant, desipramine, or the monoamine oxidase inhibitor (MAOI), nialamide, on the ability of the TRH analog, MK-771, to induce wet-dog shakes in rats was examined.	Desipramine	70-81	TRH	Canis lupus familiaris	159-162
2455193-13	1987	The NA uptake inhibitor desipramine reduces NPY release.	Desipramine	24-35	neuropeptide Y	Homo sapiens	44-47
3769385-4	1986	For desipramine the apparent oral clearance (L X min-1) was 0.19 (0.12 to 0.24) in PM compared with 1.64 (1.46 to 1.80) and 1.03 (0.77 to 1.13) in rapid EM and slow EM.	Desipramine	4-15	CD59 molecule (CD59 blood group)	Homo sapiens	49-54
2872321-3	1986	Prolonged administration of desipramine and citalopram, but not amitriptyline, elevated the microsomal level of cytochrome P-450 and accelerated the rate of ethylmorphine demethylation.	Desipramine	28-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	112-128
2418913-3	1986	In this study, we have determined the effect of neonatal 5,7-DHT and desipramine (DMI) treatment on the biochemical content and immunocytochemical localization of substance P and TRH throughout the brain.	Desipramine	69-80	thyrotropin releasing hormone	Rattus norvegicus	179-182
2874504-8	1986	co-administration of atenolol or practolol, beta 1-adrenoceptor antagonists, together with DMI attenuated both beta-adrenoceptor down regulation and the behavioural activation by chronic DMI.	Desipramine	187-190	adrenoceptor beta 1	Rattus norvegicus	44-63
2418913-3	1986	In this study, we have determined the effect of neonatal 5,7-DHT and desipramine (DMI) treatment on the biochemical content and immunocytochemical localization of substance P and TRH throughout the brain.	Desipramine	82-85	thyrotropin releasing hormone	Rattus norvegicus	179-182
3028722-5	1986	The alpha 2-mediated growth hormone response to clonidine was increased after one week"s treatment with desipramine and then reduced during the second and third weeks of treatment.	Desipramine	104-115	growth hormone 1	Homo sapiens	21-35
3709653-3	1986	2-hydroxylation of DMI is probably mediated by debrisoquine hydroxylase, a cytochrome P-450 isozyme that is monogenically controlled.	Desipramine	19-22	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	75-91
3005903-4	1986	Since the inhibitors of the uptake of noradrenaline, desipramine and CPP 199 antagonized this preference for noradrenergic MAO it is concluded that these MAO inhibitors are accumulated in the noradrenergic neurones by the membranal uptake carrier.	Desipramine	53-64	monoamine oxidase A	Rattus norvegicus	123-126
3005903-4	1986	Since the inhibitors of the uptake of noradrenaline, desipramine and CPP 199 antagonized this preference for noradrenergic MAO it is concluded that these MAO inhibitors are accumulated in the noradrenergic neurones by the membranal uptake carrier.	Desipramine	53-64	monoamine oxidase A	Rattus norvegicus	154-157
3031716-2	1986	In this report the effects of various receptor blockers on desimipramine (DMI)-induced growth hormone (GH) secretion in healthy male subjects are presented.	Desipramine	59-72	growth hormone 1	Homo sapiens	87-101
3031716-2	1986	In this report the effects of various receptor blockers on desimipramine (DMI)-induced growth hormone (GH) secretion in healthy male subjects are presented.	Desipramine	59-72	growth hormone 1	Homo sapiens	103-105
3031716-2	1986	In this report the effects of various receptor blockers on desimipramine (DMI)-induced growth hormone (GH) secretion in healthy male subjects are presented.	Desipramine	74-77	growth hormone 1	Homo sapiens	87-101
3031716-2	1986	In this report the effects of various receptor blockers on desimipramine (DMI)-induced growth hormone (GH) secretion in healthy male subjects are presented.	Desipramine	74-77	growth hormone 1	Homo sapiens	103-105
3031716-6	1986	DMI-induced GH stimulation was not significantly different after DMI i.v.	Desipramine	0-3	growth hormone 1	Homo sapiens	12-14
3031716-10	1986	), GH secretion was significantly increased by 25 mg DMI (p less than 0.05) and 50 mg DMI (incomplete block design, n = 18).	Desipramine	53-56	growth hormone 1	Homo sapiens	3-5
3031716-10	1986	), GH secretion was significantly increased by 25 mg DMI (p less than 0.05) and 50 mg DMI (incomplete block design, n = 18).	Desipramine	86-89	growth hormone 1	Homo sapiens	3-5
3031716-11	1986	GH secretion was significantly lower (p less than 0.01) after DMI in combination with 60 mg phentolamine i.v.	Desipramine	62-65	growth hormone 1	Homo sapiens	0-2
3031716-15	1986	The DMI-induced GH increase following DMI plus 1 mg prazosin p.o.	Desipramine	4-7	growth hormone 1	Homo sapiens	16-18
3031716-15	1986	The DMI-induced GH increase following DMI plus 1 mg prazosin p.o.	Desipramine	38-41	growth hormone 1	Homo sapiens	16-18
3031716-17	1986	The results indicate that the GH-stimulating effect of DMI is primarily related to the ability of DMI to inhibit noradrenaline (NA) reuptake.	Desipramine	55-58	growth hormone 1	Homo sapiens	30-32
3031716-17	1986	The results indicate that the GH-stimulating effect of DMI is primarily related to the ability of DMI to inhibit noradrenaline (NA) reuptake.	Desipramine	98-101	growth hormone 1	Homo sapiens	30-32
3739365-5	1986	By monitoring the hydroxylation of DMI in various fractions during separation and purification of cytochrome P-450 from human liver microsomes we have purified a cytochrome P-450 which efficiently hydroxylates this drug.	Desipramine	35-38	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	98-114
3739365-5	1986	By monitoring the hydroxylation of DMI in various fractions during separation and purification of cytochrome P-450 from human liver microsomes we have purified a cytochrome P-450 which efficiently hydroxylates this drug.	Desipramine	35-38	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	162-178
3160963-7	1985	Pretreatment with the blocker of the uptake of norepinephrine, desipramine did not prevent the initial (30 min) effect but completely prevented the delayed (4 hr) effect of fenfluramine on plasma renin activity.	Desipramine	63-74	renin	Rattus norvegicus	196-201
3031718-2	1986	In this report the effects of various receptor blockers on the desimipramine (DMI)-induced cortisol (ACTH) secretion in healthy male subjects are presented.	Desipramine	63-76	proopiomelanocortin	Homo sapiens	101-105
3031718-2	1986	In this report the effects of various receptor blockers on the desimipramine (DMI)-induced cortisol (ACTH) secretion in healthy male subjects are presented.	Desipramine	78-81	proopiomelanocortin	Homo sapiens	101-105
3031718-6	1986	In addition, the effect of prazosin on DMI-induced ACTH stimulation was examined.	Desipramine	39-42	proopiomelanocortin	Homo sapiens	51-55
3031718-15	1986	n = 12), as was DMI-induced ACTH secretion (p less than 0.05) in these subjects.	Desipramine	16-19	proopiomelanocortin	Homo sapiens	28-32
3031718-16	1986	The findings of these trials, especially those of the prazosin trial, indicate that DMI-induced stimulation of cortisol and ACTH secretion is attributable to the noradrenaline (NA) reuptake inhibiting effect of DMI, and that the stimulus is transmitted with the aid of noradrenergic alpha-1 receptors.	Desipramine	84-87	proopiomelanocortin	Homo sapiens	124-128
3031718-16	1986	The findings of these trials, especially those of the prazosin trial, indicate that DMI-induced stimulation of cortisol and ACTH secretion is attributable to the noradrenaline (NA) reuptake inhibiting effect of DMI, and that the stimulus is transmitted with the aid of noradrenergic alpha-1 receptors.	Desipramine	84-87	adrenoceptor alpha 1D	Homo sapiens	283-290
3031718-16	1986	The findings of these trials, especially those of the prazosin trial, indicate that DMI-induced stimulation of cortisol and ACTH secretion is attributable to the noradrenaline (NA) reuptake inhibiting effect of DMI, and that the stimulus is transmitted with the aid of noradrenergic alpha-1 receptors.	Desipramine	211-214	proopiomelanocortin	Homo sapiens	124-128
3928818-9	1985	DMI pretreatment blocked the increase in hippocampal TRH, but not in brainstem TRH.	Desipramine	0-3	thyrotropin releasing hormone	Rattus norvegicus	53-56
3031716-18	1986	Should serotonergic receptors be involved in the DMI-induced GH secretion at all, they transmit a positive stimulus.	Desipramine	49-52	growth hormone 1	Homo sapiens	61-63
3031717-2	1986	In this report the effects of various receptor blockers on desimipramine (DMI)-induced prolactin (PRL) secretion in healthy male subjects are presented.	Desipramine	59-72	prolactin	Homo sapiens	87-96
3031717-2	1986	In this report the effects of various receptor blockers on desimipramine (DMI)-induced prolactin (PRL) secretion in healthy male subjects are presented.	Desipramine	74-77	prolactin	Homo sapiens	87-96
6098913-5	1984	DMI acutely increased plasma PRL, whereas ZIM had an effect only after chronic pretreatment.	Desipramine	0-3	prolactin	Homo sapiens	29-32
4092710-0	1985	Growth hormone release after desipramine in depressive illness.	Desipramine	29-40	growth hormone 1	Homo sapiens	0-14
4092710-2	1985	administration of 75 mg of desipramine on growth hormone (GH) secretion was investigated in a sample of 87 patients with major depressive disorders and in 31 normal controls.	Desipramine	27-38	growth hormone 1	Homo sapiens	42-56
4092710-2	1985	administration of 75 mg of desipramine on growth hormone (GH) secretion was investigated in a sample of 87 patients with major depressive disorders and in 31 normal controls.	Desipramine	27-38	growth hormone 1	Homo sapiens	58-60
4001280-2	1985	In previous studies it was shown that the tricyclic antidepressant desimipramine (DMI) had different stimulatory effects on growth hormone (GH), prolactin (PRL), ACTH and cortisol secretion in healthy subjects, depending on the mode of administration.	Desipramine	67-80	growth hormone 1	Homo sapiens	124-138
4001280-2	1985	In previous studies it was shown that the tricyclic antidepressant desimipramine (DMI) had different stimulatory effects on growth hormone (GH), prolactin (PRL), ACTH and cortisol secretion in healthy subjects, depending on the mode of administration.	Desipramine	67-80	prolactin	Homo sapiens	145-154
4001280-2	1985	In previous studies it was shown that the tricyclic antidepressant desimipramine (DMI) had different stimulatory effects on growth hormone (GH), prolactin (PRL), ACTH and cortisol secretion in healthy subjects, depending on the mode of administration.	Desipramine	67-80	prolactin	Homo sapiens	156-159
4001280-2	1985	In previous studies it was shown that the tricyclic antidepressant desimipramine (DMI) had different stimulatory effects on growth hormone (GH), prolactin (PRL), ACTH and cortisol secretion in healthy subjects, depending on the mode of administration.	Desipramine	67-80	proopiomelanocortin	Homo sapiens	162-166
4001280-2	1985	In previous studies it was shown that the tricyclic antidepressant desimipramine (DMI) had different stimulatory effects on growth hormone (GH), prolactin (PRL), ACTH and cortisol secretion in healthy subjects, depending on the mode of administration.	Desipramine	82-85	growth hormone 1	Homo sapiens	124-138
4001280-2	1985	In previous studies it was shown that the tricyclic antidepressant desimipramine (DMI) had different stimulatory effects on growth hormone (GH), prolactin (PRL), ACTH and cortisol secretion in healthy subjects, depending on the mode of administration.	Desipramine	82-85	prolactin	Homo sapiens	145-154
4001280-2	1985	In previous studies it was shown that the tricyclic antidepressant desimipramine (DMI) had different stimulatory effects on growth hormone (GH), prolactin (PRL), ACTH and cortisol secretion in healthy subjects, depending on the mode of administration.	Desipramine	82-85	prolactin	Homo sapiens	156-159
4001280-2	1985	In previous studies it was shown that the tricyclic antidepressant desimipramine (DMI) had different stimulatory effects on growth hormone (GH), prolactin (PRL), ACTH and cortisol secretion in healthy subjects, depending on the mode of administration.	Desipramine	82-85	proopiomelanocortin	Homo sapiens	162-166
4001280-6	1985	Compared to placebo, significant increases occurred in GH (p less than 0.05) and in PRL (p less than 0.05) from a dose of DMI 25 mg on, and in cortisol (p less than 0.05) from 15 mg on.	Desipramine	122-125	prolactin	Homo sapiens	84-87
2937389-2	1985	In rat but not in mouse thymocytes the ecto-ATPase was inhibited in vitro by HgCl2, tricyclohexyltin chloride, di-n-butyltin dichloride, DDT, gamma HCH and desipramine.	Desipramine	156-167	CEA cell adhesion molecule 1	Rattus norvegicus	39-50
2857613-1	1985	In the present studies the effects of desipramine on the functional sensitivity of the prejunctional alpha 2-adrenoceptors of the vas deferens were studied in pithed rats; contractions of the tissue were evoked by electrical stimulation (6 Hz) of the spinal sympathetic outflow.	Desipramine	38-49	arginine vasopressin	Rattus norvegicus	130-133
2857613-4	1985	In acute studies desipramine (0.3-4.3 mg/kg, intravenously) inhibited electrically induced contractions of the vas deferens of pithed rats.	Desipramine	17-28	arginine vasopressin	Rattus norvegicus	111-114
6098913-6	1984	Chronic DMI but not ZIM increased baseline PRL.	Desipramine	8-11	prolactin	Homo sapiens	43-46
6237705-7	1984	Desipramine given orally (27 mg kg-1 per day, 14 days) decreased both the behaviour and number of 5-HT2 binding sites.	Desipramine	0-11	hypothermia due to alcohol sensitivity 2	Mus musculus	100-103
6087965-4	1984	By contrast, the growth hormone response to clonidine tended to be increased after one week of desipramine, reduced after three weeks of treatment, and further reduced after discontinuation.	Desipramine	95-106	growth hormone 1	Homo sapiens	17-31
6703855-4	1984	Both desipramine (N = 7) and amitriptyline (N = 6) significantly increased the PRL rise induced by tryptophan compared with a preceding placebo period.	Desipramine	5-16	prolactin	Homo sapiens	79-82
6735152-3	1984	Similarly inhibition of NE reuptake by imipramine or desmethylimipramine were followed by reduced GH secretion.	Desipramine	53-72	growth hormone 1	Homo sapiens	98-100
6703855-5	1984	In contrast, following long-term amitriptyline and desipramine treatment, the ability of tryptophan to increase PRL was enhanced two weeks following abrupt cessation of amitriptyline therapy (N = 5), but not after discontinuation of desipramine therapy.	Desipramine	51-62	prolactin	Homo sapiens	112-115
6703855-5	1984	In contrast, following long-term amitriptyline and desipramine treatment, the ability of tryptophan to increase PRL was enhanced two weeks following abrupt cessation of amitriptyline therapy (N = 5), but not after discontinuation of desipramine therapy.	Desipramine	233-244	prolactin	Homo sapiens	112-115
6693882-4	1984	In aorta and vas deferens, about 45% and 65%, respectively, of the total [3H]XYL accumulation was blocked by 100 mumol/L desmethylimipramine (DMI), l-NA, or bretylium.	Desipramine	121-140	arginine vasopressin	Rattus norvegicus	13-16
6141282-7	1984	The decrease and recovery of enzyme activity in the heart after administration of the reversible noradrenergic neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4) were parallel to the recovery of norepinephrine content and desmethylimipramine binding.	Desipramine	234-253	dual specificity phosphatase 26	Homo sapiens	168-172
6693882-4	1984	In aorta and vas deferens, about 45% and 65%, respectively, of the total [3H]XYL accumulation was blocked by 100 mumol/L desmethylimipramine (DMI), l-NA, or bretylium.	Desipramine	142-145	arginine vasopressin	Rattus norvegicus	13-16
6098855-3	1984	Desimipramine therapy (50-100 mg/day per os for 3-5 weeks) induced in parallel psychological improvement and fall in beta LPH-beta EP in 6 of 8 PAD patients treated, and a normalization of beta EP-beta LPH levels with minimal mood improvement in the 2 schizoaffective subjects.	Desipramine	0-13	proopiomelanocortin	Homo sapiens	117-125
6098855-3	1984	Desimipramine therapy (50-100 mg/day per os for 3-5 weeks) induced in parallel psychological improvement and fall in beta LPH-beta EP in 6 of 8 PAD patients treated, and a normalization of beta EP-beta LPH levels with minimal mood improvement in the 2 schizoaffective subjects.	Desipramine	0-13	proopiomelanocortin	Homo sapiens	197-205
6093182-2	1984	Desimipramine (DMI) (50 mg IV) significantly stimulated ACTH secretion.	Desipramine	0-13	proopiomelanocortin	Homo sapiens	56-60
6093182-2	1984	Desimipramine (DMI) (50 mg IV) significantly stimulated ACTH secretion.	Desipramine	15-18	proopiomelanocortin	Homo sapiens	56-60
6420832-0	1984	Comparison of growth hormone and prolactin stimulation induced by chlorimipramine and desimipramine in man in connection with chlorimipramine metabolism.	Desipramine	86-99	prolactin	Homo sapiens	33-42
6420832-1	1984	In order to compare the effects of chlorimipramine (CI) and desimipramine (DMI) on growth hormone (GH) and on prolactin (PRL) secretion equal doses of 25 mg CI or DMI were administered i.v.	Desipramine	75-78	growth hormone 1	Homo sapiens	83-97
6644379-2	1983	The label is incorporated by reaction of C-11 methyl iodide (11CH3I) upon desipramine in dimethylsulfoxide.	Desipramine	74-85	aldo-keto reductase family 1 member C4	Homo sapiens	41-45
6646243-8	1983	Since pretreatment of the rats with norzimeldine or desipramine antagonized the preferences for serotonergic or noradrenergic MAO, it is plausible to conclude that the compounds showing these preferences are accumulated in the neurons by the membranal uptake systems.	Desipramine	52-63	monoamine oxidase A	Rattus norvegicus	126-129
6299918-3	1983	When in these patients brain norepinephrine receptor activity was increased by desipramine, the normally negative differential feedback mechanism was converted into a positive one (paradoxical ACTH response).	Desipramine	79-90	proopiomelanocortin	Homo sapiens	193-197
6888570-7	1983	The liver/intestine ratio of DMI and 2-OH-IMP formation is proportional to the cytochrome P-450 ratio in the microsomes, in contrast to N-oxide formation.	Desipramine	29-32	cytochrome P450 3A14	Cavia porcellus	79-95
6130811-3	1983	The beta(2)-adrenoceptor agonist, terbutaline (5.0 mg kg(-1)), produced a moderate increase in pineal melatonin content.2 Repeated daily administration of desmethylimipramine (10 mg kg(-1) for 10 days) and maprotiline (10 mg kg(-1) for 10 days), antidepressants predominantly inhibiting noradrenaline (NA) uptake, reduced the isoprenaline-induced increase in pineal melatonin content.	Desipramine	155-174	adrenoceptor beta 2	Rattus norvegicus	4-24
6840904-5	1983	There was a difference between the drug-free period and desmethylimipramine or imipramine on the PEPc (P less than 0.05) and the PEP/LVET ratio (P less than 0.05); on the R-R (P less than 0.05), PR (P less than 0.05), QRS (P less than 0.05), and QTc (P less than 0.05) intervals; but no difference on the LVETc or shortening fraction or the mean velocity of circumferential shortening.	Desipramine	56-75	peptidase C	Homo sapiens	97-101
6840904-5	1983	There was a difference between the drug-free period and desmethylimipramine or imipramine on the PEPc (P less than 0.05) and the PEP/LVET ratio (P less than 0.05); on the R-R (P less than 0.05), PR (P less than 0.05), QRS (P less than 0.05), and QTc (P less than 0.05) intervals; but no difference on the LVETc or shortening fraction or the mean velocity of circumferential shortening.	Desipramine	56-75	progestagen associated endometrial protein	Homo sapiens	97-100
6840904-6	1983	Drugs such as desmethylimipramine and imipramine which prolong intraventricular conduction can probably be expected to prolong the PEP and PEP/LVET.	Desipramine	14-33	progestagen associated endometrial protein	Homo sapiens	131-134
6840904-6	1983	Drugs such as desmethylimipramine and imipramine which prolong intraventricular conduction can probably be expected to prolong the PEP and PEP/LVET.	Desipramine	14-33	progestagen associated endometrial protein	Homo sapiens	139-142
6959166-1	1982	The effect of 4 to 6 weeks of treatment with the antidepressants, desmethylimipramine and amitriptyline, on the growth hormone response to clonidine was studied in 12 depressed patients.	Desipramine	66-85	growth hormone 1	Homo sapiens	112-126
6126334-7	1982	These data suggest that DMI decreases both transport of 5-HT across the pulmonary endothelium and MAO activity.	Desipramine	24-27	monoamine oxidase A	Rattus norvegicus	98-101
7090425-3	1982	The enzyme system involved was dependent on cytochrome P-450 and the main metabolites were desmethylimipramine (DMI), formaldehyde and p-chlorobenzoic acid.	Desipramine	91-110	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	44-60
7090425-3	1982	The enzyme system involved was dependent on cytochrome P-450 and the main metabolites were desmethylimipramine (DMI), formaldehyde and p-chlorobenzoic acid.	Desipramine	112-115	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	44-60
7178370-0	1982	Comparison of growth hormone stimulation induced by desimipramine, diazepam and metaclazepam in man.	Desipramine	52-65	growth hormone 1	Homo sapiens	14-28
6457138-4	1981	Plasma renin activity was also reduced in rats that had received intraventricular 5,7-dihydroxytryptamine after pretreatment with desmethylimipramine.	Desipramine	130-149	renin	Rattus norvegicus	7-12
6314168-0	1983	Involvement of alpha- and beta 1-adrenergic mechanisms in the immobility-reducing action of desipramine in the forced swimming test.	Desipramine	92-103	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	15-32
6135776-0	1983	Stereoselectivity of catecholamines: differential effects of cocaine and desipramine on catecholamine-induced contractions of the rat isolated vas deferens.	Desipramine	73-84	arginine vasopressin	Rattus norvegicus	143-146
6135776-1	1983	The effect of uptake inhibitors, cocaine and desipramine, on the contractile response of the rat isolated vas deferens to the enantiomers of noradrenaline and adrenaline and to the corresponding deoxy-derivatives, dopamine and epinephline, was investigated.	Desipramine	45-56	arginine vasopressin	Rattus norvegicus	106-109
6135776-4	1983	This selective antagonism of dopamine by desipramine was also observed for the separated epididymal and prostatic ends of the rat vas deferens.	Desipramine	41-52	arginine vasopressin	Rattus norvegicus	130-133
6124090-10	1982	It is likely that such studies will enrich our understanding of how these agents work, of the difference between agents which have been classed together on the basis of preclinical studies (e.g., DMI, which appears to increase PRL and GH, and NT which appears not to) and provided additional evidence to test current hypotheses about the biological basis of their antidepressant action.	Desipramine	196-199	prolactin	Homo sapiens	227-230
7320735-6	1981	Desipramine treatment increase NAT activity in 8-day-old animals; hydrocortisone-treated animals were least affected.	Desipramine	0-11	bromodomain containing 2	Homo sapiens	31-34
6971560-8	1981	Desipramine, acutely, had no effect on any of the above paradigms but after chronic administration, potentiated the effect of low dose 5-HTP on prolactin secretion.	Desipramine	0-11	prolactin	Rattus norvegicus	144-153
6452790-4	1981	In the same individuals, desipramine concentrations were highly correlated with decreases of MHPG in the CSF.	Desipramine	25-36	colony stimulating factor 2	Homo sapiens	105-108
119692-3	1979	TRH (10(-7)--10(--3)M) alone did not increase the DA release into the incubation medium, but it clearly enhanced the DA release in the concomitant presence of desipramine (5 x 10(-5)M).	Desipramine	159-170	thyrotropin releasing hormone	Rattus norvegicus	0-3
1000130-12	1976	5 The long-term effects of DSP 4 on the noradrenaline accumulation, the DBH activity and noradrenaline concentration in the rat brain were antagonized by desipramine (10 mg/kg i.p.).	Desipramine	154-165	dopamine beta-hydroxylase	Rattus norvegicus	72-75
215414-1	1978	Intravenous infusion of two separate doses of angiotensin II in pentobarbital-anesthetized, desipramine-treated animals produced dose-related increases in arterial blood pressure and caused significant potentiation of the cardioacceleration observed during the stimulation of the right postganglionic cardiac sympathetic nerve fibers.	Desipramine	92-103	angiotensinogen	Homo sapiens	46-60
365126-3	1978	The levels of both drugs were approximately equal in plasma, but desipramine predominated in CSF (imipramine/desipramine ratio of 0.8).	Desipramine	65-76	colony stimulating factor 2	Homo sapiens	93-96
582390-0	1978	[Influence of single and repeated administration of desipramine (DMI) on the secretion of growth hormone (GH) (author"s transl)].	Desipramine	52-63	growth hormone 1	Homo sapiens	90-104
582390-0	1978	[Influence of single and repeated administration of desipramine (DMI) on the secretion of growth hormone (GH) (author"s transl)].	Desipramine	52-63	growth hormone 1	Homo sapiens	106-108
582390-0	1978	[Influence of single and repeated administration of desipramine (DMI) on the secretion of growth hormone (GH) (author"s transl)].	Desipramine	65-68	growth hormone 1	Homo sapiens	90-104
582390-0	1978	[Influence of single and repeated administration of desipramine (DMI) on the secretion of growth hormone (GH) (author"s transl)].	Desipramine	65-68	growth hormone 1	Homo sapiens	106-108
582390-1	1978	DMI leads to stimulation of GH in healthy male subjects 60--120 min after i.m.	Desipramine	0-3	growth hormone 1	Homo sapiens	28-30
582390-3	1978	During a 20-day administration of 2 x 75 mg DMI per day a repeated stimulation of GH was provable on days 0, 10 and 20 in two male patients, whereas no stimulation of GH occurred in two female patients who underwent the same treatment.	Desipramine	44-47	growth hormone 1	Homo sapiens	82-84
582390-6	1978	The increase in PRL and TSH, which is induced by the thyrotrophin releasing hormone (TRH), is provable after acute as well as after chronic administration of DMI.	Desipramine	158-161	prolactin	Homo sapiens	16-19
1012341-3	1976	In vas deferens from non-reserpinized rats the release of noradrenaline evoked by veratridine was partially antagonized by omission of Ca2+ in the incubation medium and partially inhibited by low concentrations of desipramine.	Desipramine	214-225	arginine vasopressin	Rattus norvegicus	3-6
958507-0	1976	Persistent enhancement of potassium-induced responses of the rat vas deferens by desipramine.	Desipramine	81-92	arginine vasopressin	Rattus norvegicus	65-68
991921-2	1976	Org 6582 was approximately twice as potent as fluoxetine, five times more potent than chlorimipramine and 14 times more potent than desipramine in blocking the ability of p-chloroamphetamine to lower rat brain 5-HT content.	Desipramine	132-143	POU class 6 homeobox 1	Rattus norvegicus	204-211
186834-6	1976	By that time the MUA changes of PH and MRF showed similar characteristics in response to TRH administration which was observed following the injection of desipramine and imipramine.	Desipramine	154-165	thyrotropin releasing hormone	Felis catus	89-92
958507-1	1976	The effect of desipramine on the cumulative dose-response curves of noradrenaline and potassium (K+) was examined on the isolated rat vas deferens.	Desipramine	14-25	arginine vasopressin	Rattus norvegicus	134-137
5348466-4	1969	In slices of rat vas deferens incubated with various concentrations of (3)H-NA, cocaine and desipramine and phenoxybenzamine were also shown to act as competitive inhibitors of NA uptake.	Desipramine	92-103	arginine vasopressin	Rattus norvegicus	17-20
5067380-0	1972	Oxidation and glucuronidation of certain drugs in various subcellular fractions of rat liver: binding of desmethylimipramine and hexobarbital to cytochrome P-450 and oxidation and glucuronidation of desmethylimipramine, aminopyrine, p-nitrophenol and 1-naphthol.	Desipramine	105-124	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	145-161
5314401-0	1970	Binding to cytochrome P-450 and metabolism of desmethylimipramine and metabolites in rat liver microsomes.	Desipramine	46-65	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	11-27
476283-2	1979	Detection limits of 0.2 ng ml-1 for imipramine and 0.1 ng ml-1 for desipramine were demonstrated with a signal-to-noise ratio maintained at 2:1 or better.	Desipramine	67-78	interleukin 17F	Homo sapiens	58-62
1187753-2	1975	The administration of NE, DOPA, amphetamine, phenelzine, desipramine and clonidine induced the reappearance of the CAR.	Desipramine	57-68	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	115-118
33220685-2	2021	It poorly infects mice deficient in acid sphingomyelinase (ASM), a lysosomal enzyme critical for cholesterol efflux, and wild-type mice treated with desipramine that functionally inhibits ASM.	Desipramine	149-160	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	188-191
33496295-4	2021	Layer-resolved DMI calculations revealed that the sign of the spin-orbit coupling (SOC) energy was changed for Au near the interface of Au/Fe under tensile stress, subsequently reversing the chirality of the i-DMI from left-handed to right-handed.	Desipramine	15-18	spindlin 1	Homo sapiens	62-66
4382642-0	1967	Potentiation of noradrenaline isomers by cocaine and desipramine in the isolated vas deferens of the rat.	Desipramine	53-64	arginine vasopressin	Rattus norvegicus	81-84
33513512-8	2021	For example, IC50 value of desipramine for the zSERT was 1/200 of that for the hSERT.	Desipramine	27-38	solute carrier family 6 member 4	Homo sapiens	79-84
33220685-8	2021	Infection was markedly lower in ASM-deficient and desipramine-treated wild-type mice versus desipramine-treated SCID mice.	Desipramine	92-103	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	32-35
32294250-9	2020	Desipramine administration downregulated mRNA expressions of IL-1beta, iNOS, COX-2 and TIMP-1 when compared to vehicle alone in the ligature group (P<0.05).	Desipramine	0-11	interleukin 1 alpha	Rattus norvegicus	61-69
32294250-9	2020	Desipramine administration downregulated mRNA expressions of IL-1beta, iNOS, COX-2 and TIMP-1 when compared to vehicle alone in the ligature group (P<0.05).	Desipramine	0-11	nitric oxide synthase 2	Rattus norvegicus	71-75
32294250-9	2020	Desipramine administration downregulated mRNA expressions of IL-1beta, iNOS, COX-2 and TIMP-1 when compared to vehicle alone in the ligature group (P<0.05).	Desipramine	0-11	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	77-82
32294250-9	2020	Desipramine administration downregulated mRNA expressions of IL-1beta, iNOS, COX-2 and TIMP-1 when compared to vehicle alone in the ligature group (P<0.05).	Desipramine	0-11	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	87-93
32294250-10	2020	MMP-9 expression and MMP-9/TIMP-1 ratio were similar among rats with ligature-induced periodontitis (P>0.05); however, MMP-9 activity was lower in the group treated with desipramine (P<0.05).	Desipramine	170-181	matrix metallopeptidase 9	Rattus norvegicus	0-5
32294250-10	2020	MMP-9 expression and MMP-9/TIMP-1 ratio were similar among rats with ligature-induced periodontitis (P>0.05); however, MMP-9 activity was lower in the group treated with desipramine (P<0.05).	Desipramine	170-181	matrix metallopeptidase 9	Rattus norvegicus	21-26
32294250-10	2020	MMP-9 expression and MMP-9/TIMP-1 ratio were similar among rats with ligature-induced periodontitis (P>0.05); however, MMP-9 activity was lower in the group treated with desipramine (P<0.05).	Desipramine	170-181	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	27-33
32294250-10	2020	MMP-9 expression and MMP-9/TIMP-1 ratio were similar among rats with ligature-induced periodontitis (P>0.05); however, MMP-9 activity was lower in the group treated with desipramine (P<0.05).	Desipramine	170-181	matrix metallopeptidase 9	Rattus norvegicus	21-26
32679212-1	2020	Single-crystal X-ray diffraction and DFT calculation have been carried out for an atomic-level understanding of beta-cyclodextrin (beta-CD) inclusion complexation with two tricyclic antidepressants (TCAs), desipramine and imipramine.	Desipramine	206-217	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	131-138
32697958-8	2020	Taken together with existing literature, concurrent blockade of OCTs and/or PMAT merits further investigation as an adjunctive therapeutic for desipramine-like antidepressant drugs.	Desipramine	143-154	solute carrier family 29 member 4	Homo sapiens	76-80
32642907-12	2020	In contrast, treatment with desipramine, a NET selective inhibitor, resulted in profoundly decreased xenograft [125I]MIBG levels (p < 0.0001).	Desipramine	28-39	solute carrier family 6 member 2	Homo sapiens	43-46
33117297-7	2020	Results indicate a positive response in terms of growth performance and gastrointestinal digestibility to REE supplementation, and 400 mg/kg DMI treatment presented the most average daily feed intake (ADFI), the best average daily weight gain (ADG), and the least F/G.	Desipramine	141-144	ADFI	Bos taurus	201-205
33117297-7	2020	Results indicate a positive response in terms of growth performance and gastrointestinal digestibility to REE supplementation, and 400 mg/kg DMI treatment presented the most average daily feed intake (ADFI), the best average daily weight gain (ADG), and the least F/G.	Desipramine	141-144	ADG	Bos taurus	244-247
31090092-6	2019	The predicted versus observed geometric mean ratio (GMR) of AUCinf for CYP2D6 substrates desipramine and metoprolol coadministered with mirabegron 100 or 160 mg once daily were 3.47 versus 3.41 and 2.97 versus 3.29, respectively, indicating that the mirabegron model can be used to predict clinical CYP2D6 inhibition.	Desipramine	89-100	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	71-77
33344693-8	2020	Further, Adcy1 tg mice show reduced immobility under acute physical stress conditions in the forced swimming test and are more sensitive to the antidepressant desipramine.	Desipramine	159-170	adenylate cyclase 1	Mus musculus	9-14
32425895-9	2020	Nonetheless, inhibition of ASMase by desipramine did not affect IAV infection.	Desipramine	37-48	sphingomyelin phosphodiesterase 1	Homo sapiens	27-33
32481596-9	2020	Treatment of immortalized cell in vision research (ARPE-19) cells with high glucose resulted in a 25% +- 1.6% decrease in citrate synthase activity at 72 h. Inhibition of ASM with desipramine (15 muM, 1 h daily) abolished the decreases in metabolic functional parameters.	Desipramine	180-191	citrate synthase	Homo sapiens	122-138
32481596-9	2020	Treatment of immortalized cell in vision research (ARPE-19) cells with high glucose resulted in a 25% +- 1.6% decrease in citrate synthase activity at 72 h. Inhibition of ASM with desipramine (15 muM, 1 h daily) abolished the decreases in metabolic functional parameters.	Desipramine	180-191	sphingomyelin phosphodiesterase 1	Homo sapiens	171-174
31788096-11	2019	Treatment with Desi inhibited the activation of insulin-like growth factor-1 receptor and inhibited the activation of proteins in the PI3K/Akt signaling pathway.	Desipramine	15-19	insulin like growth factor 1 receptor	Homo sapiens	48-85
31442583-7	2019	CD spectroscopic analysis of protein stability allowed identifying CHS and POPX as stabilizing components, which increased hSERT thermostability by 7  C. The kinetic dissociation constant KD of 2.8 muM (+-0.05) for of the inhibitor Desipramine was determined with a ka of 10,848 M - 1 s-1 (+-220) and a kd of 0.03 s-1 (+-4.7 x 10-5).	Desipramine	232-243	solute carrier family 6 member 4	Homo sapiens	123-128
31090092-6	2019	The predicted versus observed geometric mean ratio (GMR) of AUCinf for CYP2D6 substrates desipramine and metoprolol coadministered with mirabegron 100 or 160 mg once daily were 3.47 versus 3.41 and 2.97 versus 3.29, respectively, indicating that the mirabegron model can be used to predict clinical CYP2D6 inhibition.	Desipramine	89-100	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	299-305
31624238-9	2019	DMI treatment restored the mRNA expression of AVP in the SCN and enhanced GR-mediated signaling by upregulating GR expression and nuclear translocation in the hippocampus.	Desipramine	0-3	arginine vasopressin	Mus musculus	46-49
31090092-4	2019	Models predicted and verified mirabegron and desipramine (CYP2D6 substrate) and 5-HMT and ketoconazole (strong CYP3A inhibitor) DDIs.	Desipramine	45-56	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	58-64
31624238-9	2019	DMI treatment restored the mRNA expression of AVP in the SCN and enhanced GR-mediated signaling by upregulating GR expression and nuclear translocation in the hippocampus.	Desipramine	0-3	nuclear receptor subfamily 3, group C, member 1	Mus musculus	74-76
31624238-9	2019	DMI treatment restored the mRNA expression of AVP in the SCN and enhanced GR-mediated signaling by upregulating GR expression and nuclear translocation in the hippocampus.	Desipramine	0-3	nuclear receptor subfamily 3, group C, member 1	Mus musculus	112-114
31624238-11	2019	Taken together, our data indicate that DMI treatment enhances GR-mediated signaling and restores the synchronization of peripheral clocks with the SCN and support the hypothesis that altered circadian entrainment is a modifiable risk factor for depression.	Desipramine	39-42	nuclear receptor subfamily 3, group C, member 1	Mus musculus	62-64
30550872-3	2019	RAW 264.7 cells were pretreated with desipramine, an ASM inhibitor, prior to LPS challenge in vitro.	Desipramine	37-48	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	53-56
30546074-5	2019	The neutral SMase inhibitor GW4869 as well as the genetic inhibition of nSMase with small interfering RNA (siRNA) against sphingomyelin phosphodiesterase 3 (SMPD3) prevented the inhibition by TNFalpha, but not the acid SMase inhibitor desipramine.	Desipramine	235-246	sphingomyelin phosphodiesterase 2	Homo sapiens	72-78
30546074-5	2019	The neutral SMase inhibitor GW4869 as well as the genetic inhibition of nSMase with small interfering RNA (siRNA) against sphingomyelin phosphodiesterase 3 (SMPD3) prevented the inhibition by TNFalpha, but not the acid SMase inhibitor desipramine.	Desipramine	235-246	sphingomyelin phosphodiesterase 3	Homo sapiens	157-162
30985942-7	2019	The PBPK model predicted that the AUC for mirabegron with itraconazole (a CYP3A4 inhibitor) was 4.12-times that in healthy elderly subjects administered mirabegron alone, and predicted that the proportional change in AUC for desipramine (a CYP2D6 substrate) with mirabegron was greater than that in healthy subjects.	Desipramine	225-236	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	74-80
30985942-7	2019	The PBPK model predicted that the AUC for mirabegron with itraconazole (a CYP3A4 inhibitor) was 4.12-times that in healthy elderly subjects administered mirabegron alone, and predicted that the proportional change in AUC for desipramine (a CYP2D6 substrate) with mirabegron was greater than that in healthy subjects.	Desipramine	225-236	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	240-246
30689930-5	2019	Calm heifers (mean REV minus 1 SD) had 4% greater (P &lt; 0.001) initial BW, 12% greater (P &lt; 0.001) ADG, 8% greater (P &lt; 0.001) DMI, and 4% greater (P &lt; 0.02) G:F than heifers with excitable temperaments (mean REV plus 1 SD).	Desipramine	135-138	synaptosome associated protein 91	Homo sapiens	0-4
30728250-7	2019	5-HT elicited concentration-dependent contractions of the CE duct (pEC50 = 6.5 +- 0.1) that were potentiated with high potency by the norepinephrine transporter (NET) inhibitor desipramine and with low potency by the highly selective serotonin transporter inhibitor paroxetine, indicating that the NET is the major mediator of 5-HT reuptake in vitro.	Desipramine	177-188	solute carrier family 6 member 2	Rattus norvegicus	134-160
30728250-7	2019	5-HT elicited concentration-dependent contractions of the CE duct (pEC50 = 6.5 +- 0.1) that were potentiated with high potency by the norepinephrine transporter (NET) inhibitor desipramine and with low potency by the highly selective serotonin transporter inhibitor paroxetine, indicating that the NET is the major mediator of 5-HT reuptake in vitro.	Desipramine	177-188	solute carrier family 6 member 2	Rattus norvegicus	162-165
31262782-6	2019	Treatment of mice with pharmacological inhibitors of acid sphingomyelinase (ASMase), desipramine and imipramine, attenuated ATP-induced TF decryption.	Desipramine	85-96	coagulation factor III	Mus musculus	136-138
30910852-2	2019	Here, we show that elevated aSMase activity and ceramide content were reduced by desipramine treatment in diabetic animals.	Desipramine	81-92	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	28-34
30910852-3	2019	The inhibitor of aSMase, desipramine, improved vascular dysfunction in db/db mice.	Desipramine	25-36	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	17-23
30910852-4	2019	High glucose (HG)-induced up-regulation of aSMase activity and ceramide levels were restored by treatment with aSMase siRNA or desipramine in endothelial cells.	Desipramine	127-138	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	43-49
30910852-5	2019	In addition, aSMase siRNA or desipramine treatment increased the release of nitric oxide (NO) and the phosphorylation of endothelial NO synthase (eNOS) in diabetic mouse aortas and aortic endothelial cells with HG.These results indicate that inhibition of aSMase/ceramide pathway improves endothelium-dependent vascular relaxation (EDR) largely through regulating the eNOS/NO pathway in diabetic animals.	Desipramine	29-40	nitric oxide synthase 3, endothelial cell	Mus musculus	121-144
30910852-5	2019	In addition, aSMase siRNA or desipramine treatment increased the release of nitric oxide (NO) and the phosphorylation of endothelial NO synthase (eNOS) in diabetic mouse aortas and aortic endothelial cells with HG.These results indicate that inhibition of aSMase/ceramide pathway improves endothelium-dependent vascular relaxation (EDR) largely through regulating the eNOS/NO pathway in diabetic animals.	Desipramine	29-40	nitric oxide synthase 3, endothelial cell	Mus musculus	146-150
30910852-5	2019	In addition, aSMase siRNA or desipramine treatment increased the release of nitric oxide (NO) and the phosphorylation of endothelial NO synthase (eNOS) in diabetic mouse aortas and aortic endothelial cells with HG.These results indicate that inhibition of aSMase/ceramide pathway improves endothelium-dependent vascular relaxation (EDR) largely through regulating the eNOS/NO pathway in diabetic animals.	Desipramine	29-40	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	256-262
30910852-5	2019	In addition, aSMase siRNA or desipramine treatment increased the release of nitric oxide (NO) and the phosphorylation of endothelial NO synthase (eNOS) in diabetic mouse aortas and aortic endothelial cells with HG.These results indicate that inhibition of aSMase/ceramide pathway improves endothelium-dependent vascular relaxation (EDR) largely through regulating the eNOS/NO pathway in diabetic animals.	Desipramine	29-40	nitric oxide synthase 3, endothelial cell	Mus musculus	368-372
30550872-5	2019	Conversely, inhibition of ASM activity by desipramine diminished LPS induced ASM activities and TNF production of RAW 264.7 cells.	Desipramine	42-53	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	26-29
30550872-5	2019	Conversely, inhibition of ASM activity by desipramine diminished LPS induced ASM activities and TNF production of RAW 264.7 cells.	Desipramine	42-53	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	77-80
30550872-8	2019	Desipramine administration overrode ASM activities in colon, and ameliorated DSS-induced colitis evidenced with the reduced disease activities and the decreased cytokine levels.	Desipramine	0-11	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	36-39
30284474-4	2018	The Dmi group was gavaged with the p38 MAPK inhibitor SB203580 for 9 weeks, and the effects on beta cell dysfunction and apoptosis were investigated.	Desipramine	4-7	mitogen-activated protein kinase 14	Mus musculus	35-43
30326559-11	2018	Since we were also able to show that the functional inhibitor of SMPD1, desipramine, ameliorates downregulation of CYP mRNA expression and activities in the acute phase of sepsis in wild-type mice, SMPD1 might be an interesting pharmacological target, which should be further investigated.	Desipramine	72-83	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	65-70
30326559-11	2018	Since we were also able to show that the functional inhibitor of SMPD1, desipramine, ameliorates downregulation of CYP mRNA expression and activities in the acute phase of sepsis in wild-type mice, SMPD1 might be an interesting pharmacological target, which should be further investigated.	Desipramine	72-83	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	115-118
30326559-11	2018	Since we were also able to show that the functional inhibitor of SMPD1, desipramine, ameliorates downregulation of CYP mRNA expression and activities in the acute phase of sepsis in wild-type mice, SMPD1 might be an interesting pharmacological target, which should be further investigated.	Desipramine	72-83	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	198-203
29758252-8	2018	In contrast, selective noradrenaline reuptake inhibitor desipramine had a significant effect on RGS8tg in the FST.	Desipramine	56-67	regulator of G-protein signaling 8	Mus musculus	96-100
30126999-6	2018	The antidepressant desipramine, which decreases ceramide levels by inhibiting acid sphingomyelinase, corrects EE defects in the RPE of Abca4-/- mice.	Desipramine	19-30	ATP-binding cassette, sub-family A (ABC1), member 4	Mus musculus	135-140
29068103-2	2018	The level of LC3-II was elevated and that of p62 was reduced in desipramine-treated L929 cells, indicating the induction of autophagy by desipramine.	Desipramine	64-75	nucleoporin 62	Mus musculus	45-48
29496989-6	2018	Results: The half-maximal inhibitory concentrations of desipramine, escitalopram, venlafaxine, and bupropion on 131I-MIBG cellular uptake were 11.9 nM, 7.5 muM, 4.92 muM, and 12.9 muM, respectively.	Desipramine	55-66	latexin	Homo sapiens	156-159
29496989-6	2018	Results: The half-maximal inhibitory concentrations of desipramine, escitalopram, venlafaxine, and bupropion on 131I-MIBG cellular uptake were 11.9 nM, 7.5 muM, 4.92 muM, and 12.9 muM, respectively.	Desipramine	55-66	latexin	Homo sapiens	166-169
29496989-6	2018	Results: The half-maximal inhibitory concentrations of desipramine, escitalopram, venlafaxine, and bupropion on 131I-MIBG cellular uptake were 11.9 nM, 7.5 muM, 4.92 muM, and 12.9 muM, respectively.	Desipramine	55-66	latexin	Homo sapiens	166-169
29401225-17	2018	It will be most effective if ADG over the period coinciding with intake recording and ADG over a much longer period of time are simultaneously included in a multiple-trait genetic evaluation with DMI and used in a selection index for efficiency.	Desipramine	196-199	ADG	Bos taurus	29-32
29068103-2	2018	The level of LC3-II was elevated and that of p62 was reduced in desipramine-treated L929 cells, indicating the induction of autophagy by desipramine.	Desipramine	137-148	nucleoporin 62	Mus musculus	45-48
29068103-5	2018	Furthermore, desipramine-induced vacuolization was observed in autophagy-deficient Atg7-/- mouse embryonic fibroblasts (MEFs) as well as wild-type Atg7+/+ MEFs.	Desipramine	13-24	autophagy related 7	Mus musculus	83-87
29068103-5	2018	Furthermore, desipramine-induced vacuolization was observed in autophagy-deficient Atg7-/- mouse embryonic fibroblasts (MEFs) as well as wild-type Atg7+/+ MEFs.	Desipramine	13-24	autophagy related 7	Mus musculus	147-151
29414147-5	2018	RESULTS: In SH-SY5Y cells, [3H]-dopamine uptake was inhibited by desipramine (selective NET inhibitor), GBR-12909 (selective DAT inhibitor), and fluoxetine (selective inhibitor of the serotonin transporter, SERT) with IC50 values 37, 537, and 2800nM, respectively.	Desipramine	65-76	solute carrier family 6 member 4	Homo sapiens	207-211
28359918-9	2017	Chronic administration of desipramine, fluoxetine, or tianeptine increased the BDNF mRNA expression and protein levels in the LPS-injected stressed rats.	Desipramine	26-37	brain-derived neurotrophic factor	Rattus norvegicus	79-83
29038231-4	2018	For static and dynamic predictions, midazolam, repaglinide, and desipramine were used as probe substrates for CYP3A4/5, CYP2C8, and CYP2D6, respectively.	Desipramine	64-75	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	110-116
28955042-5	2017	Strikingly, similar to heterozygote expression of SMPD1, either preventative (p-smpd1+/+) or therapeutic (t-smpd1+/+) pharmacological treatment strategies with desipramine - a functional inhibitor of acid sphingomyelinase (FIASMA) - significantly improved liver function and survival.	Desipramine	160-171	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	200-221
29468173-2	2018	Desipramine, a noradrenaline reuptake inhibitor, reduced the number of apneas in Mecp2-deficient mice, a model of RTT.	Desipramine	0-11	methyl CpG binding protein 2	Mus musculus	81-86
28842312-8	2017	Moreover, desipramine treatment was able to reduce the oxidative damage to rat liver, and to increase the expression of telomerase reverse transcriptase (TERT), leading to correspondingly restored telomerase activity.	Desipramine	10-21	telomerase reverse transcriptase	Rattus norvegicus	120-152
28842312-8	2017	Moreover, desipramine treatment was able to reduce the oxidative damage to rat liver, and to increase the expression of telomerase reverse transcriptase (TERT), leading to correspondingly restored telomerase activity.	Desipramine	10-21	telomerase reverse transcriptase	Rattus norvegicus	154-158
28675459-10	2017	The combination of desipramine and G-CSF is safe and signals improved mobilization over G-CSF alone, providing a possible alternative means of mobilization that needs further investigation.	Desipramine	19-30	colony stimulating factor 3	Homo sapiens	88-93
29169412-8	2017	Accordingly, Cer content was increase in MCF-7 cells treated by TNF-alpha, which was blocked by the pretreatment of ASM inhibitor Des.	Desipramine	130-133	tumor necrosis factor	Homo sapiens	64-73
29169412-8	2017	Accordingly, Cer content was increase in MCF-7 cells treated by TNF-alpha, which was blocked by the pretreatment of ASM inhibitor Des.	Desipramine	130-133	sphingomyelin phosphodiesterase 1	Homo sapiens	116-119
29169412-10	2017	Des and DMS could respectively reverse the TNF-alpha-induced decrease and increase of proliferation in MCF-7 and MDA-MB-231 cells.	Desipramine	0-3	tumor necrosis factor	Homo sapiens	43-52
28627696-6	2017	In addition, desipramine activated MAPKs (ERK 1/2, JNK, and p38) and increased intracellular Ca2+ levels.	Desipramine	13-24	mitogen-activated protein kinase 3	Homo sapiens	42-49
28627696-6	2017	In addition, desipramine activated MAPKs (ERK 1/2, JNK, and p38) and increased intracellular Ca2+ levels.	Desipramine	13-24	mitogen-activated protein kinase 8	Homo sapiens	51-54
28627696-6	2017	In addition, desipramine activated MAPKs (ERK 1/2, JNK, and p38) and increased intracellular Ca2+ levels.	Desipramine	13-24	mitogen-activated protein kinase 1	Homo sapiens	60-63
28627696-7	2017	Pro-apoptotic effects of desipramine were abolished after MAPK inhibitors (PD98059, SB203580, and SP600125) or N-acetyl-L-cysteine (NAC), as a ROS scavenger, treatments.	Desipramine	25-36	mitogen-activated protein kinase 3	Homo sapiens	58-62
28627696-7	2017	Pro-apoptotic effects of desipramine were abolished after MAPK inhibitors (PD98059, SB203580, and SP600125) or N-acetyl-L-cysteine (NAC), as a ROS scavenger, treatments.	Desipramine	25-36	X-linked Kx blood group	Homo sapiens	132-135
28627696-8	2017	These findings suggest that desipramine shows anti-proliferative effects in Hep3B cells mediated by promotion of apoptosis, activation of MAPK signaling, and increase in intracellular Ca2+ levels.	Desipramine	28-39	mitogen-activated protein kinase 3	Homo sapiens	138-142
31994095-9	2017	Chronic administration of desipramine, fluoxetine, or tianeptine increased the BDNF mRNA expression and protein levels in the LPS-injected stressed rats.	Desipramine	26-37	brain-derived neurotrophic factor	Rattus norvegicus	79-83
27654664-12	2017	RESULTS: We show dose-dependent inhibition of [125 I]MIBG uptake by dexmedetomidine, but at several logs lower potency than the known NET inhibitor desipramine.	Desipramine	148-159	solute carrier family 6 member 2	Homo sapiens	134-137
28420138-8	2017	Furthermore, similar results in desipramine-pretreated SMPD1-/- littermates suggest an SMPD1-independent pathway.	Desipramine	32-43	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	55-60
28420138-8	2017	Furthermore, similar results in desipramine-pretreated SMPD1-/- littermates suggest an SMPD1-independent pathway.	Desipramine	32-43	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	87-92
27900470-0	2017	Influence of the selective antagonist of the NR2B subunit of the NMDA receptor, traxoprodil, on the antidepressant-like activity of desipramine, paroxetine, milnacipran, and bupropion in mice.	Desipramine	132-143	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	45-49
28520379-6	2012	Imipramine is primarily metabolized via CYP2C19 to active metabolites, including desipramine, also a tricyclic antidepressant.	Desipramine	81-92	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
28352358-5	2017	Then, the effect of 28-day daily treatment with desipramine (DMI; 10 mg/kg), fluoxetine (5 mg/kg) or tianeptine (10 mg/kg) on the number of copies of VEGF mRNA in the amygdala, hippocampus and hypothalamus, and on serum VEGF protein levels, of rats subjected to chronic stress was determined.	Desipramine	48-59	vascular endothelial growth factor A	Rattus norvegicus	150-154
28352358-11	2017	Furthermore, the results identified that the stress-induced increase in VEGF mRNA expression in the amygdala and hypothalamus was attenuated by long-term administration of DMI.	Desipramine	172-175	vascular endothelial growth factor A	Rattus norvegicus	72-76
28352358-13	2017	In conclusion, the current study suggests that under conditions of stress, VEGF serves a role in the mechanism of action of DMI, through modulating activity of the norepinephrine system.	Desipramine	124-127	vascular endothelial growth factor A	Rattus norvegicus	75-79
27831486-5	2017	We investigated the relation between antidepressant-like response to the TCA desipramine using the tail suspension test and saturation binding of [3H]nisoxetine to the norepinephrine transporter (NET), the primary target of desipramine, in juvenile (21 days postnatal [P21]), adolescent (P28), and adult (P90) wild-type (SERT+/+) mice.	Desipramine	77-88	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	196-199
27773824-8	2016	By contrast, cannabinoid CB1 and CB2 receptor antagonists partially attenuated the antinociceptive actions of desipramine in a manner that was restricted to the development phase of paclitaxel-induced neuropathic pain only.	Desipramine	110-121	cannabinoid receptor 1	Homo sapiens	25-28
27773824-8	2016	By contrast, cannabinoid CB1 and CB2 receptor antagonists partially attenuated the antinociceptive actions of desipramine in a manner that was restricted to the development phase of paclitaxel-induced neuropathic pain only.	Desipramine	110-121	cannabinoid receptor 2	Homo sapiens	33-36
27773824-10	2016	Notably, desipramine (1nM-1muM) alone did not alter tumor cell viability and did not prevent the cytotoxic effects of paclitaxel under identical conditions.	Desipramine	9-20	latexin	Homo sapiens	27-30
27571014-12	2016	The ischemia-induced increase in retinal TNF-alpha levels was suppressed by the administration of the ASMase inhibitor desipramine, or by reducing ASMase expression.	Desipramine	119-130	tumor necrosis factor	Mus musculus	41-50
27799387-5	2016	AHI was quantified off CPAP.Desipramine reduced active Pcrit (median (interquartile range) -5.2 (4.3) cmH2O on desipramine versus -1.9 (2.7) cmH2O on placebo; p=0.049) but not passive Pcrit (-2.2 (3.4) versus -0.7 (2.1) cmH2O; p=0.135).	Desipramine	28-39	troponin T2, cardiac type	Homo sapiens	102-106
27799387-5	2016	AHI was quantified off CPAP.Desipramine reduced active Pcrit (median (interquartile range) -5.2 (4.3) cmH2O on desipramine versus -1.9 (2.7) cmH2O on placebo; p=0.049) but not passive Pcrit (-2.2 (3.4) versus -0.7 (2.1) cmH2O; p=0.135).	Desipramine	28-39	troponin T2, cardiac type	Homo sapiens	141-145
26923251-9	2016	ASM was inhibited by siRNA or desipramine (DES), and/or ceramide was degraded by recombinant acid ceramidase (AC).	Desipramine	30-41	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
26923251-9	2016	ASM was inhibited by siRNA or desipramine (DES), and/or ceramide was degraded by recombinant acid ceramidase (AC).	Desipramine	43-46	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
27341515-9	2016	Hydrolysis of sphingomyelin, clustering of receptor complexes, such as the CD95L/Fas-receptor, as well as formation of ceramide enriched macrodomains was abrogated using functional inhibitors (desipramine and NB6).	Desipramine	193-204	Fas ligand	Homo sapiens	75-80
27341515-10	2016	Strikingly, the stimulation of HMECs with serum obtained from sepsis patients or mixture of proinflammatory cytokines resulted in cytotoxicity and ADAMTS13 downregulation which was abrogated using desipramine, amino bisphosphonates and genetic inhibitors.	Desipramine	197-208	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	147-155
27831486-5	2017	We investigated the relation between antidepressant-like response to the TCA desipramine using the tail suspension test and saturation binding of [3H]nisoxetine to the norepinephrine transporter (NET), the primary target of desipramine, in juvenile (21 days postnatal [P21]), adolescent (P28), and adult (P90) wild-type (SERT+/+) mice.	Desipramine	224-235	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	168-194
27831486-5	2017	We investigated the relation between antidepressant-like response to the TCA desipramine using the tail suspension test and saturation binding of [3H]nisoxetine to the norepinephrine transporter (NET), the primary target of desipramine, in juvenile (21 days postnatal [P21]), adolescent (P28), and adult (P90) wild-type (SERT+/+) mice.	Desipramine	224-235	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	196-199
27831486-7	2017	The potency and maximal antidepressant-like effect of desipramine was greater in P21 mice than in P90 mice and was SERT genotype independent.	Desipramine	54-65	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	81-84
27831486-7	2017	The potency and maximal antidepressant-like effect of desipramine was greater in P21 mice than in P90 mice and was SERT genotype independent.	Desipramine	54-65	transferrin receptor	Mus musculus	98-101
27831486-7	2017	The potency and maximal antidepressant-like effect of desipramine was greater in P21 mice than in P90 mice and was SERT genotype independent.	Desipramine	54-65	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	115-119
27831486-10	2017	These data show age-dependent shifts for desipramine to produce antidepressant-like effects that correlate with NET expression in the locus coeruleus and suggest that drugs with NET-blocking activity may be an effective alternative to SSRIs in juveniles.	Desipramine	41-52	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	112-115
27831486-10	2017	These data show age-dependent shifts for desipramine to produce antidepressant-like effects that correlate with NET expression in the locus coeruleus and suggest that drugs with NET-blocking activity may be an effective alternative to SSRIs in juveniles.	Desipramine	41-52	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	178-181
27440861-3	2016	Imipramine undergoes N-demethylation to form the active metabolite desipramine, and both imipramine and desipramine are converted to hydroxylated metabolites by the polymorphic enzyme CYP2D6.	Desipramine	67-78	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	184-190
27440861-3	2016	Imipramine undergoes N-demethylation to form the active metabolite desipramine, and both imipramine and desipramine are converted to hydroxylated metabolites by the polymorphic enzyme CYP2D6.	Desipramine	104-115	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	184-190
27440861-4	2016	The objective of the present study is to determine whether the human pharmacokinetics of desipramine following dosing of imipramine can be predicted using static and dynamic physiologically-based pharmacokinetic (PBPK) models from in vitro input data for CYP2D6 extensive metabolizer (EM) and poor metabolizer (PM) populations.	Desipramine	89-100	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	255-261
27440861-9	2016	Moreover, the PBPK model was able to recover simultaneously plasma profiles of imipramine and desipramine in populations with different phenotypes of CYP2D6.	Desipramine	94-105	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	150-156
27571014-12	2016	The ischemia-induced increase in retinal TNF-alpha levels was suppressed by the administration of the ASMase inhibitor desipramine, or by reducing ASMase expression.	Desipramine	119-130	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	102-108
27259485-10	2016	Chronic (14 days) desipramine and fluoxetine, but not phenelzine, increased p-FADD (up to 59 %), p-FADD/FADD ratio (up to 1.8-fold), and pro-survival p-PEA-15 (up to 46 %) in rat brain cortex.	Desipramine	18-29	proliferation and apoptosis adaptor protein 15	Rattus norvegicus	152-158
26970016-5	2016	In this study, we similarly show that Crtc1(-/-) mice are resistant to the antidepressant effect of chronic desipramine in a behavioral despair paradigm.	Desipramine	108-119	CREB regulated transcription coactivator 1	Mus musculus	38-43
26785076-9	2016	The co-administration of DMI with the Src inhibitor SU6656, which blocks EphA4 forward signalling, could partially reverse the LTP attenuation, further supporting the targeting of the ephrinA3/EphA4 pathway by DMI.	Desipramine	210-213	ephrin A3	Homo sapiens	184-192
27338163-0	2016	Desipramine improves depression-like behavior and working memory by up-regulating p-CREB in Alzheimer"s disease associated mice.	Desipramine	0-11	cAMP responsive element binding protein 1	Mus musculus	84-88
27338163-8	2016	The neuroprotection of desipramine may be involved in the up-regulation of p-CREB level in the hippocampus of mice.	Desipramine	23-34	cAMP responsive element binding protein 1	Mus musculus	77-81
26785076-0	2016	Desipramine targets astrocytes to attenuate synaptic plasticity via modulation of the ephrinA3/EphA4 signalling.	Desipramine	0-11	ephrin A3	Homo sapiens	86-94
26785076-9	2016	The co-administration of DMI with the Src inhibitor SU6656, which blocks EphA4 forward signalling, could partially reverse the LTP attenuation, further supporting the targeting of the ephrinA3/EphA4 pathway by DMI.	Desipramine	210-213	EPH receptor A4	Homo sapiens	193-198
26785076-0	2016	Desipramine targets astrocytes to attenuate synaptic plasticity via modulation of the ephrinA3/EphA4 signalling.	Desipramine	0-11	EPH receptor A4	Homo sapiens	95-100
26785076-8	2016	DMI enhanced EphA4 clustering, which favoured an increased ephrinA3-mediated EphA4 phosphorylation and elevated EphA4 forward signalling.	Desipramine	0-3	EPH receptor A4	Homo sapiens	13-18
26785076-8	2016	DMI enhanced EphA4 clustering, which favoured an increased ephrinA3-mediated EphA4 phosphorylation and elevated EphA4 forward signalling.	Desipramine	0-3	ephrin A3	Homo sapiens	59-67
26785076-8	2016	DMI enhanced EphA4 clustering, which favoured an increased ephrinA3-mediated EphA4 phosphorylation and elevated EphA4 forward signalling.	Desipramine	0-3	EPH receptor A4	Homo sapiens	77-82
26785076-8	2016	DMI enhanced EphA4 clustering, which favoured an increased ephrinA3-mediated EphA4 phosphorylation and elevated EphA4 forward signalling.	Desipramine	0-3	EPH receptor A4	Homo sapiens	77-82
26785076-9	2016	The co-administration of DMI with the Src inhibitor SU6656, which blocks EphA4 forward signalling, could partially reverse the LTP attenuation, further supporting the targeting of the ephrinA3/EphA4 pathway by DMI.	Desipramine	25-28	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	38-41
26785076-9	2016	The co-administration of DMI with the Src inhibitor SU6656, which blocks EphA4 forward signalling, could partially reverse the LTP attenuation, further supporting the targeting of the ephrinA3/EphA4 pathway by DMI.	Desipramine	25-28	EPH receptor A4	Homo sapiens	73-78
26785076-9	2016	The co-administration of DMI with the Src inhibitor SU6656, which blocks EphA4 forward signalling, could partially reverse the LTP attenuation, further supporting the targeting of the ephrinA3/EphA4 pathway by DMI.	Desipramine	25-28	ephrin A3	Homo sapiens	184-192
26785076-9	2016	The co-administration of DMI with the Src inhibitor SU6656, which blocks EphA4 forward signalling, could partially reverse the LTP attenuation, further supporting the targeting of the ephrinA3/EphA4 pathway by DMI.	Desipramine	25-28	EPH receptor A4	Homo sapiens	193-198
26785076-9	2016	The co-administration of DMI with the Src inhibitor SU6656, which blocks EphA4 forward signalling, could partially reverse the LTP attenuation, further supporting the targeting of the ephrinA3/EphA4 pathway by DMI.	Desipramine	210-213	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	38-41
26777153-3	2016	METHODS: We used diethylpyrocarbonate (DEPC) to specifically modify His(18) and obtained mono-ethyloxyformylated hIAPP (DMI).	Desipramine	120-123	islet amyloid polypeptide	Homo sapiens	113-118
26937856-0	2016	Desipramine administered chronically inhibits lipopolysaccharide-stimulated production of IL-1beta in the brain and plasma of rats.	Desipramine	0-11	interleukin 1 beta	Rattus norvegicus	90-98
26937856-2	2016	The present study investigated for the first time the effect of 21-day oral administration of desipramine on the lipopolysaccharide (LPS)-stimulated IL-1beta concentration in the olfactory bulb, hypothalamus, frontal cortex, hippocampus and plasma of rats, and on the LPS-induced IL-1beta mRNA level in the olfactory bulb.	Desipramine	94-105	interleukin 1 beta	Rattus norvegicus	149-157
26937856-2	2016	The present study investigated for the first time the effect of 21-day oral administration of desipramine on the lipopolysaccharide (LPS)-stimulated IL-1beta concentration in the olfactory bulb, hypothalamus, frontal cortex, hippocampus and plasma of rats, and on the LPS-induced IL-1beta mRNA level in the olfactory bulb.	Desipramine	94-105	interleukin 1 beta	Rattus norvegicus	280-288
26937856-6	2016	By using the alpha1/alpha2-adrenoceptor antagonist prazosin and the unspecific beta-adrenoceptor antagonist propranolol given prior to LPS, we found that the effect of desipramine on LPS-induced IL-1beta production was partially mediated by both adrenoceptors in the olfactory bulb and plasma, and that beta-adrenoceptors contributed also to its effect on the stimulated IL-1beta concentration in the hypothalamus.	Desipramine	168-179	interleukin 1 beta	Rattus norvegicus	195-203
26785076-10	2016	Thus, our findings suggest a putative novel mechanism for DMI to modulate LTP through the regulation of the ephrinA3/EphA4 signalling pathway.	Desipramine	58-61	ephrin A3	Homo sapiens	108-116
26785076-10	2016	Thus, our findings suggest a putative novel mechanism for DMI to modulate LTP through the regulation of the ephrinA3/EphA4 signalling pathway.	Desipramine	58-61	EPH receptor A4	Homo sapiens	117-122
26785076-11	2016	A further exploration of the molecular and behavioral consequences of targeting ephrinA3/EphA4 might help to improve the clinical use of DMI.	Desipramine	137-140	ephrin A3	Homo sapiens	80-88
26785076-11	2016	A further exploration of the molecular and behavioral consequences of targeting ephrinA3/EphA4 might help to improve the clinical use of DMI.	Desipramine	137-140	EPH receptor A4	Homo sapiens	89-94
26452722-11	2016	Similarly, quinidine-mediated CYP2D6 inhibition reduced clearance of dextromethorphan and desipramine by 71 and 22%, respectively.	Desipramine	90-101	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	30-36
26809095-8	2016	Desipramine, a functional ASMase inhibitor, prevented RSV-induced ceramide increase.	Desipramine	0-11	sphingomyelin phosphodiesterase 1	Homo sapiens	26-32
26250357-8	2015	Desipramine was less potent in middle-aged SERT(+/+) and SERT(+/-) mice than in adult SERT(+/+) or SERT(+/-) mice.	Desipramine	0-11	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	43-47
26056032-6	2015	Previously defeated rats and controls were pre-treated with the norepinephrine transporter (NET) inhibitor desipramine (20 mg/kg, ip.)	Desipramine	107-118	solute carrier family 6 member 2	Rattus norvegicus	64-90
26453893-9	2015	And desipramine significantly decreased AO fluorescence intensity and the expression of the p53 protein and gene.	Desipramine	4-15	tumor protein p53	Homo sapiens	92-95
26305935-3	2015	Prevention of RGS9-2 action in the NAc increases the efficacy of the TCA desipramine and dramatically accelerates its onset of action.	Desipramine	73-84	regulator of G-protein signaling 9	Mus musculus	14-20
26250357-8	2015	Desipramine was less potent in middle-aged SERT(+/+) and SERT(+/-) mice than in adult SERT(+/+) or SERT(+/-) mice.	Desipramine	0-11	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	57-61
26250357-8	2015	Desipramine was less potent in middle-aged SERT(+/+) and SERT(+/-) mice than in adult SERT(+/+) or SERT(+/-) mice.	Desipramine	0-11	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	57-61
26250357-8	2015	Desipramine was less potent in middle-aged SERT(+/+) and SERT(+/-) mice than in adult SERT(+/+) or SERT(+/-) mice.	Desipramine	0-11	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	57-61
25639149-10	2015	We also found that desipramine inhibits the increase in membrane aquaporin-5 level triggered by carbachol and histamine treatments.	Desipramine	19-30	aquaporin 5	Homo sapiens	65-76
26135316-5	2015	The ASM inhibitor desipramine significantly reduced EGCG-induced cell death.	Desipramine	18-29	sphingomyelin phosphodiesterase 1	Homo sapiens	4-7
25873594-5	2015	We exemplify our approach by measuring the kinetics of cocaine, methylphenidate, and desipramine binding to SERT and DAT.	Desipramine	85-96	solute carrier family 6 member 4	Homo sapiens	108-112
25873594-5	2015	We exemplify our approach by measuring the kinetics of cocaine, methylphenidate, and desipramine binding to SERT and DAT.	Desipramine	85-96	solute carrier family 6 member 3	Homo sapiens	117-120
25873594-6	2015	Our analysis revealed that the selectivity of methylphenidate and desipramine for DAT and SERT, respectively, can be accounted for by their rate of association and not by the residence time in their respective binding sites.	Desipramine	66-77	solute carrier family 6 member 3	Homo sapiens	82-85
25873594-6	2015	Our analysis revealed that the selectivity of methylphenidate and desipramine for DAT and SERT, respectively, can be accounted for by their rate of association and not by the residence time in their respective binding sites.	Desipramine	66-77	solute carrier family 6 member 4	Homo sapiens	90-94
25840741-4	2015	The results showed that short- (3 days) or long-term (21 days) systemic treatment with the tricyclic ADs imipramine, clomipramine or desipramine increased BDNF levels in the DPAG.	Desipramine	133-144	brain-derived neurotrophic factor	Rattus norvegicus	155-159
25771452-6	2015	MMC and MDMA both induced concentration-dependently [(3)H]1-methyl-4-phenylpyridinium-release from NET-, DAT or SERT-expressing cells which was clearly transporter-mediated release as demonstrated by the selective inhibitory effects of nmolar to low micromolar concentrations of desipramine, GBR 12909 and fluoxetine, respectively.	Desipramine	279-290	solute carrier family 6 member 4	Homo sapiens	112-116
25903729-0	2015	Changes in blood CD4+T and CD8+T lymphocytes in stressed rats pretreated chronically with desipramine are more pronounced after chronic open field stress challenge.	Desipramine	90-101	Cd4 molecule	Rattus norvegicus	17-20
25637091-3	2015	Systemic injections of antidepressants: the tricyclic antidepressant desipramine (DMI), the selective serotonin reuptake inhibitor fluoxetine, and the NMDA-antagonist ketamine selectively increased cFos expression (a marker of neuronal activity) in the deep layers of the ventromedial PFC (vmPFC) in rats.	Desipramine	69-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-202
25637091-3	2015	Systemic injections of antidepressants: the tricyclic antidepressant desipramine (DMI), the selective serotonin reuptake inhibitor fluoxetine, and the NMDA-antagonist ketamine selectively increased cFos expression (a marker of neuronal activity) in the deep layers of the ventromedial PFC (vmPFC) in rats.	Desipramine	82-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-202
25639149-11	2015	CONCLUSIONS: These results imply that desipramine blocks muscarinic and histamine receptor-mediated Ca(2+) signaling and the subsequent translocation of aquaporin-5 in human salivary gland cells, suggesting a novel mechanism for the xerogenic effects of desipramine.	Desipramine	38-49	aquaporin 5	Homo sapiens	153-164
25639149-11	2015	CONCLUSIONS: These results imply that desipramine blocks muscarinic and histamine receptor-mediated Ca(2+) signaling and the subsequent translocation of aquaporin-5 in human salivary gland cells, suggesting a novel mechanism for the xerogenic effects of desipramine.	Desipramine	254-265	aquaporin 5	Homo sapiens	153-164
25855965-7	2015	Inhibition of ceramide accumulation in lysosomes using an ASM inhibitor, desipramine, decreased cytosolic activation of CTSB by inhibiting its transfer into cytosol from the lysosome.	Desipramine	73-84	H19 imprinted maternally expressed transcript	Homo sapiens	58-61
25855965-7	2015	Inhibition of ceramide accumulation in lysosomes using an ASM inhibitor, desipramine, decreased cytosolic activation of CTSB by inhibiting its transfer into cytosol from the lysosome.	Desipramine	73-84	cathepsin B	Homo sapiens	120-124
25451113-3	2015	Moreover, biochemical studies have revealed the up-regulation of other monoamine transporters (dopamine and serotonin) in the brains of NET-KO mice, similar to the phenomenon observed after the chronic pharmacological blockade of norepinephrine transporter by desipramine in wild-type (WT) animals.	Desipramine	260-271	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	230-256
25038868-0	2015	Effects of desipramine treatment on stress-induced up-regulation of norepinephrine transporter expression in rat brains.	Desipramine	11-22	solute carrier family 6 member 2	Rattus norvegicus	68-94
25296725-0	2015	Evaluation of the likelihood of a selective CHK1 inhibitor (LY2603618) to inhibit CYP2D6 with desipramine as a probe substrate in cancer patients.	Desipramine	94-105	checkpoint kinase 1	Homo sapiens	44-48
25296725-2	2015	The study described was to assess the potential interaction between LY2603618 and cytochrome P450 isoform 2D6 (CYP2D6) substrate desipramine in patients with cancer.	Desipramine	129-140	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	82-109
25296725-2	2015	The study described was to assess the potential interaction between LY2603618 and cytochrome P450 isoform 2D6 (CYP2D6) substrate desipramine in patients with cancer.	Desipramine	129-140	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	111-117
25038868-1	2015	RATIONALE: Many studies demonstrate down-regulation of the norepinephrine transporter (NET) by desipramine (DMI) in vitro and in stress-naive rats.	Desipramine	95-106	solute carrier family 6 member 2	Rattus norvegicus	59-85
25038868-1	2015	RATIONALE: Many studies demonstrate down-regulation of the norepinephrine transporter (NET) by desipramine (DMI) in vitro and in stress-naive rats.	Desipramine	108-111	solute carrier family 6 member 2	Rattus norvegicus	59-85
25463972-0	2014	Leptin receptor deficiency confers resistance to behavioral effects of fluoxetine and desipramine via separable substrates.	Desipramine	86-97	leptin	Mus musculus	0-6
25463972-5	2014	In this study, we determined the functional role of the leptin receptor (LepRb) in behavioral responses to the selective serotonergic antidepressant fluoxetine and the noradrenergic antidepressant desipramine.	Desipramine	197-208	leptin	Mus musculus	56-62
25463972-5	2014	In this study, we determined the functional role of the leptin receptor (LepRb) in behavioral responses to the selective serotonergic antidepressant fluoxetine and the noradrenergic antidepressant desipramine.	Desipramine	197-208	leptin receptor	Mus musculus	73-78
25463972-6	2014	While acute and chronic treatment with fluoxetine or desipramine in wild-type mice elicited antidepressant-like effects in the forced swim test, mice null for LepRb (db/db) displayed resistance to treatment with either fluoxetine or desipramine.	Desipramine	233-244	leptin receptor	Mus musculus	159-164
25463972-9	2014	Deletion of LepRb specifically from hippocampal and cortical neurons resulted in fluoxetine insensitivity in the forced swim test and tail suspension test while leaving the response to desipramine intact.	Desipramine	185-196	leptin receptor	Mus musculus	12-17
25463972-10	2014	These results suggest that functional LepRb is critically involved in regulating the antidepressant-like behavioral effects of both fluoxetine and desipramine.	Desipramine	147-158	leptin receptor	Mus musculus	38-43
25208966-0	2014	Norepinephrine transporter inhibition with desipramine exacerbates L-DOPA-induced dyskinesia: role for synaptic dopamine regulation in denervated nigrostriatal terminals.	Desipramine	43-54	solute carrier family 6 member 2	Rattus norvegicus	0-26
25414111-2	2014	Circulating ghrelin concentrations could potentially be used as a predictor of DMI in cattle.	Desipramine	79-82	ghrelin and obestatin prepropeptide	Bos taurus	12-19
25414111-3	2014	The objective of this experiment was to determine the association of circulating ghrelin concentrations with DMI and other production traits.	Desipramine	109-112	ghrelin and obestatin prepropeptide	Bos taurus	81-88
25414111-6	2014	Active ghrelin was not correlated to DMI (P=0.36), but when DMI was modeled using a multivariate analysis including plasma metabolites and sex, active ghrelin was shown to be positively associated with DMI (P&lt;0.01) and accounted for 6.2% of the variation accounted for by the regression model (R2=0.33).	Desipramine	60-63	ghrelin and obestatin prepropeptide	Bos taurus	151-158
25414111-6	2014	Active ghrelin was not correlated to DMI (P=0.36), but when DMI was modeled using a multivariate analysis including plasma metabolites and sex, active ghrelin was shown to be positively associated with DMI (P&lt;0.01) and accounted for 6.2% of the variation accounted for by the regression model (R2=0.33).	Desipramine	60-63	ghrelin and obestatin prepropeptide	Bos taurus	151-158
25414111-7	2014	Total ghrelin was negatively correlated to DMI (P&lt;0.01), but was not significant in a multivariate regression analysis (P=0.13).	Desipramine	43-46	ghrelin and obestatin prepropeptide	Bos taurus	6-13
25414111-8	2014	The ratio of active:total ghrelin was positively associated with DMI (P&lt;0.01) and accounted for 10.2% of the variation in the model (R2=0.35).	Desipramine	65-68	ghrelin and obestatin prepropeptide	Bos taurus	26-33
25414111-14	2014	Results indicated that ghrelin concentrations are associated with DMI in beef cattle and that there is genetic variation that leads to differences in the amount and form of circulating ghrelin which could contribute to variation observed in DMI of beef cattle.	Desipramine	66-69	ghrelin and obestatin prepropeptide	Bos taurus	23-30
25414111-14	2014	Results indicated that ghrelin concentrations are associated with DMI in beef cattle and that there is genetic variation that leads to differences in the amount and form of circulating ghrelin which could contribute to variation observed in DMI of beef cattle.	Desipramine	241-244	ghrelin and obestatin prepropeptide	Bos taurus	185-192
25373053-8	2014	Vasopressin alone was shown to be the most effective treatment in the management of desipramine overdose.	Desipramine	84-95	vasopressin	Sus scrofa	0-11
24576687-3	2014	METHODS: This study assessed the following: 1) brain reward function in rats (using the intracranial self-stimulation procedure) and protein levels of brain-derived neurotrophic factor and related signaling molecules in response to chronic social defeat, 2) brain reward function during social defeat and long-term treatment with the antidepressants fluoxetine (5 mg/kg/day) and desipramine (10 mg/kg/day), and 3) forced swim test behavior after social defeat and fluoxetine treatment.	Desipramine	379-390	brain-derived neurotrophic factor	Rattus norvegicus	151-184
25129807-4	2014	This increase in prodynorphin immunoreactivity in the dBNST and CeL was blocked by desipramine and citalopram treatments.	Desipramine	83-94	carboxyl ester lipase	Mus musculus	64-67
25048970-9	2014	GSH loss was associated with an increase in acid sphingomyelinase (ASMase) activity and lipid raft formation, which could be inhibited by the ASMase inhibitor desipramine.	Desipramine	159-170	sphingomyelin phosphodiesterase 1	Homo sapiens	44-65
25048970-9	2014	GSH loss was associated with an increase in acid sphingomyelinase (ASMase) activity and lipid raft formation, which could be inhibited by the ASMase inhibitor desipramine.	Desipramine	159-170	sphingomyelin phosphodiesterase 1	Homo sapiens	67-73
25048970-9	2014	GSH loss was associated with an increase in acid sphingomyelinase (ASMase) activity and lipid raft formation, which could be inhibited by the ASMase inhibitor desipramine.	Desipramine	159-170	sphingomyelin phosphodiesterase 1	Homo sapiens	142-148
25048970-10	2014	27OH-C and total lipids from LDL and oxLDL independently increased Abeta production by SH-SY5Y cells, and Abeta accumulation could be inhibited by desipramine and by N-acetylcysteine.	Desipramine	147-158	amyloid beta precursor protein	Homo sapiens	106-111
25129807-8	2014	These results suggest that regulation of prodynorphin in the dBNST and CeL before the test swim may be involved in the antidepressant-like effect of desipramine and citalopram in the FST and suggest that changes in pCREB immunoreactivity in these areas may not play an important role in the regulation of prodynorphin in the dBNST and CeA.	Desipramine	149-160	carboxyl ester lipase	Mus musculus	71-74
24880753-4	2014	Desipramine was selected as a model drug because it is mainly metabolized by CYP2D6, which is inhibited by almorexant in vitro.	Desipramine	0-11	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	77-83
24951586-5	2014	Moreover, treating cells with siRNA to ASM or with the indirect pharmacologic inhibitor desipramine resulted in significant inhibition of TNFalpha- and PMA-induced IL-6 production in MDA-MB-231 and HeLa cells.	Desipramine	88-99	tumor necrosis factor	Homo sapiens	138-146
24951586-5	2014	Moreover, treating cells with siRNA to ASM or with the indirect pharmacologic inhibitor desipramine resulted in significant inhibition of TNFalpha- and PMA-induced IL-6 production in MDA-MB-231 and HeLa cells.	Desipramine	88-99	interleukin 6	Homo sapiens	164-168
24951586-7	2014	Further, ASM knockdown or desipramine blunted p38 MAPK activation in response to TNFalpha, revealing a key role for ASM in activating p38, a signaling pathway known to regulate IL-6 induction.	Desipramine	26-37	mitogen-activated protein kinase 14	Homo sapiens	46-49
24951586-7	2014	Further, ASM knockdown or desipramine blunted p38 MAPK activation in response to TNFalpha, revealing a key role for ASM in activating p38, a signaling pathway known to regulate IL-6 induction.	Desipramine	26-37	tumor necrosis factor	Homo sapiens	81-89
25247592-8	2014	Serum levels of interleukin-1beta (IL-1beta) and IL-6 were elevated in the PTSD-like group compared with the control group, and were decreased by MPH, FLU, DES or the combination drug treatments, with the combination of DES+MPH producing the most complete rescue of the inflammatory response.	Desipramine	156-159	interleukin 1 beta	Rattus norvegicus	16-33
25247592-8	2014	Serum levels of interleukin-1beta (IL-1beta) and IL-6 were elevated in the PTSD-like group compared with the control group, and were decreased by MPH, FLU, DES or the combination drug treatments, with the combination of DES+MPH producing the most complete rescue of the inflammatory response.	Desipramine	156-159	interleukin 1 beta	Rattus norvegicus	35-43
25247592-8	2014	Serum levels of interleukin-1beta (IL-1beta) and IL-6 were elevated in the PTSD-like group compared with the control group, and were decreased by MPH, FLU, DES or the combination drug treatments, with the combination of DES+MPH producing the most complete rescue of the inflammatory response.	Desipramine	156-159	interleukin 6	Rattus norvegicus	49-53
25247592-8	2014	Serum levels of interleukin-1beta (IL-1beta) and IL-6 were elevated in the PTSD-like group compared with the control group, and were decreased by MPH, FLU, DES or the combination drug treatments, with the combination of DES+MPH producing the most complete rescue of the inflammatory response.	Desipramine	220-223	interleukin 1 beta	Rattus norvegicus	16-33
25247592-8	2014	Serum levels of interleukin-1beta (IL-1beta) and IL-6 were elevated in the PTSD-like group compared with the control group, and were decreased by MPH, FLU, DES or the combination drug treatments, with the combination of DES+MPH producing the most complete rescue of the inflammatory response.	Desipramine	220-223	interleukin 1 beta	Rattus norvegicus	35-43
25247592-8	2014	Serum levels of interleukin-1beta (IL-1beta) and IL-6 were elevated in the PTSD-like group compared with the control group, and were decreased by MPH, FLU, DES or the combination drug treatments, with the combination of DES+MPH producing the most complete rescue of the inflammatory response.	Desipramine	220-223	interleukin 6	Rattus norvegicus	49-53
24648162-1	2014	Proteasome modulator 9 (PSMD9) gene single nucleotide polymorphism (SNP) rs1043307/rs2514259 (E197G) is associated with significant clinical response to the anti-depressant desipramine.	Desipramine	173-184	proteasome 26S subunit, non-ATPase 9	Homo sapiens	0-22
24648162-1	2014	Proteasome modulator 9 (PSMD9) gene single nucleotide polymorphism (SNP) rs1043307/rs2514259 (E197G) is associated with significant clinical response to the anti-depressant desipramine.	Desipramine	173-184	proteasome 26S subunit, non-ATPase 9	Homo sapiens	24-29
25128275-3	2014	Our previous work established a particular TCA, desipramine, as an arrestin-biased alpha2AAR ligand driving receptor endocytosis and downregulation but not canonical heterotrimeric G protein-mediated signaling.	Desipramine	48-59	adrenoceptor alpha 2A	Homo sapiens	83-92
24657329-8	2014	Sertraline and desipramine tended to inhibit OCT2 activity via a competitive mechanism.	Desipramine	15-26	solute carrier family 22 member 2	Homo sapiens	45-49
24880753-7	2014	Almorexant increased the exposure to desipramine 3.7-fold, suggesting that almorexant is a moderate inhibitor of desipramine metabolism through inhibition of CYP2D6.	Desipramine	37-48	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	158-164
24880753-7	2014	Almorexant increased the exposure to desipramine 3.7-fold, suggesting that almorexant is a moderate inhibitor of desipramine metabolism through inhibition of CYP2D6.	Desipramine	113-124	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	158-164
24748481-6	2014	These results suggest common and distinct regulation of CART by desipramine and citalopram treatments in the FST and raise the possibility that CART in the AcbSh, dBNST, and CeA may be involved in antidepressant-like effect in the FST.	Desipramine	64-75	CART prepropeptide	Mus musculus	56-60
24742525-0	2014	The tricyclic antidepressant desipramine inhibited the neurotoxic, kainate-induced [Ca(2+)]i increases in CA1 pyramidal cells in acute hippocampal slices.	Desipramine	29-40	carbonic anhydrase 1	Rattus norvegicus	106-109
24742525-3	2014	We used [Ca(2+)]i imaging and patch clamp electrophysiology to decipher the mechanism of KA-evoked [Ca(2+)]i rise and its inhibition by the tricyclic antidepressant desipramine (DMI) in CA1 pyramidal cells in rat hippocampal slices and in cultured hippocampal cells.	Desipramine	165-176	carbonic anhydrase 1	Rattus norvegicus	186-189
24528439-0	2014	Acute desipramine restores presynaptic cortical defects in murine experimental autoimmune encephalomyelitis by suppressing central CCL5 overproduction.	Desipramine	6-17	chemokine (C-C motif) ligand 5	Mus musculus	131-135
24528439-11	2014	Acute, but not chronic, DMI reduced CCL5 levels in cortical homogenates of EAE mice at 13 d.p.i., but did not affect peripheral IL-17 and TNF-alpha contents or CCL5 plasma levels.	Desipramine	24-27	chemokine (C-C motif) ligand 5	Mus musculus	36-40
24528439-12	2014	Acute DMI caused a long-lasting restoration of glutamate exocytosis, restored endogenous cAMP production and impeded the shift from inhibition to facilitation of the CCL5-mediated control of glutamate exocytosis.	Desipramine	6-9	chemokine (C-C motif) ligand 5	Mus musculus	166-170
24663212-3	2014	Phenotypic RFI was calculated as actual DMI minus expected DMI.	Desipramine	40-43	RFI	Bos taurus	11-14
24663212-3	2014	Phenotypic RFI was calculated as actual DMI minus expected DMI.	Desipramine	59-62	RFI	Bos taurus	11-14
24663212-8	2014	Live weight and ADG were not correlated (P &gt; 0.05), and DMI was positively correlated (r = 0.80; P &lt; 0.001) with RFI.	Desipramine	59-62	RFI	Bos taurus	119-122
24748481-0	2014	Effect of desipramine and citalopram treatment on forced swimming test-induced changes in cocaine- and amphetamine-regulated transcript (CART) immunoreactivity in mice.	Desipramine	10-21	CART prepropeptide	Mus musculus	90-135
24748481-0	2014	Effect of desipramine and citalopram treatment on forced swimming test-induced changes in cocaine- and amphetamine-regulated transcript (CART) immunoreactivity in mice.	Desipramine	10-21	CART prepropeptide	Mus musculus	137-141
24748481-2	2014	To explore this possibility, we assessed the treatment effects of desipramine and citalopram, which inhibit the reuptake of norepinephrine and serotonin into the presynaptic terminals, respectively, on changes in levels of CART-IR before and after the test swim in mouse brain.	Desipramine	66-77	CART prepropeptide	Mus musculus	223-227
24748481-4	2014	This increase in CART-IR in the AcbSh, dBNST, and PVN before the test swim remained elevated by desipramine treatment after the test swim, but this increase in these brain areas returned to near control levels after test swim by citalopram treatment.	Desipramine	96-107	CART prepropeptide	Mus musculus	17-21
24461377-3	2014	Chronic desipramine pretreatment did not protect against OF stress-induced suppression of blood anti-tumor natural killer cell activity but increased plasma interleukin-10 and decreased interferon-gamma and corticosterone concentration.	Desipramine	8-19	interleukin 10	Rattus norvegicus	157-171
24461377-3	2014	Chronic desipramine pretreatment did not protect against OF stress-induced suppression of blood anti-tumor natural killer cell activity but increased plasma interleukin-10 and decreased interferon-gamma and corticosterone concentration.	Desipramine	8-19	interferon gamma	Rattus norvegicus	186-202
24132698-0	2014	Dexamethasone in the presence of desipramine enhances MAPK/ERK1/2 signaling possibly via its interference with beta-arrestin.	Desipramine	33-44	mitogen-activated protein kinase 3	Homo sapiens	59-65
24730055-0	2014	Chronic desipramine treatment rescues depression-related, social and cognitive deficits in Engrailed-2 knockout mice.	Desipramine	8-19	engrailed 2	Mus musculus	91-102
24730055-4	2014	This study evaluated the ability of chronic treatment with desipramine (DMI), a selective norepinephrine (NE) reuptake inhibitor and classical antidepressant, to reverse behavioral abnormalities in En2-/- mice.	Desipramine	59-70	engrailed 2	Mus musculus	198-201
24730055-4	2014	This study evaluated the ability of chronic treatment with desipramine (DMI), a selective norepinephrine (NE) reuptake inhibitor and classical antidepressant, to reverse behavioral abnormalities in En2-/- mice.	Desipramine	72-75	engrailed 2	Mus musculus	198-201
24730055-5	2014	Desipramine treatment significantly reduced immobility in the tail suspension and forced swim tests, restored sociability in the three-chambered social approach task and reversed impairments in contextual fear conditioning in En2-/- mice.	Desipramine	0-11	engrailed 2	Mus musculus	226-229
25562160-4	2014	The present study was designed to investigate effects of desipramine (DES), as an ASMase inhibitor, on Cr(VI)-induced hepatotoxicity.	Desipramine	57-68	sphingomyelin phosphodiesterase 1	Homo sapiens	82-88
25562160-4	2014	The present study was designed to investigate effects of desipramine (DES), as an ASMase inhibitor, on Cr(VI)-induced hepatotoxicity.	Desipramine	70-73	sphingomyelin phosphodiesterase 1	Homo sapiens	82-88
25562160-6	2014	Moreover, the study investigated the role of DES played in ASMase activities and ceramide levels.	Desipramine	45-48	sphingomyelin phosphodiesterase 1	Homo sapiens	59-65
25562160-9	2014	The results demonstrated that apoptosis rates, ASMase activities and ceramide content decreased in groups treated with the combination of DES and Cr(VI) compared to Cr(VI) groups.	Desipramine	138-141	sphingomyelin phosphodiesterase 1	Homo sapiens	47-53
24268836-12	2014	Milk production decreased on the 2 feather meal treatments, partly explained by a tendency for DMI to decrease.	Desipramine	95-98	Weaning weight-maternal milk	Bos taurus	0-4
24132698-3	2014	In the present study, we show that the glucocorticoid receptor (GR) agonist dexamethasone (DEX) increased MAPK/ERK1/2 signaling in the presence of the noradrenergic antidepressant, desipramine (DMI), while no such effect was induced by DEX or DMI alone in human neuroblastoma SH-SY5Y cells.	Desipramine	181-192	nuclear receptor subfamily 3 group C member 1	Homo sapiens	39-62
24132698-3	2014	In the present study, we show that the glucocorticoid receptor (GR) agonist dexamethasone (DEX) increased MAPK/ERK1/2 signaling in the presence of the noradrenergic antidepressant, desipramine (DMI), while no such effect was induced by DEX or DMI alone in human neuroblastoma SH-SY5Y cells.	Desipramine	181-192	nuclear receptor subfamily 3 group C member 1	Homo sapiens	64-66
24132698-3	2014	In the present study, we show that the glucocorticoid receptor (GR) agonist dexamethasone (DEX) increased MAPK/ERK1/2 signaling in the presence of the noradrenergic antidepressant, desipramine (DMI), while no such effect was induced by DEX or DMI alone in human neuroblastoma SH-SY5Y cells.	Desipramine	194-197	nuclear receptor subfamily 3 group C member 1	Homo sapiens	39-62
24132698-3	2014	In the present study, we show that the glucocorticoid receptor (GR) agonist dexamethasone (DEX) increased MAPK/ERK1/2 signaling in the presence of the noradrenergic antidepressant, desipramine (DMI), while no such effect was induced by DEX or DMI alone in human neuroblastoma SH-SY5Y cells.	Desipramine	194-197	nuclear receptor subfamily 3 group C member 1	Homo sapiens	64-66
24132698-3	2014	In the present study, we show that the glucocorticoid receptor (GR) agonist dexamethasone (DEX) increased MAPK/ERK1/2 signaling in the presence of the noradrenergic antidepressant, desipramine (DMI), while no such effect was induced by DEX or DMI alone in human neuroblastoma SH-SY5Y cells.	Desipramine	243-246	nuclear receptor subfamily 3 group C member 1	Homo sapiens	39-62
24132698-3	2014	In the present study, we show that the glucocorticoid receptor (GR) agonist dexamethasone (DEX) increased MAPK/ERK1/2 signaling in the presence of the noradrenergic antidepressant, desipramine (DMI), while no such effect was induced by DEX or DMI alone in human neuroblastoma SH-SY5Y cells.	Desipramine	243-246	nuclear receptor subfamily 3 group C member 1	Homo sapiens	64-66
24132698-10	2014	We suggest that such an interaction in the presence of DMI can enhance MAPK/ERK1/2 signaling, a key player in neural plasticity and neurogenesis processes, which is impaired in MDD, while stimulated by antidepressants.	Desipramine	55-58	mitogen-activated protein kinase 3	Homo sapiens	76-82
23906970-4	2013	Twenty four-hour incubation of cells with antidepressants (0.05-10 muM) and DEX (10 muM) showed that imipramine, amitriptyline, desipramine, citalopram and fluoxetine at concentrations from 0.1 up to 1 muM, reboxetine (0.1 muM) and tianeptine (0.05 muM) prevented the DEX-induced decreases in cell viability and proliferation rate.	Desipramine	128-139	latexin	Homo sapiens	67-70
23906970-4	2013	Twenty four-hour incubation of cells with antidepressants (0.05-10 muM) and DEX (10 muM) showed that imipramine, amitriptyline, desipramine, citalopram and fluoxetine at concentrations from 0.1 up to 1 muM, reboxetine (0.1 muM) and tianeptine (0.05 muM) prevented the DEX-induced decreases in cell viability and proliferation rate.	Desipramine	128-139	latexin	Homo sapiens	84-87
23906970-4	2013	Twenty four-hour incubation of cells with antidepressants (0.05-10 muM) and DEX (10 muM) showed that imipramine, amitriptyline, desipramine, citalopram and fluoxetine at concentrations from 0.1 up to 1 muM, reboxetine (0.1 muM) and tianeptine (0.05 muM) prevented the DEX-induced decreases in cell viability and proliferation rate.	Desipramine	128-139	latexin	Homo sapiens	84-87
23906970-4	2013	Twenty four-hour incubation of cells with antidepressants (0.05-10 muM) and DEX (10 muM) showed that imipramine, amitriptyline, desipramine, citalopram and fluoxetine at concentrations from 0.1 up to 1 muM, reboxetine (0.1 muM) and tianeptine (0.05 muM) prevented the DEX-induced decreases in cell viability and proliferation rate.	Desipramine	128-139	latexin	Homo sapiens	84-87
23906970-4	2013	Twenty four-hour incubation of cells with antidepressants (0.05-10 muM) and DEX (10 muM) showed that imipramine, amitriptyline, desipramine, citalopram and fluoxetine at concentrations from 0.1 up to 1 muM, reboxetine (0.1 muM) and tianeptine (0.05 muM) prevented the DEX-induced decreases in cell viability and proliferation rate.	Desipramine	128-139	latexin	Homo sapiens	84-87
23486447-3	2013	These drugs and their metabolites, along with desipramine and nortriptyline, undergo hydroxylation by CYP2D6 to less active metabolites.	Desipramine	46-57	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	102-108
23620084-5	2013	A significantly higher level of C/EBPalpha was measured at 48 h, but the levels of C/EBPbeta increased after 12 h. Levels of FABP4 significantly increased with the time of incubation after 12 h, but that of LPL was reduced (P &lt; 0.05) at 6, 24 and 48 h. FABP4 was highly expressed in cells treated with CS, DMI + CS and DMIOA + CS compared to cells treated with FBS, DMI + FBS and DMIOA + FBS.	Desipramine	309-312	fatty acid binding protein 4	Homo sapiens	125-130
23946692-0	2013	Changes in c-Fos Expression in the Forced Swimming Test: Common and Distinct Modulation in Rat Brain by Desipramine and Citalopram.	Desipramine	104-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
23946692-5	2013	Both desipramine and citalopram treatment after the pretest swim significantly increased the number of c-Fos-like immunoreactive cells in the ventral lateral septum and ventrolateral periaqueductal gray before the test swim.	Desipramine	5-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
23389997-7	2013	Furthermore, treatment with desipramine, an antidepressant with specific inhibitory effects on norepinephrine transport, prevented an increased dopamine beta-hydroxylase expression by chronic social defeat in the locus coeruleus and its main terminal regions such as the hippocampus, frontal cortex and amygdala.	Desipramine	28-39	dopamine beta-hydroxylase	Rattus norvegicus	144-169
24309563-7	2013	In DMI-treated mice, tumor VEGF, IL-6, and the prometastatic chemokines RANTES, M-CSF, and MIP-2 were reduced.	Desipramine	3-6	vascular endothelial growth factor A	Mus musculus	27-31
24309563-7	2013	In DMI-treated mice, tumor VEGF, IL-6, and the prometastatic chemokines RANTES, M-CSF, and MIP-2 were reduced.	Desipramine	3-6	interleukin 6	Mus musculus	33-37
24309563-7	2013	In DMI-treated mice, tumor VEGF, IL-6, and the prometastatic chemokines RANTES, M-CSF, and MIP-2 were reduced.	Desipramine	3-6	chemokine (C-C motif) ligand 5	Mus musculus	72-78
24309563-7	2013	In DMI-treated mice, tumor VEGF, IL-6, and the prometastatic chemokines RANTES, M-CSF, and MIP-2 were reduced.	Desipramine	3-6	colony stimulating factor 1 (macrophage)	Mus musculus	80-85
24309563-7	2013	In DMI-treated mice, tumor VEGF, IL-6, and the prometastatic chemokines RANTES, M-CSF, and MIP-2 were reduced.	Desipramine	3-6	chemokine (C-X-C motif) ligand 2	Mus musculus	91-96
24161357-0	2013	Chronic antidepressant desipramine treatment increases open field-induced brain expression and spleen production of interleukin 10 in rats.	Desipramine	23-34	interleukin 10	Rattus norvegicus	116-130
24161357-4	2013	In the desipramine pretreated groups, OF stress decreased spleen NKCC, behavioral activity, the Con A-stimulated splenocyte IFN-gamma response and plasma corticosterone concentration whereas it increased the brain and splenocyte IL-10 response.	Desipramine	7-18	interferon gamma	Rattus norvegicus	124-133
24161357-4	2013	In the desipramine pretreated groups, OF stress decreased spleen NKCC, behavioral activity, the Con A-stimulated splenocyte IFN-gamma response and plasma corticosterone concentration whereas it increased the brain and splenocyte IL-10 response.	Desipramine	7-18	interleukin 10	Rattus norvegicus	229-234
24406179-12	2013	CONCLUSION: TNF-alpha can induce DUOX-1 expression increasing in lipid raft, then the DUOX-1 can be activated to increase reactive oxygen species level; acidic sphingomyelinase inhibitor desipramine can inhibit this process, the results disclose that the process will depend on the ceramide of lipid raft.	Desipramine	187-198	tumor necrosis factor	Homo sapiens	12-21
24406179-12	2013	CONCLUSION: TNF-alpha can induce DUOX-1 expression increasing in lipid raft, then the DUOX-1 can be activated to increase reactive oxygen species level; acidic sphingomyelinase inhibitor desipramine can inhibit this process, the results disclose that the process will depend on the ceramide of lipid raft.	Desipramine	187-198	dual oxidase 1	Homo sapiens	33-39
24406179-12	2013	CONCLUSION: TNF-alpha can induce DUOX-1 expression increasing in lipid raft, then the DUOX-1 can be activated to increase reactive oxygen species level; acidic sphingomyelinase inhibitor desipramine can inhibit this process, the results disclose that the process will depend on the ceramide of lipid raft.	Desipramine	187-198	dual oxidase 1	Homo sapiens	86-92
23620084-5	2013	A significantly higher level of C/EBPalpha was measured at 48 h, but the levels of C/EBPbeta increased after 12 h. Levels of FABP4 significantly increased with the time of incubation after 12 h, but that of LPL was reduced (P &lt; 0.05) at 6, 24 and 48 h. FABP4 was highly expressed in cells treated with CS, DMI + CS and DMIOA + CS compared to cells treated with FBS, DMI + FBS and DMIOA + FBS.	Desipramine	322-325	fatty acid binding protein 4	Homo sapiens	125-130
23508024-7	2013	Substitution of the G allele of SNP rs42670353 was associated with ADG (0.043 +- 0.02 kg/d; P &lt; 0.01) and FCR (0.114 +- 0.05 kg BW gain kg(-1) DMI; P &lt; 0.05).	Desipramine	146-149	ADG	Bos taurus	67-70
23508024-7	2013	Substitution of the G allele of SNP rs42670353 was associated with ADG (0.043 +- 0.02 kg/d; P &lt; 0.01) and FCR (0.114 +- 0.05 kg BW gain kg(-1) DMI; P &lt; 0.05).	Desipramine	146-149	FCR	Bos taurus	109-112
22422821-6	2012	Whereas desipramine did not by itself elicit circulating HSPCs, it increased G-CSF-triggered mobilization efficiency significantly and rescued mobilization in a model mimicking "poor mobilizers."	Desipramine	8-19	peripheral blood stem cell response to granulocyte colony stimulating factor 1	Mus musculus	77-82
23582643-7	2013	Similarly, the cyclophilin D-inhibiting drug alisporivir and the acid sphingomyelinase-inactivating drug, desipramine, synergize to reverse susceptibility, suggesting the therapeutic potential of these orally active drugs against tuberculosis and possibly other TNF-mediated diseases.	Desipramine	106-117	tumor necrosis factor b (TNF superfamily, member 2)	Danio rerio	262-265
24399720-4	2013	RESULTS: The investigated antidepressant drugs added to control liver microsomes produced certain inhibitory effects on CYP2C11 activity, which were moderate (sertraline, nefazodone and clomipramine: Ki = 39, 56 and 66 muM, respectively), modest (fluoxetine and amitriptyline: Ki = 98 and 108 muM, respectively) or weak (imipramine and desipramine: Ki = 191 and 212 muM, respectively).	Desipramine	336-347	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	120-127
24399720-6	2013	One-day exposure of rats to the antidepressant drugs did not significantly change the activity of CYP2C11 in liver microsomes; however, imipramine, desipramine and fluoxetine showed a tendency to diminish the activity of CYP2C11.	Desipramine	148-159	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	221-228
24399720-7	2013	Of the antidepressants studied, only desipramine and fluoxetine administered chronically elevated CYP2C11 activity; those effects were positively correlated with the observed increases in the enzyme protein level.	Desipramine	37-48	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	98-105
22250926-3	2012	Therefore, the present study aimed to investigate the effect of P-gp inhibition on the transport of the tricyclic antidepressant imipramine and its active metabolite desipramine across the BBB.	Desipramine	166-177	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	64-68
23221858-1	2013	The results of two single-center, two-period, open-label trials that evaluated the effects of multiple doses of desvenlafaxine on the pharmacokinetics of desipramine, a cytochrome P450 (CYP) 2D6 enzyme substrate, are presented.	Desipramine	154-165	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	169-194
22934693-4	2013	Our previous study revealed that DMI at the clinical relevant concentrations could induce CHOP-dependent apoptotic death in C6 glioma cells.	Desipramine	33-36	DNA damage inducible transcript 3	Homo sapiens	90-94
22934693-6	2013	Treatment with DMI could induce autophagic cell death characterized by the formation of autophagosome and the elevated level of autophagic protein Beclin-1 and cellular redistribution of marker LC3.	Desipramine	15-18	beclin 1	Homo sapiens	147-155
22934693-7	2013	Meanwhile, DMI inhibited the activation of PI3K-AKT-mTOR pathway which is considered as a negative regulator of autophagy.	Desipramine	11-14	mechanistic target of rapamycin kinase	Homo sapiens	52-56
22934693-8	2013	Furthermore, DMI activated PERK-eIF2alpha and ATF6 of endoplasmic reticulum (ER) stress pathway, while knockdown of PERK with the PERK-specific short interfering RNA (siRNA) could obviously attenuate the autophagy.	Desipramine	13-16	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	27-31
22934693-8	2013	Furthermore, DMI activated PERK-eIF2alpha and ATF6 of endoplasmic reticulum (ER) stress pathway, while knockdown of PERK with the PERK-specific short interfering RNA (siRNA) could obviously attenuate the autophagy.	Desipramine	13-16	eukaryotic translation initiation factor 2A	Homo sapiens	32-41
22934693-8	2013	Furthermore, DMI activated PERK-eIF2alpha and ATF6 of endoplasmic reticulum (ER) stress pathway, while knockdown of PERK with the PERK-specific short interfering RNA (siRNA) could obviously attenuate the autophagy.	Desipramine	13-16	activating transcription factor 6	Homo sapiens	46-50
22934693-9	2013	The results strongly suggested that DMI could induce autophagy through the PERK-ER stress pathway in C6 glioma cells.	Desipramine	36-39	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	75-79
23527713-12	2013	Desipramine also suppressed the serum OVA-specific IgE and IL-4 levels, but had no effect on IFN-gamma level.	Desipramine	0-11	interleukin 4	Mus musculus	59-63
23527713-15	2013	These results suggest that the antidepressant drug, desipramine, also has anti-allergic action, which was possibly achieved by reducing allergen-specific IgE and Th2 cytokine production and maintaining a balance between Treg and Th17 cells.	Desipramine	52-63	heart and neural crest derivatives expressed 2	Mus musculus	162-165
22806583-6	2012	At their upper therapeutic plasma concentrations, several drugs are expected to inhibit by more than 20 % hOCT1 and could thus interfere with the pharmacokinetics of hOCT1-transported drugs in the kidney and liver, namely trimipramine, desipramine and fluoxetine (by about 37 %), levomepromazine and nefazodone (by about 32 %), and clozapine and amitriptyline (by about 22 %).	Desipramine	236-247	solute carrier family 22 member 1	Homo sapiens	106-111
22806583-6	2012	At their upper therapeutic plasma concentrations, several drugs are expected to inhibit by more than 20 % hOCT1 and could thus interfere with the pharmacokinetics of hOCT1-transported drugs in the kidney and liver, namely trimipramine, desipramine and fluoxetine (by about 37 %), levomepromazine and nefazodone (by about 32 %), and clozapine and amitriptyline (by about 22 %).	Desipramine	236-247	solute carrier family 22 member 1	Homo sapiens	166-171
22369787-0	2012	Noradrenergic antidepressant responses to desipramine in vivo are reciprocally regulated by arrestin3 and spinophilin.	Desipramine	42-53	protein phosphatase 1, regulatory subunit 9B	Mus musculus	106-117
22369787-7	2012	As well, mice deficient in arrestin3 lack antidepressant response to DMI, while spinophilin-null mice have enhanced antidepressant response to DMI compared with wild-type controls, indicating that this alpha(2A)AR-mediated response is reciprocally regulated by arrestin and spinophilin.	Desipramine	143-146	protein phosphatase 1, regulatory subunit 9B	Mus musculus	80-91
22369787-9	2012	Our results implicate arrestin- and spinophilin-mediated regulation of the alpha(2A)AR in the pharmacology of the noradrenergic antidepressant DMI, and suggest that manipulation of this mode of receptor regulation may represent a novel and viable therapeutic strategy.	Desipramine	143-146	protein phosphatase 1, regulatory subunit 9B	Mus musculus	36-47
22342816-7	2012	Additionally, desipramine had an IC(50) value of 0.7 muM for the uptake of NE by OCT3, while the IC(50) value of sertraline was 2.3 muM for 5-HT uptake.	Desipramine	14-25	OCTN3	Homo sapiens	81-85
22342816-8	2012	Both desipramine and sertraline appeared to inhibit OCT3 activity via a non-competitive mechanism.	Desipramine	5-16	OCTN3	Homo sapiens	52-56
22405824-0	2012	Desipramine selectively potentiates norepinephrine-elicited ERK1/2 activation through the alpha2A adrenergic receptor.	Desipramine	0-11	mitogen-activated protein kinase 3	Homo sapiens	60-66
22405824-0	2012	Desipramine selectively potentiates norepinephrine-elicited ERK1/2 activation through the alpha2A adrenergic receptor.	Desipramine	0-11	adrenoceptor alpha 2A	Homo sapiens	90-117
22405824-2	2012	We have recently identified the tricyclic antidepressant drug desipramine (DMI) as a direct ligand at the alpha(2A) adrenergic receptor (AR) without itself driving heterotrimeric G protein/downstream effector activation [5].	Desipramine	62-73	adrenoceptor alpha 2A	Homo sapiens	106-135
22405824-2	2012	We have recently identified the tricyclic antidepressant drug desipramine (DMI) as a direct ligand at the alpha(2A) adrenergic receptor (AR) without itself driving heterotrimeric G protein/downstream effector activation [5].	Desipramine	75-78	adrenoceptor alpha 2A	Homo sapiens	106-135
22405824-4	2012	DMI acted as a signaling potentiator, selectively enhancing NE-induced alpha(2A)AR-mediated ERK1/2 MAPK signaling.	Desipramine	0-3	mitogen-activated protein kinase 3	Homo sapiens	92-98
22405824-4	2012	DMI acted as a signaling potentiator, selectively enhancing NE-induced alpha(2A)AR-mediated ERK1/2 MAPK signaling.	Desipramine	0-3	mitogen-activated protein kinase 3	Homo sapiens	99-103
22405824-6	2012	DMI in a physiologically relevant ratio with NE effectively turned on ERK1/2 signaling that is lacking in response to physiological NE alone.	Desipramine	0-3	mitogen-activated protein kinase 3	Homo sapiens	70-76
22405824-7	2012	Further, the DMI-induced ERK1/2 potentiation relied on heterotrimeric G(i/o) proteins and was arrestin-independent.	Desipramine	13-16	mitogen-activated protein kinase 3	Homo sapiens	25-31
21976621-4	2012	The inhibition profiles of 20 known inhibitors of CYP2D6 were characterized in vitro against four clinically relevant CYP2D6 substrates (desipramine, dextromethorphan, metoprolol, and thioridazine) and bufuralol.	Desipramine	137-148	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	50-56
22442074-6	2012	Finally, the depressive-like behaviors in BDNF(+/Met) mice could be selectively rescued by acute administration of desipramine but not fluoxetine.	Desipramine	115-126	brain derived neurotrophic factor	Mus musculus	42-46
22442074-8	2012	Importantly, desipramine but not fluoxetine has antidepressant effects on BDNF(+/Met) mice, suggesting that specific classes of antidepressant may be a more effective treatment option for depressive symptoms in humans with this genetic variant BDNF.	Desipramine	13-24	brain derived neurotrophic factor	Mus musculus	74-78
22442074-8	2012	Importantly, desipramine but not fluoxetine has antidepressant effects on BDNF(+/Met) mice, suggesting that specific classes of antidepressant may be a more effective treatment option for depressive symptoms in humans with this genetic variant BDNF.	Desipramine	13-24	brain derived neurotrophic factor	Homo sapiens	244-248
22089316-12	2012	This study was registered with ClinicalTrials.gov, registration number NCT00338962 and URL: http://clinicaltrials.gov/ct2/show/NCT00338962?term=desipramine+AND+alcohol+dependence+AND+depression&amp;recr=Closed&amp;rank=1.	Desipramine	144-155	solute carrier family 6 member 10, pseudogene	Homo sapiens	118-121
21976621-9	2012	The in vivo sensitivities of the clinically relevant CYP2D6 substrates desipramine, dextromethorphan, and metoprolol were determined on the basis of literature drug-drug interaction (DDI) outcomes.	Desipramine	71-82	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	53-59
21976621-11	2012	Finally, the magnitude of in vivo CYP2D6 DDIs caused by quinidine was predicted using desipramine, dextromethorphan, and metoprolol.	Desipramine	86-97	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	34-40
21918844-6	2012	The desipramine/cisplatin combination resulted in increased levels of p53 as well as mitochondrial damage, caspase activation, and poly(ADP ribose) polymerase cleavage, suggesting that desipramine may synergize with cisplatin more than with other platinum chemotherapeutics partly by activating distinct apoptotic pathways.	Desipramine	4-15	tumor protein p53	Homo sapiens	70-73
21918844-6	2012	The desipramine/cisplatin combination resulted in increased levels of p53 as well as mitochondrial damage, caspase activation, and poly(ADP ribose) polymerase cleavage, suggesting that desipramine may synergize with cisplatin more than with other platinum chemotherapeutics partly by activating distinct apoptotic pathways.	Desipramine	4-15	poly(ADP-ribose) polymerase 1	Homo sapiens	131-158
21918844-6	2012	The desipramine/cisplatin combination resulted in increased levels of p53 as well as mitochondrial damage, caspase activation, and poly(ADP ribose) polymerase cleavage, suggesting that desipramine may synergize with cisplatin more than with other platinum chemotherapeutics partly by activating distinct apoptotic pathways.	Desipramine	185-196	tumor protein p53	Homo sapiens	70-73
21918844-6	2012	The desipramine/cisplatin combination resulted in increased levels of p53 as well as mitochondrial damage, caspase activation, and poly(ADP ribose) polymerase cleavage, suggesting that desipramine may synergize with cisplatin more than with other platinum chemotherapeutics partly by activating distinct apoptotic pathways.	Desipramine	185-196	poly(ADP-ribose) polymerase 1	Homo sapiens	131-158
21867719-12	2012	and desipramine (16 mg/kg, i.p) prevented the depressant-like effect induced by TNF-alpha (0.1 fg/site, i.c.v.)	Desipramine	4-15	tumor necrosis factor	Mus musculus	80-89
22197911-8	2012	Our data show that fluoxetine is a selective inhibitor of GluN2B-containing NMDARs, whereas desipramine inhibits both GluN1/GluN2A and GluN1/GluN2B subtypes.	Desipramine	92-103	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	118-123
22197911-8	2012	Our data show that fluoxetine is a selective inhibitor of GluN2B-containing NMDARs, whereas desipramine inhibits both GluN1/GluN2A and GluN1/GluN2B subtypes.	Desipramine	92-103	glutamate ionotropic receptor NMDA type subunit 2A	Homo sapiens	124-130
22197911-8	2012	Our data show that fluoxetine is a selective inhibitor of GluN2B-containing NMDARs, whereas desipramine inhibits both GluN1/GluN2A and GluN1/GluN2B subtypes.	Desipramine	92-103	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	135-140
22197911-8	2012	Our data show that fluoxetine is a selective inhibitor of GluN2B-containing NMDARs, whereas desipramine inhibits both GluN1/GluN2A and GluN1/GluN2B subtypes.	Desipramine	92-103	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	141-147
21963947-0	2011	Regulation of CCL2/MCP-1 production in astrocytes by desipramine and atomoxetine: involvement of alpha2 adrenergic receptors.	Desipramine	53-64	C-C motif chemokine ligand 2	Rattus norvegicus	14-18
22814024-10	2012	Desipramine decreased also relative weight of inguinal lymph nodes and spleens whereas desipramine and fluoxetine increased production of IL-10 in comparison to positive control.	Desipramine	87-98	interleukin 10	Homo sapiens	138-143
23209658-0	2012	Desipramine protects neuronal cell death and induces heme oxygenase-1 expression in Mes23.5 dopaminergic neurons.	Desipramine	0-11	heme oxygenase 1	Homo sapiens	53-69
23209658-6	2012	Desipramine induces endogenous anti-oxidative enzyme, heme oxygenase-1 (HO-1) protein and mRNA expression in concentration- and time-dependent manners.	Desipramine	0-11	heme oxygenase 1	Homo sapiens	54-70
23209658-6	2012	Desipramine induces endogenous anti-oxidative enzyme, heme oxygenase-1 (HO-1) protein and mRNA expression in concentration- and time-dependent manners.	Desipramine	0-11	heme oxygenase 1	Homo sapiens	72-76
23209658-7	2012	A different type of antidepressant SSRI (selective serotonin reuptake inhibitor), fluoxetine also shows similar effects of desipramine on HO-1 expression.	Desipramine	123-134	heme oxygenase 1	Homo sapiens	138-142
23209658-8	2012	Moreover, desipramine induces HO-1 expression through activation of ERK and JNK signaling pathways.	Desipramine	10-21	heme oxygenase 1	Homo sapiens	30-34
23209658-8	2012	Moreover, desipramine induces HO-1 expression through activation of ERK and JNK signaling pathways.	Desipramine	10-21	mitogen-activated protein kinase 1	Homo sapiens	68-71
23209658-8	2012	Moreover, desipramine induces HO-1 expression through activation of ERK and JNK signaling pathways.	Desipramine	10-21	mitogen-activated protein kinase 8	Homo sapiens	76-79
23209658-9	2012	Desipramine also increases NF-E2-related factor-2 (Nrf2) accumulation in the nucleus and enhances Nrf2-DNA binding activity.	Desipramine	0-11	NFE2 like bZIP transcription factor 2	Homo sapiens	27-49
23209658-9	2012	Desipramine also increases NF-E2-related factor-2 (Nrf2) accumulation in the nucleus and enhances Nrf2-DNA binding activity.	Desipramine	0-11	NFE2 like bZIP transcription factor 2	Homo sapiens	51-55
23209658-9	2012	Desipramine also increases NF-E2-related factor-2 (Nrf2) accumulation in the nucleus and enhances Nrf2-DNA binding activity.	Desipramine	0-11	NFE2 like bZIP transcription factor 2	Homo sapiens	98-102
23209658-10	2012	Moreover, desipramine-mediated increase of HO-1 expression is reduced by transfection with siRNA against Nrf2.	Desipramine	10-21	heme oxygenase 1	Homo sapiens	43-47
23209658-10	2012	Moreover, desipramine-mediated increase of HO-1 expression is reduced by transfection with siRNA against Nrf2.	Desipramine	10-21	NFE2 like bZIP transcription factor 2	Homo sapiens	105-109
23209658-12	2012	Furthermore, inhibition of HO-1 activity by a HO-1 pharmacological inhibitor, ZnPP IX, attenuates the neuroprotective effect of desipramine.	Desipramine	128-139	heme oxygenase 1	Homo sapiens	27-31
23209658-12	2012	Furthermore, inhibition of HO-1 activity by a HO-1 pharmacological inhibitor, ZnPP IX, attenuates the neuroprotective effect of desipramine.	Desipramine	128-139	heme oxygenase 1	Homo sapiens	46-50
23209658-14	2012	CONCLUSIONS/SIGNIFICANCE: These findings suggest that desipramine-increased HO-1 expression is mediated by Nrf2 activation through the ERK and JNK signaling pathways.	Desipramine	54-65	heme oxygenase 1	Homo sapiens	76-80
23209658-14	2012	CONCLUSIONS/SIGNIFICANCE: These findings suggest that desipramine-increased HO-1 expression is mediated by Nrf2 activation through the ERK and JNK signaling pathways.	Desipramine	54-65	NFE2 like bZIP transcription factor 2	Homo sapiens	107-111
23209658-14	2012	CONCLUSIONS/SIGNIFICANCE: These findings suggest that desipramine-increased HO-1 expression is mediated by Nrf2 activation through the ERK and JNK signaling pathways.	Desipramine	54-65	mitogen-activated protein kinase 1	Homo sapiens	135-138
23209658-14	2012	CONCLUSIONS/SIGNIFICANCE: These findings suggest that desipramine-increased HO-1 expression is mediated by Nrf2 activation through the ERK and JNK signaling pathways.	Desipramine	54-65	mitogen-activated protein kinase 8	Homo sapiens	143-146
22563449-0	2012	Desipramine inhibits histamine H1 receptor-induced Ca2+ signaling in rat hypothalamic cells.	Desipramine	0-11	histamine receptor H 1	Rattus norvegicus	21-42
22563449-4	2012	In primary cultured rat hypothalamic cells, desipramine markedly suppressed the elevation of intracellular Ca(2+) evoked by histamine H1 receptor activation.	Desipramine	44-55	histamine receptor H 1	Rattus norvegicus	124-145
22563449-8	2012	Our results reveal that desipramine and sibutramine have different effects on histamine H1 receptor signaling in hypothalamic cells and suggest that distinct regulation of hypothalamic histamine signaling might underlie the differential regulation of food intake between antidepressants.	Desipramine	24-35	histamine receptor H 1	Rattus norvegicus	78-99
21963947-0	2011	Regulation of CCL2/MCP-1 production in astrocytes by desipramine and atomoxetine: involvement of alpha2 adrenergic receptors.	Desipramine	53-64	C-C motif chemokine ligand 2	Rattus norvegicus	19-24
21963947-2	2011	The treatment of primary rat astrocyte cultures with the noradrenaline transporter inhibitors desipramine or atomoxetine induced the expression and synthesis of CCL2/MCP-1 in these cells.	Desipramine	94-105	C-C motif chemokine ligand 2	Rattus norvegicus	161-165
21963947-2	2011	The treatment of primary rat astrocyte cultures with the noradrenaline transporter inhibitors desipramine or atomoxetine induced the expression and synthesis of CCL2/MCP-1 in these cells.	Desipramine	94-105	chemokine (C-C motif) ligand 2	Mus musculus	166-171
21859713-0	2011	The antidepressant desipramine is an arrestin-biased ligand at the alpha(2A)-adrenergic receptor driving receptor down-regulation in vitro and in vivo.	Desipramine	19-30	adrenoceptor alpha 2A	Homo sapiens	67-96
23049887-11	2012	Importantly, we have found that two drugs known to inhibit mammalian ASM activities, desipramine and clomipramine, markedly extend the lifespan of wild-type animals, in a manner similar to that achieved by genetic inactivation of the asm genes.	Desipramine	85-96	sphingomyelin phosphodiesterase 1	Homo sapiens	69-72
23049887-11	2012	Importantly, we have found that two drugs known to inhibit mammalian ASM activities, desipramine and clomipramine, markedly extend the lifespan of wild-type animals, in a manner similar to that achieved by genetic inactivation of the asm genes.	Desipramine	85-96	sphingomyelin phosphodiesterase 1	Homo sapiens	234-237
21859713-4	2011	In the present study, we have characterized the direct interaction between DMI and the alpha(2A)-adrenergic receptor (alpha(2A)AR), a key regulator of noradrenergic neurotransmission with altered expression and function in depression.	Desipramine	75-78	adrenoceptor alpha 2A	Homo sapiens	87-116
21859713-4	2011	In the present study, we have characterized the direct interaction between DMI and the alpha(2A)-adrenergic receptor (alpha(2A)AR), a key regulator of noradrenergic neurotransmission with altered expression and function in depression.	Desipramine	75-78	adrenoceptor alpha 2A	Homo sapiens	118-129
21859713-5	2011	DMI alone was found to be sufficient to drive receptor internalization acutely and a robust down-regulation of alpha(2A)AR expression and signaling following prolonged stimulation in vitro.	Desipramine	0-3	adrenoceptor alpha 2A	Homo sapiens	111-122
21859713-8	2011	Prolonged in vivo administration of DMI resulted in significant down-regulation of synaptic alpha(2A)AR expression, a response that was lost in arrestin3-null animals.	Desipramine	36-39	adrenoceptor alpha 2A	Homo sapiens	92-103
21442465-7	2011	The administration of desipramine, a specific inhibitor of noradrenaline reuptake, prevented the increase in Nur77-like immunoreactivity and mRNA induced by stress in rats subjected to repeated exposure to immobilization stress.	Desipramine	22-33	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	109-114
21208501-0	2011	Chronic desipramine treatment alters tyrosine hydroxylase but not norepinephrine transporter immunoreactivity in norepinephrine axons in the rat prefrontal cortex.	Desipramine	8-19	tyrosine hydroxylase	Rattus norvegicus	37-57
21208501-4	2011	Following DMI treatment (21 d, 15 mg/kg.d), NET-immunoreactive (ir) axons were significantly less likely to co-localize TH.	Desipramine	10-13	solute carrier family 6 member 2	Rattus norvegicus	44-47
21481537-4	2011	Using an in situ brain/choroid plexus perfusion method, we tested the hypothesis that the antidepressant desipramine increases glucocorticoid accumulation in the mouse brain by inhibiting P-gp, following either chronic treatment (8 days, 20 mg/kg/day, IP) or acute administration (20 min brain perfusion in the presence of either 0.9 muM or 10 muM desipramine).	Desipramine	105-116	phosphoglycolate phosphatase	Mus musculus	188-192
21832094-3	2011	Importantly, desipramine belongs to a group of tricyclic antidepressant compounds that can simultaneously block hERG and inhibit its surface expression.	Desipramine	13-24	ETS transcription factor ERG	Homo sapiens	112-116
21832094-5	2011	Here, we have studied in detail how desipramine inhibits hERG surface expression.	Desipramine	36-47	ETS transcription factor ERG	Homo sapiens	57-61
21832094-6	2011	We find a previously unrecognized combination of two entirely different mechanisms; desipramine increases hERG endocytosis and degradation as a consequence of drug-induced channel ubiquitination and simultaneously inhibits hERG forward trafficking from the endoplasmic reticulum.	Desipramine	84-95	ETS transcription factor ERG	Homo sapiens	106-110
21832094-6	2011	We find a previously unrecognized combination of two entirely different mechanisms; desipramine increases hERG endocytosis and degradation as a consequence of drug-induced channel ubiquitination and simultaneously inhibits hERG forward trafficking from the endoplasmic reticulum.	Desipramine	84-95	ETS transcription factor ERG	Homo sapiens	223-227
21540358-5	2011	Moreover, the transfection of siRNA for nuclear factor erythroid 2-related factor 2 (Nrf2) to decrease the cellular expression level of Nrf2 exacerbated the cytotoxicity of some drugs (troglitazone, flutamide, acetaminophen, clozapine, terbinafine, and desipramine), suggesting that the genes regulated by Nrf2 are associated with the detoxification of the cytotoxicities mediated by CYP3A4.	Desipramine	253-264	NFE2 like bZIP transcription factor 2	Homo sapiens	40-83
21605631-8	2011	Administration of desipramine (a norepinephrine reuptake inhibitor) to Sprague-Dawley rats was sufficient either alone or in combination with stress to increase IL-1beta mRNA in the hypothalamus and desipramine combined with stress was sufficient to increase IL-1R2 mRNA in the hypothalamus.	Desipramine	18-29	interleukin 1 beta	Rattus norvegicus	161-169
21605631-8	2011	Administration of desipramine (a norepinephrine reuptake inhibitor) to Sprague-Dawley rats was sufficient either alone or in combination with stress to increase IL-1beta mRNA in the hypothalamus and desipramine combined with stress was sufficient to increase IL-1R2 mRNA in the hypothalamus.	Desipramine	18-29	interleukin 1 receptor type 2	Rattus norvegicus	259-265
21540358-5	2011	Moreover, the transfection of siRNA for nuclear factor erythroid 2-related factor 2 (Nrf2) to decrease the cellular expression level of Nrf2 exacerbated the cytotoxicity of some drugs (troglitazone, flutamide, acetaminophen, clozapine, terbinafine, and desipramine), suggesting that the genes regulated by Nrf2 are associated with the detoxification of the cytotoxicities mediated by CYP3A4.	Desipramine	253-264	NFE2 like bZIP transcription factor 2	Homo sapiens	85-89
21540358-5	2011	Moreover, the transfection of siRNA for nuclear factor erythroid 2-related factor 2 (Nrf2) to decrease the cellular expression level of Nrf2 exacerbated the cytotoxicity of some drugs (troglitazone, flutamide, acetaminophen, clozapine, terbinafine, and desipramine), suggesting that the genes regulated by Nrf2 are associated with the detoxification of the cytotoxicities mediated by CYP3A4.	Desipramine	253-264	NFE2 like bZIP transcription factor 2	Homo sapiens	136-140
21540358-5	2011	Moreover, the transfection of siRNA for nuclear factor erythroid 2-related factor 2 (Nrf2) to decrease the cellular expression level of Nrf2 exacerbated the cytotoxicity of some drugs (troglitazone, flutamide, acetaminophen, clozapine, terbinafine, and desipramine), suggesting that the genes regulated by Nrf2 are associated with the detoxification of the cytotoxicities mediated by CYP3A4.	Desipramine	253-264	NFE2 like bZIP transcription factor 2	Homo sapiens	136-140
21389273-6	2011	Functionally, TNF-alpha-stimulated H(2)O(2) production was also blocked by MCD and DES (194.6 +- 15.4% vs. 90.6 +- 15.9% and 148.8 +- 20.4%), and the activation of the pivotal proinflammatory transcription factor, NF-kappaB, by TNF-alpha was reversed by MCD and DES as well as by small interfering RNAs of Duox1 or ASMase.	Desipramine	83-86	tumor necrosis factor	Homo sapiens	14-23
21621196-5	2011	We found that CUS led to depressive-like behavior and reduced the amplitude of PER2 oscillation in the SCN, which were blocked by 3 weeks of desipramine (DMI) treatment.	Desipramine	141-152	period circadian regulator 2	Homo sapiens	79-83
21621196-5	2011	We found that CUS led to depressive-like behavior and reduced the amplitude of PER2 oscillation in the SCN, which were blocked by 3 weeks of desipramine (DMI) treatment.	Desipramine	154-157	period circadian regulator 2	Homo sapiens	79-83
21389273-6	2011	Functionally, TNF-alpha-stimulated H(2)O(2) production was also blocked by MCD and DES (194.6 +- 15.4% vs. 90.6 +- 15.9% and 148.8 +- 20.4%), and the activation of the pivotal proinflammatory transcription factor, NF-kappaB, by TNF-alpha was reversed by MCD and DES as well as by small interfering RNAs of Duox1 or ASMase.	Desipramine	83-86	nuclear factor kappa B subunit 1	Homo sapiens	214-223
21389273-6	2011	Functionally, TNF-alpha-stimulated H(2)O(2) production was also blocked by MCD and DES (194.6 +- 15.4% vs. 90.6 +- 15.9% and 148.8 +- 20.4%), and the activation of the pivotal proinflammatory transcription factor, NF-kappaB, by TNF-alpha was reversed by MCD and DES as well as by small interfering RNAs of Duox1 or ASMase.	Desipramine	83-86	tumor necrosis factor	Homo sapiens	228-237
21389273-6	2011	Functionally, TNF-alpha-stimulated H(2)O(2) production was also blocked by MCD and DES (194.6 +- 15.4% vs. 90.6 +- 15.9% and 148.8 +- 20.4%), and the activation of the pivotal proinflammatory transcription factor, NF-kappaB, by TNF-alpha was reversed by MCD and DES as well as by small interfering RNAs of Duox1 or ASMase.	Desipramine	83-86	dual oxidase 1	Homo sapiens	306-311
21389273-6	2011	Functionally, TNF-alpha-stimulated H(2)O(2) production was also blocked by MCD and DES (194.6 +- 15.4% vs. 90.6 +- 15.9% and 148.8 +- 20.4%), and the activation of the pivotal proinflammatory transcription factor, NF-kappaB, by TNF-alpha was reversed by MCD and DES as well as by small interfering RNAs of Duox1 or ASMase.	Desipramine	83-86	sphingomyelin phosphodiesterase 1	Homo sapiens	315-321
21248719-9	2011	This effect of DMI on spine density was severely attenuated following ATR deletion.	Desipramine	15-18	ataxia telangiectasia and Rad3 related	Mus musculus	70-73
21278119-12	2011	Because RFI is the error of the DMI equation, any inaccuracy when estimating intake will lead to a bias in the prediction of RFI.	Desipramine	32-35	RFI	Bos taurus	8-11
21278119-12	2011	Because RFI is the error of the DMI equation, any inaccuracy when estimating intake will lead to a bias in the prediction of RFI.	Desipramine	32-35	RFI	Bos taurus	125-128
21120454-0	2011	hERG K+ channel-associated cardiac effects of the antidepressant drug desipramine.	Desipramine	70-81	ETS transcription factor ERG	Homo sapiens	0-4
21052032-11	2011	CONCLUSION: The MC1R gene might be associated with major depressive disorder and with treatment response to desipramine.	Desipramine	108-119	melanocortin 1 receptor	Homo sapiens	16-20
21229608-5	2011	Moreover, desipramine attenuated THDF-mediated cell death, indicating a crucial role of ASMase in the mechanism of cell death.	Desipramine	10-21	sphingomyelin phosphodiesterase 1	Homo sapiens	88-94
21130737-6	2011	Both Desipramine and FTY720 treatment reduced ASMase without significant inhibition of other lysosomal hydrolases but most hydrolases showed increased secretion (up to a 50% increase) providing more evidence of lysosomal disruption by these drugs.	Desipramine	5-16	sphingomyelin phosphodiesterase 1	Homo sapiens	46-52
21178181-11	2011	Feeding fat and infusion of GLP-1 tended (linear, P = 0.12; quadratic, P = 0.13) to decrease DMI.	Desipramine	93-96	glucagon like peptide 1 receptor	Homo sapiens	28-33
20549303-0	2011	Desipramine induces apoptosis in rat glioma cells via endoplasmic reticulum stress-dependent CHOP pathway.	Desipramine	0-11	DNA-damage inducible transcript 3	Rattus norvegicus	93-97
20549303-3	2011	DMI induced typical apoptotic morphology of chromatin condensation in rat glioma C6 cells and activated intracellular caspase 9 and caspase 3 with no change in mitochondrial membrane potential.	Desipramine	0-3	caspase 9	Rattus norvegicus	118-127
20549303-3	2011	DMI induced typical apoptotic morphology of chromatin condensation in rat glioma C6 cells and activated intracellular caspase 9 and caspase 3 with no change in mitochondrial membrane potential.	Desipramine	0-3	caspase 3	Rattus norvegicus	132-141
20549303-5	2011	However, knockdown of CHOP by CHOP-specific short interfering RNA (siRNA) could decrease the activity of intracellular caspase 3 and the cytotoxicity of DMI to C6 cells.	Desipramine	153-156	DNA-damage inducible transcript 3	Rattus norvegicus	22-26
20549303-5	2011	However, knockdown of CHOP by CHOP-specific short interfering RNA (siRNA) could decrease the activity of intracellular caspase 3 and the cytotoxicity of DMI to C6 cells.	Desipramine	153-156	DNA-damage inducible transcript 3	Rattus norvegicus	30-34
20549303-6	2011	These results revealed that the CHOP-dependent endoplasmic reticulum (ER) stress pathway is responsible for DMI-induced apoptosis in C6 cells.	Desipramine	108-111	DNA-damage inducible transcript 3	Rattus norvegicus	32-36
22076148-6	2011	In vivo, chronic treatment with the non-selective antidepressant imipramine as well as the norepinephrine-selective reuptake inhibitor desipramine or the serotonin-selective reuptake inhibitor fluoxetine all decrease p21 expression, and this was associated with increased neurogenesis.	Desipramine	135-146	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	217-220
21120454-8	2011	We found that desipramine reduced hERG currents by binding to a receptor site inside the channel pore.	Desipramine	14-25	ETS transcription factor ERG	Homo sapiens	34-38
21120454-12	2011	Finally, desipramine triggered apoptosis in cells expressing hERG channels.	Desipramine	9-20	ETS transcription factor ERG	Homo sapiens	61-65
21120454-13	2011	Desipramine exerts at least four different cellular effects: (1) direct hERG channel block, (2) acute reduction of hERG surface expression, (3) chronic disruption of hERG trafficking, and (4) induction of apoptosis.	Desipramine	0-11	ETS transcription factor ERG	Homo sapiens	72-76
21120454-13	2011	Desipramine exerts at least four different cellular effects: (1) direct hERG channel block, (2) acute reduction of hERG surface expression, (3) chronic disruption of hERG trafficking, and (4) induction of apoptosis.	Desipramine	0-11	ETS transcription factor ERG	Homo sapiens	115-119
21120454-13	2011	Desipramine exerts at least four different cellular effects: (1) direct hERG channel block, (2) acute reduction of hERG surface expression, (3) chronic disruption of hERG trafficking, and (4) induction of apoptosis.	Desipramine	0-11	ETS transcription factor ERG	Homo sapiens	115-119
20878594-7	2010	Evidence of cytochrome P450 (CYP)2D6 inhibition in clinical trials highlighted a concern for pharmacokinetic interaction with other drugs that are CYP2D6 substrates, as confirmed by a rise in the pharmacokinetic parameters of desipramine with concomitant administration of mirabegron.	Desipramine	226-237	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	12-36
20926613-7	2010	In HEPES buffer the pH-sensitive current expressed by RTN astrocytes reversed near E(K(+)) (the equilibrium potential for K(+)) and was inhibited by Ba(2+) and desipramine (blocker of Kir4.1-containing channels), characteristics most consistent with heteromeric Kir4.1-Kir5.1 channels.	Desipramine	160-171	potassium inwardly rectifying channel subfamily J member 10	Homo sapiens	184-190
20926613-7	2010	In HEPES buffer the pH-sensitive current expressed by RTN astrocytes reversed near E(K(+)) (the equilibrium potential for K(+)) and was inhibited by Ba(2+) and desipramine (blocker of Kir4.1-containing channels), characteristics most consistent with heteromeric Kir4.1-Kir5.1 channels.	Desipramine	160-171	potassium inwardly rectifying channel subfamily J member 10	Homo sapiens	262-268
20974006-5	2010	Functional knockdown of ASMase with either the chemical inhibitor, desipramine, or siRNA markedly reduces alpha-TEA-induced cell surface membrane accumulation of ceramide and its co-localization with Fas, DR5, and FADD, cleavage of caspases-8 and -9 and apoptosis, suggesting an early and critical role for ASMase in alpha-TEA-induced apoptosis.	Desipramine	67-78	sphingomyelin phosphodiesterase 1	Homo sapiens	24-30
20840444-0	2010	Desipramine, substrate for CYP2D6 activity: population pharmacokinetic model and design elements of drug-drug interaction trials.	Desipramine	0-11	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	27-33
20840444-2	2010	Additional objectives were to develop a semi-mechanistic population pharmacokinetic model for desipramine, which allowed simulation of CYP2D6-mediated inhibition, when using desipramine as a probe substrate, and to evaluate certain study design elements, such as duration of desipramine pharmacokinetic sampling, required sample size and optimal pharmacokinetic sampling schedule for intermediate, extensive and ultrarapid metabolizers of CYP2D6 substrates.	Desipramine	94-105	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	135-141
20840444-2	2010	Additional objectives were to develop a semi-mechanistic population pharmacokinetic model for desipramine, which allowed simulation of CYP2D6-mediated inhibition, when using desipramine as a probe substrate, and to evaluate certain study design elements, such as duration of desipramine pharmacokinetic sampling, required sample size and optimal pharmacokinetic sampling schedule for intermediate, extensive and ultrarapid metabolizers of CYP2D6 substrates.	Desipramine	94-105	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	439-445
20878594-7	2010	Evidence of cytochrome P450 (CYP)2D6 inhibition in clinical trials highlighted a concern for pharmacokinetic interaction with other drugs that are CYP2D6 substrates, as confirmed by a rise in the pharmacokinetic parameters of desipramine with concomitant administration of mirabegron.	Desipramine	226-237	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	147-153
20435089-4	2010	We have found that desipramine (DMI), a tricyclic antidepressant, acts as an inhibitor of thyroid hormone transport by MCT8.	Desipramine	19-30	solute carrier family 16 member 2	Homo sapiens	119-123
20435089-4	2010	We have found that desipramine (DMI), a tricyclic antidepressant, acts as an inhibitor of thyroid hormone transport by MCT8.	Desipramine	32-35	solute carrier family 16 member 2	Homo sapiens	119-123
20435089-7	2010	In a heterologous expression system, both human MCT8 and its close homolog, MCT10, were sensitive to inhibition by DMI.	Desipramine	115-118	solute carrier family 16 member 2	Homo sapiens	48-52
20435089-7	2010	In a heterologous expression system, both human MCT8 and its close homolog, MCT10, were sensitive to inhibition by DMI.	Desipramine	115-118	solute carrier family 16 member 10	Homo sapiens	76-81
19749024-3	2010	Feed conversion ratio (FCR) is the inverse of gross feed efficiency and is the ratio of DMI to ADG.	Desipramine	88-91	FCR	Bos taurus	0-21
20136837-4	2010	KEY RESULTS: NTUA fluorescence accumulated linearly in nerve terminals, an effect that was prevented with NET inhibition with desipramine (1 microM).	Desipramine	126-137	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	106-109
20158296-7	2010	Chronic administration of the antidepressant drugs fluoxetine and desipramine produced robust elevations in hippocampal cell proliferation and brain-derived neurotrophic factor (BDNF) protein levels in MRL/MpJ mice.	Desipramine	66-77	brain derived neurotrophic factor	Mus musculus	143-176
20158296-7	2010	Chronic administration of the antidepressant drugs fluoxetine and desipramine produced robust elevations in hippocampal cell proliferation and brain-derived neurotrophic factor (BDNF) protein levels in MRL/MpJ mice.	Desipramine	66-77	brain derived neurotrophic factor	Mus musculus	178-182
21364631-3	2010	Inhibition of JNK activation with sphingomyelinase inhibitors (20 muM desipramine, 20 muM imipramine), with the protein kinase C-delta (PKCdelta) inhibitor rottlerin (10 muM), and with the specific PKCtheta pseudosubstrate inhibitor (30 muM) indicates that ceramide and phosphorylation by PKCdelta and PKCtheta mediate gal-1-induced JNK activation.	Desipramine	70-81	mitogen-activated protein kinase 8	Homo sapiens	14-17
19635928-9	2010	Inhalation of the Asm inhibitors amitriptyline, trimipramine, desipramine, chlorprothixene, fluoxetine, amlodipine, or sertraline restored normal ceramide concentrations in murine bronchial epithelial cells, reduced inflammation in the lung of CF mice and prevented infection with Pseudomonas aeruginosa.	Desipramine	62-73	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	18-21
20428789-1	2010	Desipramine (DMI) has been reported to induce glucocorticoid receptor-mediated signal transduction in recent studies.	Desipramine	0-11	nuclear receptor subfamily 3, group C, member 1	Mus musculus	46-69
20428789-1	2010	Desipramine (DMI) has been reported to induce glucocorticoid receptor-mediated signal transduction in recent studies.	Desipramine	13-16	nuclear receptor subfamily 3, group C, member 1	Mus musculus	46-69
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	125-128	B cell leukemia/lymphoma 2	Mus musculus	248-253
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	125-128	baculoviral IAP repeat-containing 5	Mus musculus	258-266
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	125-128	BCL2-like 1	Mus musculus	275-281
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	125-128	BCL2-associated X protein	Mus musculus	335-338
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	125-128	apoptotic peptidase activating factor 1	Mus musculus	340-346
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	125-128	caspase 3	Mus musculus	348-357
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	125-128	caspase 7	Mus musculus	362-371
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	223-226	B cell leukemia/lymphoma 2	Mus musculus	248-253
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	223-226	baculoviral IAP repeat-containing 5	Mus musculus	258-266
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	223-226	BCL2-like 1	Mus musculus	275-281
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	223-226	BCL2-associated X protein	Mus musculus	335-338
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	223-226	apoptotic peptidase activating factor 1	Mus musculus	340-346
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	223-226	caspase 3	Mus musculus	348-357
20428789-5	2010	Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 microM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose- and time-dependent manner.	Desipramine	223-226	caspase 7	Mus musculus	362-371
20428789-7	2010	Quantitative RT-PCR revealed that DMI decreased the expression of the PCNA gene and caused an increase in the expression of the p21 and p27 genes in the Ca3/7 cells.	Desipramine	34-37	proliferating cell nuclear antigen	Mus musculus	70-74
20428789-7	2010	Quantitative RT-PCR revealed that DMI decreased the expression of the PCNA gene and caused an increase in the expression of the p21 and p27 genes in the Ca3/7 cells.	Desipramine	34-37	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	128-131
20428789-7	2010	Quantitative RT-PCR revealed that DMI decreased the expression of the PCNA gene and caused an increase in the expression of the p21 and p27 genes in the Ca3/7 cells.	Desipramine	34-37	cyclin-dependent kinase inhibitor 1B	Mus musculus	136-139
19884907-1	2010	CYP2C19 converts the tricyclic antidepressant imipramine to its active metabolite desipramine, which is subsequently inactivated by CYP2D6.	Desipramine	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
19884907-1	2010	CYP2C19 converts the tricyclic antidepressant imipramine to its active metabolite desipramine, which is subsequently inactivated by CYP2D6.	Desipramine	82-93	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	132-138
19884907-6	2010	In a multivariate analysis, we found a significant, but limited effect (P=0.035, eta(2)=0.031) of the CYP2C19*17 genotype on imipramine+desipramine concentrations.	Desipramine	136-147	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	102-109
20211602-0	2010	Block of the human ether-a-go-go-related gene (hERG) K+ channel by the antidepressant desipramine.	Desipramine	86-97	ETS transcription factor ERG	Homo sapiens	47-51
20211602-2	2010	Since blockade of cardiac human ether-a-go-go-related gene (hERG) channels is an important cause of acquired long QT syndrome, we investigated the acute effects of desipramine on hERG channels to determine the electrophysiological basis for its pro-arrhythmic potential.	Desipramine	164-175	ETS transcription factor ERG	Homo sapiens	179-183
20211602-3	2010	We examined the effects of desipramine on the hERG channels expressed in Xenopus oocytes using two-microelectrode voltage-clamp techniques.	Desipramine	27-38	ETS transcription factor ERG	Homo sapiens	46-50
20211602-4	2010	Desipramine-induced concentration-dependent decreases in the current amplitude at the end of the voltage steps and hERG tail currents.	Desipramine	0-11	ETS transcription factor ERG	Homo sapiens	115-119
20211602-5	2010	The IC(50) for desipramine needed to block the hERG current in Xenopus oocytes decreased progressively relative to the degree of depolarization.	Desipramine	15-26	ETS transcription factor ERG	Homo sapiens	47-51
20211602-7	2010	The S6 domain mutations, Tyr-652 located in the S6 domain of the hERG channel reduced the potency of the channel block by desipramine more than a mutation of Phe-656 in the same region.	Desipramine	122-133	ETS transcription factor ERG	Homo sapiens	65-69
20211602-8	2010	These results suggest that desipramine is a blocker of the hERG channels, providing a molecular mechanism for the arrhythmogenic side effects during the clinical administration of desipramine.	Desipramine	27-38	ETS transcription factor ERG	Homo sapiens	59-63
20211602-8	2010	These results suggest that desipramine is a blocker of the hERG channels, providing a molecular mechanism for the arrhythmogenic side effects during the clinical administration of desipramine.	Desipramine	180-191	ETS transcription factor ERG	Homo sapiens	59-63
20132473-8	2010	Desipramine (an inhibitor of NA reuptake) also caused an increase of MCP-1 in cortex.	Desipramine	0-11	C-C motif chemokine ligand 2	Rattus norvegicus	69-74
19749024-3	2010	Feed conversion ratio (FCR) is the inverse of gross feed efficiency and is the ratio of DMI to ADG.	Desipramine	88-91	FCR	Bos taurus	23-26
20722995-1	2010	OBJECTIVES: In rats with diabetes mellitus induced by alloxan (DMIA) or streptozocin (DMIS), changes in the cytochrome P450 (CYP) isozymes in the liver, lung, kidney, intestine, brain, and testis have been reported based on Western blot analysis, Northern blot analysis, and various enzyme activities.	Desipramine	86-90	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	108-123
20722995-1	2010	OBJECTIVES: In rats with diabetes mellitus induced by alloxan (DMIA) or streptozocin (DMIS), changes in the cytochrome P450 (CYP) isozymes in the liver, lung, kidney, intestine, brain, and testis have been reported based on Western blot analysis, Northern blot analysis, and various enzyme activities.	Desipramine	86-90	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	125-128
19995332-0	2009	Difference in desipramine metabolic profile between wild-type and CYP2D6-humanized mice.	Desipramine	14-25	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	66-72
21200377-7	2010	MAO-A was inhibited by the following drugs: pargyline &gt; clorgyline &gt; iproniazid &gt; fluoxetine &gt; desipramine &gt; amitriptyline &gt; imipramine &gt; citalopram &gt; venlafaxine &gt; reboxetine &gt; olanzapine &gt; mirtazapine &gt; tianeptine &gt; moclobemide, cocaine &gt;&gt; lithium, valproate.	Desipramine	107-118	monoamine oxidase A	Sus scrofa	0-5
21200377-8	2010	MAO-B was inhibited by the following drugs: pargyline &gt; clorgyline &gt; iproniazid &gt; fluoxetine &gt; venlafaxine &gt; amitriptyline &gt; olanzapine &gt; citalopram &gt; desipramine &gt; reboxetine &gt; imipramine &gt; tianeptine &gt; mirtazapine, cocaine &gt;&gt; moclobemide, lithium, valproate.	Desipramine	175-186	monoamine oxidase B	Sus scrofa	0-5
19818834-0	2009	Desipramine induced changes in the norepinephrine transporter, alpha- and gamma-synuclein in the hippocampus, amygdala and striatum.	Desipramine	0-11	solute carrier family 6 member 2	Rattus norvegicus	35-61
19818834-0	2009	Desipramine induced changes in the norepinephrine transporter, alpha- and gamma-synuclein in the hippocampus, amygdala and striatum.	Desipramine	0-11	synuclein alpha	Rattus norvegicus	63-89
19995332-1	2009	Desipramine (DMI), a CYP2D6 probe, was used as a model drug to test whether CYP2D6-humanized (Tg-CYP2D6) and wild-type control mice could be used as preclinical animal models to identify the effects of CYP2D6 genotype/phenotype on drug metabolic profiles.	Desipramine	0-11	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	21-27
19995332-4	2009	Three metabolites, 2-hydroxyl-, 10-hydroxyl, and N-desmethyl-desipramine were identified in the incubations of DMI with both wild-type and Tg-CYP2D6 MLM, as well as in human CYP2D6 extensive metabolizer liver microsomes.	Desipramine	111-114	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	142-148
19995332-4	2009	Three metabolites, 2-hydroxyl-, 10-hydroxyl, and N-desmethyl-desipramine were identified in the incubations of DMI with both wild-type and Tg-CYP2D6 MLM, as well as in human CYP2D6 extensive metabolizer liver microsomes.	Desipramine	111-114	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	174-180
19575421-0	2009	Desipramine inhibits the growth of a mouse skin squamous cell carcinoma cell line and affects glucocorticoid receptor-mediated transcription.	Desipramine	0-11	nuclear receptor subfamily 3, group C, member 1	Mus musculus	94-117
19575421-1	2009	The purpose of this study was to examine the effect of tricyclic antidepressant desipramine (DMI) on the growth inhibition and translocation of the glucocorticoid receptor (GR) from the cytoplasm to the nucleus in cancerous and noncancerous cell lines and the effect of DMI on GR-mediated transcription.	Desipramine	80-91	nuclear receptor subfamily 3, group C, member 1	Mus musculus	148-171
19575421-1	2009	The purpose of this study was to examine the effect of tricyclic antidepressant desipramine (DMI) on the growth inhibition and translocation of the glucocorticoid receptor (GR) from the cytoplasm to the nucleus in cancerous and noncancerous cell lines and the effect of DMI on GR-mediated transcription.	Desipramine	80-91	nuclear receptor subfamily 3, group C, member 1	Mus musculus	173-175
19575421-1	2009	The purpose of this study was to examine the effect of tricyclic antidepressant desipramine (DMI) on the growth inhibition and translocation of the glucocorticoid receptor (GR) from the cytoplasm to the nucleus in cancerous and noncancerous cell lines and the effect of DMI on GR-mediated transcription.	Desipramine	93-96	nuclear receptor subfamily 3, group C, member 1	Mus musculus	148-171
19575421-1	2009	The purpose of this study was to examine the effect of tricyclic antidepressant desipramine (DMI) on the growth inhibition and translocation of the glucocorticoid receptor (GR) from the cytoplasm to the nucleus in cancerous and noncancerous cell lines and the effect of DMI on GR-mediated transcription.	Desipramine	93-96	nuclear receptor subfamily 3, group C, member 1	Mus musculus	173-175
19575421-1	2009	The purpose of this study was to examine the effect of tricyclic antidepressant desipramine (DMI) on the growth inhibition and translocation of the glucocorticoid receptor (GR) from the cytoplasm to the nucleus in cancerous and noncancerous cell lines and the effect of DMI on GR-mediated transcription.	Desipramine	93-96	nuclear receptor subfamily 3, group C, member 1	Mus musculus	277-279
19575421-1	2009	The purpose of this study was to examine the effect of tricyclic antidepressant desipramine (DMI) on the growth inhibition and translocation of the glucocorticoid receptor (GR) from the cytoplasm to the nucleus in cancerous and noncancerous cell lines and the effect of DMI on GR-mediated transcription.	Desipramine	270-273	nuclear receptor subfamily 3, group C, member 1	Mus musculus	148-171
19575421-1	2009	The purpose of this study was to examine the effect of tricyclic antidepressant desipramine (DMI) on the growth inhibition and translocation of the glucocorticoid receptor (GR) from the cytoplasm to the nucleus in cancerous and noncancerous cell lines and the effect of DMI on GR-mediated transcription.	Desipramine	270-273	nuclear receptor subfamily 3, group C, member 1	Mus musculus	173-175
19575421-6	2009	The translocation of GR was induced by FA alone, DMI alone, and combination of both agents.	Desipramine	49-52	nuclear receptor subfamily 3, group C, member 1	Mus musculus	21-23
19575421-8	2009	However, DMI inhibited FA-induced, GR-mediated transcription when both agents were given together.	Desipramine	9-12	nuclear receptor subfamily 3, group C, member 1	Mus musculus	35-37
19575421-9	2009	Pretreatment with DMI followed by combination of DMI and FA decreased GR-mediated transcription more than pretreatment with FA.	Desipramine	18-21	nuclear receptor subfamily 3, group C, member 1	Mus musculus	70-72
19575421-9	2009	Pretreatment with DMI followed by combination of DMI and FA decreased GR-mediated transcription more than pretreatment with FA.	Desipramine	49-52	nuclear receptor subfamily 3, group C, member 1	Mus musculus	70-72
19575421-10	2009	The expression of metallothionein-1 (Mt-1) gene, which is regulated by GR, was induced significantly by the combination of DMI and FA, and enhanced significantly by pretreatment with FA but not DMI.	Desipramine	123-126	metallothionein 1	Mus musculus	18-35
19575421-10	2009	The expression of metallothionein-1 (Mt-1) gene, which is regulated by GR, was induced significantly by the combination of DMI and FA, and enhanced significantly by pretreatment with FA but not DMI.	Desipramine	123-126	metallothionein 1	Mus musculus	37-41
19575421-10	2009	The expression of metallothionein-1 (Mt-1) gene, which is regulated by GR, was induced significantly by the combination of DMI and FA, and enhanced significantly by pretreatment with FA but not DMI.	Desipramine	123-126	nuclear receptor subfamily 3, group C, member 1	Mus musculus	71-73
19575421-10	2009	The expression of metallothionein-1 (Mt-1) gene, which is regulated by GR, was induced significantly by the combination of DMI and FA, and enhanced significantly by pretreatment with FA but not DMI.	Desipramine	194-197	metallothionein 1	Mus musculus	18-35
19575421-10	2009	The expression of metallothionein-1 (Mt-1) gene, which is regulated by GR, was induced significantly by the combination of DMI and FA, and enhanced significantly by pretreatment with FA but not DMI.	Desipramine	194-197	metallothionein 1	Mus musculus	37-41
19575421-11	2009	DMI is suggested to inhibit the growth of Ca3/7 cells and to affect GR-mediated transcription.	Desipramine	0-3	nuclear receptor subfamily 3, group C, member 1	Mus musculus	68-70
19420132-6	2009	The K(m) values for N-sulfation mediated by hSULT2A1 were as follows: 1.08 +/- 0.03 mM for ciprofloxacin, 0.53 +/- 0.01 mM for moxifloxacin, 0.19 +/- 0.01 mM for garenoxacin, 0.054 +/- 0.001 mM for desipramine, and 2.32 +/- 0.12 mM for metoclopramide.	Desipramine	198-209	sulfotransferase family 2A member 1	Homo sapiens	44-52
20081247-10	2009	The prometastatic effect of desipramine in young animals was connected with an increase of VEGF and MMP-9 plasma levels.	Desipramine	28-39	vascular endothelial growth factor A	Mus musculus	91-95
20081247-10	2009	The prometastatic effect of desipramine in young animals was connected with an increase of VEGF and MMP-9 plasma levels.	Desipramine	28-39	matrix metallopeptidase 9	Mus musculus	100-105
19015855-0	2009	Disposition of desipramine, a sensitive cytochrome P450 2D6 substrate, when coadministered with intravenous temsirolimus.	Desipramine	15-26	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	40-59
19328214-4	2009	HTC cells were found to be sensitive to exogenous ceramide and significantly protected against TNF by desipramine, an inhibitor of lysosomal acid sphingomyelinase.	Desipramine	102-113	tumor necrosis factor	Rattus norvegicus	95-98
19015855-4	2009	METHODS: This 2-period study in healthy subjects investigated the pharmacokinetics of a single oral 50-mg dose of the CYP2D6 substrate desipramine, first without and subsequently with a single coadministered i.v.	Desipramine	135-146	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	118-124
19177066-10	2009	Protein levels of brain-derived neurotrophic factor (BDNF) in MRL/MpJ mice were elevated significantly in the frontal cortex, hippocampus, and amygdala after chronic FLX treatment, but increased only in the frontal cortex by chronic DMI.	Desipramine	233-236	brain derived neurotrophic factor	Mus musculus	18-51
19457081-2	2009	We report here that PACAP-deficient (PACAP-/-) mice showed increased immobility in a forced swimming test, which was reduced by the antidepressant desipramine, to a similar extent as in wild-type mice.	Desipramine	147-158	adenylate cyclase activating polypeptide 1	Mus musculus	20-25
19457081-2	2009	We report here that PACAP-deficient (PACAP-/-) mice showed increased immobility in a forced swimming test, which was reduced by the antidepressant desipramine, to a similar extent as in wild-type mice.	Desipramine	147-158	adenylate cyclase activating polypeptide 1	Mus musculus	37-42
19177066-10	2009	Protein levels of brain-derived neurotrophic factor (BDNF) in MRL/MpJ mice were elevated significantly in the frontal cortex, hippocampus, and amygdala after chronic FLX treatment, but increased only in the frontal cortex by chronic DMI.	Desipramine	233-236	brain derived neurotrophic factor	Mus musculus	53-57
19177066-11	2009	In contrast, BDNF levels in C57BL/6J mice were decreased in the hippocampus and increased in the amygdala after chronic FLX, and were decreased in the brain stem after chronic DMI.	Desipramine	176-179	brain derived neurotrophic factor	Mus musculus	13-17
18923403-1	2009	The antidepressant desipramine inhibits the reuptake of norepinephrine (NE), leading to activation of both pre- and postsynaptic adrenergic receptors, including alpha-1, alpha-2, beta-1, and beta-2 subtypes.	Desipramine	19-30	hemoglobin, beta adult major chain	Mus musculus	179-185
18923402-1	2009	Previous work has shown that repeated desipramine treatment causes downregulation of the norepinephrine transporter (NET) and persistent antidepressant-like effects on behavior, ie effects observed 2 days after discontinuation of drug treatment when acute effects are minimized.	Desipramine	38-49	solute carrier family 6 member 2	Rattus norvegicus	89-115
18986328-0	2009	Desipramine-induced Ca-independent apoptosis in Mg63 human osteosarcoma cells: dependence on P38 mitogen-activated protein kinase-regulated activation of caspase 3.	Desipramine	0-11	mitogen-activated protein kinase 14	Homo sapiens	93-129
18986328-0	2009	Desipramine-induced Ca-independent apoptosis in Mg63 human osteosarcoma cells: dependence on P38 mitogen-activated protein kinase-regulated activation of caspase 3.	Desipramine	0-11	caspase 3	Homo sapiens	154-163
18986328-6	2009	Cells treated with 100-800 mmol/L desipramine showed typical apoptotic features, including an increase in sub-diploid nuclei and activation of caspase 3, indicating that these cells underwent apoptosis.	Desipramine	34-45	caspase 3	Homo sapiens	143-152
18986328-7	2009	Immunoblotting revealed that 100 mmol/L desipramine activated extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK).	Desipramine	40-51	mitogen-activated protein kinase 1	Homo sapiens	62-99
18986328-7	2009	Immunoblotting revealed that 100 mmol/L desipramine activated extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK).	Desipramine	40-51	mitogen-activated protein kinase 1	Homo sapiens	101-104
18986328-7	2009	Immunoblotting revealed that 100 mmol/L desipramine activated extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK).	Desipramine	40-51	mitogen-activated protein kinase 8	Homo sapiens	107-130
18986328-7	2009	Immunoblotting revealed that 100 mmol/L desipramine activated extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK).	Desipramine	40-51	mitogen-activated protein kinase 8	Homo sapiens	132-135
18986328-7	2009	Immunoblotting revealed that 100 mmol/L desipramine activated extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK).	Desipramine	40-51	mitogen-activated protein kinase 14	Homo sapiens	141-177
18986328-7	2009	Immunoblotting revealed that 100 mmol/L desipramine activated extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK).	Desipramine	40-51	mitogen-activated protein kinase 1	Homo sapiens	179-183
18986328-9	2009	Desipramine-induced caspase 3 activation required p38 MAPK activation.	Desipramine	0-11	caspase 3	Homo sapiens	20-29
18986328-9	2009	Desipramine-induced caspase 3 activation required p38 MAPK activation.	Desipramine	0-11	mitogen-activated protein kinase 14	Homo sapiens	50-53
18986328-9	2009	Desipramine-induced caspase 3 activation required p38 MAPK activation.	Desipramine	0-11	mitogen-activated protein kinase 1	Homo sapiens	54-58
18986328-13	2009	The results of the present study suggest that, in MG63 human osteosarcoma cells, desipramine causes Ca(2+)-independent apoptosis by inducing p38 MAPK-associated activation of caspase 3.	Desipramine	81-92	mitogen-activated protein kinase 14	Homo sapiens	141-144
18986328-13	2009	The results of the present study suggest that, in MG63 human osteosarcoma cells, desipramine causes Ca(2+)-independent apoptosis by inducing p38 MAPK-associated activation of caspase 3.	Desipramine	81-92	caspase 3	Homo sapiens	175-184
18952723-6	2009	Relationships between ADG and G:F with DMI as a percentage of BW and NE(g) intake also were examined in the same data set.	Desipramine	39-42	ADG	Bos taurus	22-25
18952723-7	2009	Across the wide range of average shrunk BW in the database (334.4 to 548.0 kg), ADG was positively related to DMI as a percentage of BW (P &lt; 0.01); however, this relationship was not strong (r(2) = 0.17).	Desipramine	110-113	ADG	Bos taurus	80-83
19106229-0	2009	Desipramine reduces stress-activated dynorphin expression and CREB phosphorylation in NAc tissue.	Desipramine	0-11	cAMP responsive element binding protein 1	Rattus norvegicus	62-66
19106229-7	2009	In primary cultures of NAc and striatum, DMI decreases basal and stimulated CREB phosphorylation by causing reductions in intracellular calcium (Ca(2+)) availability that are independent of norepinephrine or other monoaminergic inputs, identifying a potential mechanism for alterations in CREB-mediated gene expression.	Desipramine	41-44	cAMP responsive element binding protein 1	Rattus norvegicus	76-80
19106229-7	2009	In primary cultures of NAc and striatum, DMI decreases basal and stimulated CREB phosphorylation by causing reductions in intracellular calcium (Ca(2+)) availability that are independent of norepinephrine or other monoaminergic inputs, identifying a potential mechanism for alterations in CREB-mediated gene expression.	Desipramine	41-44	cAMP responsive element binding protein 1	Rattus norvegicus	289-293
19106229-9	2009	These findings raise the possibility that a therapeutically relevant mechanism of action of DMI occurs through attenuation of CREB-mediated gene transcription, which is mediated via previously uncharacterized mechanisms that occur directly within the NAc.	Desipramine	92-95	cAMP responsive element binding protein 1	Rattus norvegicus	126-130
18800063-7	2009	DMI administration increased sst(1/4) receptors levels in the CA1 hippocampal region.	Desipramine	0-3	carbonic anhydrase 1	Rattus norvegicus	62-65
18800064-0	2009	Desipramine modulation of alpha-, gamma-synuclein, and the norepinephrine transporter in an animal model of depression.	Desipramine	0-11	synuclein, gamma	Rattus norvegicus	34-49
18800064-0	2009	Desipramine modulation of alpha-, gamma-synuclein, and the norepinephrine transporter in an animal model of depression.	Desipramine	0-11	solute carrier family 6 member 2	Rattus norvegicus	59-85
18800064-6	2009	In WKY rats there was an overexpression of gamma-Syn which was reduced following DMI treatment.	Desipramine	81-84	synuclein, gamma	Rattus norvegicus	43-52
18800064-7	2009	In parallel, DMI caused an increase in both alpha-Syn and NET in the frontal cortex.	Desipramine	13-16	synuclein alpha	Rattus norvegicus	44-53
19424057-3	2009	Here, we investigated whether chronic restraint stress (14 days) and antidepressant treatment [desipramine (DMI), 10 mg/kg intraperitoneally] induce changes in animal behavior and hippocampal levels of phospho-ERK1/2 and its substrate phospho-cAMP response element-binding protein (CREB).	Desipramine	95-106	mitogen-activated protein kinase 3	Homo sapiens	210-216
19424057-3	2009	Here, we investigated whether chronic restraint stress (14 days) and antidepressant treatment [desipramine (DMI), 10 mg/kg intraperitoneally] induce changes in animal behavior and hippocampal levels of phospho-ERK1/2 and its substrate phospho-cAMP response element-binding protein (CREB).	Desipramine	95-106	cAMP responsive element binding protein 1	Homo sapiens	282-286
19424057-3	2009	Here, we investigated whether chronic restraint stress (14 days) and antidepressant treatment [desipramine (DMI), 10 mg/kg intraperitoneally] induce changes in animal behavior and hippocampal levels of phospho-ERK1/2 and its substrate phospho-cAMP response element-binding protein (CREB).	Desipramine	108-111	mitogen-activated protein kinase 3	Homo sapiens	210-216
19424057-7	2009	Bcl-2 mRNA was reduced in all hippocampal regions by stress, an effect independent of DMI treatment.	Desipramine	86-89	BCL2 apoptosis regulator	Homo sapiens	0-5
19424057-8	2009	However, immunoblot from hippocampal extracts revealed that stress increased BCL-2 levels, an effect prevented by chronic DMI.	Desipramine	122-125	BCL2 apoptosis regulator	Homo sapiens	77-82
19424057-9	2009	These results suggest that ERKs and BDNF may be altered in depressive disorder, modifications that are sensitive to DMI action.	Desipramine	116-119	mitogen-activated protein kinase 3	Homo sapiens	27-31
19424057-9	2009	These results suggest that ERKs and BDNF may be altered in depressive disorder, modifications that are sensitive to DMI action.	Desipramine	116-119	brain derived neurotrophic factor	Homo sapiens	36-40
18923403-1	2009	The antidepressant desipramine inhibits the reuptake of norepinephrine (NE), leading to activation of both pre- and postsynaptic adrenergic receptors, including alpha-1, alpha-2, beta-1, and beta-2 subtypes.	Desipramine	19-30	hemoglobin, beta adult minor chain	Mus musculus	191-197
18923403-11	2009	In addition, desipramine (3-30 mg/kg) produced an antidepressant-like effect on behavior under a DRL 36-s schedule in mice deficient in both beta-1 and beta-2 adrenergic receptors.	Desipramine	13-24	hemoglobin, beta adult major chain	Mus musculus	141-147
18923403-11	2009	In addition, desipramine (3-30 mg/kg) produced an antidepressant-like effect on behavior under a DRL 36-s schedule in mice deficient in both beta-1 and beta-2 adrenergic receptors.	Desipramine	13-24	hemoglobin, beta adult minor chain	Mus musculus	152-158
19001559-0	2009	The effects of desvenlafaxine and paroxetine on the pharmacokinetics of the cytochrome P450 2D6 substrate desipramine in healthy adults.	Desipramine	106-117	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	76-95
19001559-3	2009	The CYP2D6 substrate desipramine (50 mg) was administered alone on day 1 and coadministered on day 6 of dosing with either desvenlafaxine or paroxetine.	Desipramine	21-32	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	4-10
18975044-5	2009	Zn-deficient mice showed exaggerated stress-evoked immediate-early gene expression in the amygdala which was normalised following DMI treatment.	Desipramine	130-133	jun proto-oncogene	Mus musculus	51-66
19067522-5	2009	Pretreatment of the monkey with the selective NET inhibitor, desipramine, decreased the specific binding for both [(11)C]1 and [(11)C]4.	Desipramine	61-72	solute carrier family 6 member 2	Macaca mulatta	46-49
18507712-3	2009	Desipramine, a monoamine uptake blocker was able to abolish the toxic effects of MPP(+) but not H(2)O(2) in reduction of cell viability.	Desipramine	0-11	M-phase phosphoprotein 6	Homo sapiens	81-84
18809731-0	2008	An assessment of drug-drug interactions: the effect of desvenlafaxine and duloxetine on the pharmacokinetics of the CYP2D6 probe desipramine in healthy subjects.	Desipramine	129-140	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	116-122
18393297-1	2008	It has been reported that metformin was primarily metabolized via hepatic CYP2C11, 2D1, and 3A1/2 in rats, and the expression and mRNA levels of hepatic CYP2C11 and 3A1 decreased and increased, respectively, whereas the expression of CYP2D1 was not changed in rat model of diabetes induced by streptozotocin (DMIS).	Desipramine	309-313	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	74-81
18393297-1	2008	It has been reported that metformin was primarily metabolized via hepatic CYP2C11, 2D1, and 3A1/2 in rats, and the expression and mRNA levels of hepatic CYP2C11 and 3A1 decreased and increased, respectively, whereas the expression of CYP2D1 was not changed in rat model of diabetes induced by streptozotocin (DMIS).	Desipramine	309-313	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	153-160
18682257-8	2008	DMI and FLU increased FBP immunoreactivity in both cortical and hippocampal neurons.	Desipramine	0-3	far upstream element binding protein 1	Rattus norvegicus	22-25
18791062-9	2008	Desipramine at the dose of 20 mg/kg produced more decrease in the level of TNF-alpha compared with the effect of the smaller dose, but fluoxetine at 10 mg/kg diminished more in the level of IL-1beta compared with the effect of the larger dose.	Desipramine	0-11	tumor necrosis factor	Rattus norvegicus	75-84
18418364-0	2008	Norepinephrine transporter regulation mediates the long-term behavioral effects of the antidepressant desipramine.	Desipramine	102-113	solute carrier family 6 member 2	Rattus norvegicus	0-26
18418364-1	2008	The relationship between the ability of repeated desipramine treatment to cause downregulation of the norepinephrine transporter (NET) and produce antidepressant-like effects on behavior was determined.	Desipramine	49-60	solute carrier family 6 member 2	Rattus norvegicus	102-128
18418364-1	2008	The relationship between the ability of repeated desipramine treatment to cause downregulation of the norepinephrine transporter (NET) and produce antidepressant-like effects on behavior was determined.	Desipramine	49-60	solute carrier family 6 member 2	Rattus norvegicus	130-133
18418364-2	2008	Treatment of rats with 15 mg/kg per day desipramine reduced NET expression, measured by (3)H-nisoxetine binding and SDS-PAGE/immunoblotting, in cerebral cortex and hippocampus and reduced the time of immobility in the forced-swim test.	Desipramine	40-51	solute carrier family 6 member 2	Rattus norvegicus	60-63
18815045-7	2008	Desipramine and fluoxetine, specific inhibitors of NET and SERT, respectively, both enhanced the inhibitory effects of propofol but reduced the inhibitory effects of ketamine on NET and SERT functions.	Desipramine	0-11	solute carrier family 6 member 4	Homo sapiens	59-63
18418364-7	2008	The present results suggest an important role for NET regulation in the long-term behavioral effects of desipramine and are consistent with clinical data suggesting that enhanced noradrenergic neurotransmission is necessary, but not sufficient, for its antidepressant actions.	Desipramine	104-115	solute carrier family 6 member 2	Rattus norvegicus	50-53
19090348-6	2008	Biochemically, citalopram and desipramine treatment significantly restored depleted reduced glutathione, catalase activity, attenuated raised lipid peroxidation and nitrite level as compared to control (72 hr sleep-deprived) animals.	Desipramine	30-41	catalase	Mus musculus	105-113
18815045-7	2008	Desipramine and fluoxetine, specific inhibitors of NET and SERT, respectively, both enhanced the inhibitory effects of propofol but reduced the inhibitory effects of ketamine on NET and SERT functions.	Desipramine	0-11	solute carrier family 6 member 4	Homo sapiens	186-190
18478316-1	2008	PURPOSE: It has been reported that telithromycin is primarily metabolized via hepatic CYP3A1/2 in rats, the expression and/or mRNA level of hepatic CYP3A1/2 increase in rat model of diabetes mellitus induced by alloxan (DMIA) or streptozotocin (DMIS), and intestinal CYP3A1/2 enzyme activity decreases in rat model of DMIS.	Desipramine	245-249	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	148-154
18698001-9	2008	Nisoxetine and desipramine, selective norepinephrine transporter inhibitors, also reduce locomotor activity in wild-type and knockin mice.	Desipramine	15-26	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	38-64
18794257-6	2008	Data were compared with those obtained in 10 sham mice and correlated with the cardiac and hepatic tissue expression of norepinephrine transporter (NET) as assessed with a (3)H-desipramine saturation binding assay.	Desipramine	177-188	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	120-146
18794257-6	2008	Data were compared with those obtained in 10 sham mice and correlated with the cardiac and hepatic tissue expression of norepinephrine transporter (NET) as assessed with a (3)H-desipramine saturation binding assay.	Desipramine	177-188	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	148-151
18664374-4	2008	RESULTS: Compared to controls, significant reduction of mRNA levels of GR-beta under imipramine and of c-jun under desipramine treatment were found.	Desipramine	115-126	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	103-108
18791062-8	2008	Desipramine and fluoxetine, at either dose, significantly reduced TNF-alpha and IL-beta.	Desipramine	0-11	tumor necrosis factor	Rattus norvegicus	66-75
18606486-0	2008	Desipramine-induced apoptosis in human PC3 prostate cancer cells: activation of JNK kinase and caspase-3 pathways and a protective role of [Ca2+]i elevation.	Desipramine	0-11	chromobox 8	Homo sapiens	39-42
18606486-0	2008	Desipramine-induced apoptosis in human PC3 prostate cancer cells: activation of JNK kinase and caspase-3 pathways and a protective role of [Ca2+]i elevation.	Desipramine	0-11	mitogen-activated protein kinase 8	Homo sapiens	80-83
18606486-0	2008	Desipramine-induced apoptosis in human PC3 prostate cancer cells: activation of JNK kinase and caspase-3 pathways and a protective role of [Ca2+]i elevation.	Desipramine	0-11	caspase 3	Homo sapiens	95-104
18606486-1	2008	The antidepressant desipramine has been shown to induce a rise in cytosolic Ca2+ levels ([Ca2+]i) and cytotoxicity in human PC3 prostate cancer cells, but the mechanisms underlying its cytotoxic effect is unclear.	Desipramine	19-30	chromobox 8	Homo sapiens	124-127
18606486-6	2008	Immunoblotting data revealed that desipramine activated the phosphorylation of c-Jun NH2-terminal kinase (JNK), but not extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK).	Desipramine	34-45	mitogen-activated protein kinase 8	Homo sapiens	79-104
18606486-6	2008	Immunoblotting data revealed that desipramine activated the phosphorylation of c-Jun NH2-terminal kinase (JNK), but not extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK).	Desipramine	34-45	mitogen-activated protein kinase 8	Homo sapiens	106-109
18606486-6	2008	Immunoblotting data revealed that desipramine activated the phosphorylation of c-Jun NH2-terminal kinase (JNK), but not extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK).	Desipramine	34-45	mitogen-activated protein kinase 1	Homo sapiens	206-210
18606486-9	2008	Immunoblotting data suggest that BAPTA/AM pretreatment enhanced desipramine-evoked JNK phosphorylation and caspase-3 cleavage.	Desipramine	64-75	mitogen-activated protein kinase 8	Homo sapiens	83-86
18606486-10	2008	The results suggest that in PC3 cells, desipramine caused apoptosis via inducing JNK-associated caspase-3 activation, and [Ca2+]i rises may slow down or alleviate desipramine-induced cytotoxicity.	Desipramine	39-50	chromobox 8	Homo sapiens	28-31
18606486-10	2008	The results suggest that in PC3 cells, desipramine caused apoptosis via inducing JNK-associated caspase-3 activation, and [Ca2+]i rises may slow down or alleviate desipramine-induced cytotoxicity.	Desipramine	39-50	mitogen-activated protein kinase 8	Homo sapiens	81-84
18606486-10	2008	The results suggest that in PC3 cells, desipramine caused apoptosis via inducing JNK-associated caspase-3 activation, and [Ca2+]i rises may slow down or alleviate desipramine-induced cytotoxicity.	Desipramine	39-50	caspase 3	Homo sapiens	96-105
18606486-10	2008	The results suggest that in PC3 cells, desipramine caused apoptosis via inducing JNK-associated caspase-3 activation, and [Ca2+]i rises may slow down or alleviate desipramine-induced cytotoxicity.	Desipramine	163-174	chromobox 8	Homo sapiens	28-31
18478316-1	2008	PURPOSE: It has been reported that telithromycin is primarily metabolized via hepatic CYP3A1/2 in rats, the expression and/or mRNA level of hepatic CYP3A1/2 increase in rat model of diabetes mellitus induced by alloxan (DMIA) or streptozotocin (DMIS), and intestinal CYP3A1/2 enzyme activity decreases in rat model of DMIS.	Desipramine	245-249	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	148-154
18601743-6	2008	Short-term treatment (6 hours) with reboxetine or desipramine reduced total BDNF, whereas long-term treatment (48 hours) significantly increased total BDNF mRNA levels.	Desipramine	50-61	brain derived neurotrophic factor	Homo sapiens	76-80
18509851-4	2008	The influence of distinct classes of antidepressants, namely, electroconvulsive seizure, fluoxetine, tranylcypromine, and desipramine, on the gene expression of MMP-2, MMP-9, and TIMPs 1-4 in the hippocampus was determined using radioactive in situ hybridization.	Desipramine	122-133	matrix metallopeptidase 2	Rattus norvegicus	161-166
18509851-4	2008	The influence of distinct classes of antidepressants, namely, electroconvulsive seizure, fluoxetine, tranylcypromine, and desipramine, on the gene expression of MMP-2, MMP-9, and TIMPs 1-4 in the hippocampus was determined using radioactive in situ hybridization.	Desipramine	122-133	matrix metallopeptidase 9	Rattus norvegicus	168-173
18509851-4	2008	The influence of distinct classes of antidepressants, namely, electroconvulsive seizure, fluoxetine, tranylcypromine, and desipramine, on the gene expression of MMP-2, MMP-9, and TIMPs 1-4 in the hippocampus was determined using radioactive in situ hybridization.	Desipramine	122-133	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	179-188
17667959-2	2008	First, CYP2C19 converts imipramine into the active metabolite desipramine, which is then inactivated by CYP2D6.	Desipramine	62-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	7-14
18420781-1	2008	There are documented clinical drug-drug interactions between bupropion and the CYP2D6-metabolized drug desipramine resulting in marked (5-fold) increases in desipramine exposure.	Desipramine	103-114	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	79-85
18420781-1	2008	There are documented clinical drug-drug interactions between bupropion and the CYP2D6-metabolized drug desipramine resulting in marked (5-fold) increases in desipramine exposure.	Desipramine	157-168	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	79-85
18420781-7	2008	This work indicates that the reductive metabolites of bupropion are potent competitive CYP2D6 inhibitors in vivo and provides a mechanistic explanation for the clinical drug-drug interaction between bupropion and desipramine.	Desipramine	213-224	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	87-93
18266934-5	2008	drSERT has a higher affinity towards compounds of the imipramine class, desipramine in particular, exhibiting a 35-fold increased affinity compared to hSERT.	Desipramine	72-83	solute carrier family 6 member 4	Homo sapiens	151-156
17727882-0	2008	Enhanced norepinephrine output during long-term desipramine treatment: a possible role for the extraneuronal monoamine transporter (SLC22A3).	Desipramine	48-59	solute carrier family 22 member 3	Homo sapiens	132-139
18438645-6	2008	Moreover, at the neural level, DMI treatment led to a decrease in FST-induced c-fos messenger RNA levels in medial prefrontal cortex (PFC) and paraventricular nucleus of the hypothalamus (PVN) in LR but not HR animals.	Desipramine	31-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
17667959-2	2008	First, CYP2C19 converts imipramine into the active metabolite desipramine, which is then inactivated by CYP2D6.	Desipramine	62-73	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	104-110
17667959-3	2008	This retrospective single center study aimed to prove whether CYP2C19 and ample CYP2D6 genotyping (taking into consideration four null alleles and three decreased-activity alleles) could be used to predict imipramine and desipramine plasma concentrations in depressed patients, and whether genotype-based drug dose recommendations might assist in the early management of imipramine pharmacotherapy.	Desipramine	221-232	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	62-69
17667959-3	2008	This retrospective single center study aimed to prove whether CYP2C19 and ample CYP2D6 genotyping (taking into consideration four null alleles and three decreased-activity alleles) could be used to predict imipramine and desipramine plasma concentrations in depressed patients, and whether genotype-based drug dose recommendations might assist in the early management of imipramine pharmacotherapy.	Desipramine	221-232	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	80-86
17667959-5	2008	Desipramine and imipramine+desipramine plasma concentration per drug dose unit, imipramine dose at steady state, and imipramine dose requirement significantly depended on CYP2D6 genotype (Kruskal-Wallis test, P&lt;0.0001).	Desipramine	0-11	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	171-177
17667959-5	2008	Desipramine and imipramine+desipramine plasma concentration per drug dose unit, imipramine dose at steady state, and imipramine dose requirement significantly depended on CYP2D6 genotype (Kruskal-Wallis test, P&lt;0.0001).	Desipramine	27-38	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	171-177
17667959-8	2008	Our protocol for CYP2D6 genotyping will thus importantly aid in the prediction of imipramine metabolism, allowing for the use of an adjusted starting dose and faster achievement of predefined imipramine+desipramine plasma levels in all genetic patient subgroups.	Desipramine	203-214	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	17-23
18342622-4	2008	Dopamine transporter (DAT) mutant flies or flies treated with the DAT inhibitor desipramine exhibited poor memory retention.	Desipramine	80-91	Dopamine transporter	Drosophila melanogaster	66-69
18420612-7	2008	The level of DMI had less effect on plasma concentrations of IGF-I at d 14 (72.2 vs. 57.1 ng/mL).	Desipramine	13-16	insulin like growth factor 1	Bos taurus	61-66
18420612-14	2008	Altering the ME or DMI components of the pasture-based diets produced changes in plasma IGF-I concentrations that did not become stabilized for 3 wk, but were then highly repeatable for individual cows within each dietary group.	Desipramine	19-22	insulin like growth factor 1	Bos taurus	88-93
17981365-2	2008	The co-administration of local anesthetics with desipramine reversed the behavioral sensitization and down-regulation of NET function induced by desipramine.	Desipramine	48-59	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	121-124
18243568-7	2008	Fluoxetine and desipramine administration significantly attenuated plasma ACTH and CORT levels in male and female Avpr1b KO mice when compared to their wild-type counterparts.	Desipramine	15-26	cortistatin	Mus musculus	83-87
18243568-7	2008	Fluoxetine and desipramine administration significantly attenuated plasma ACTH and CORT levels in male and female Avpr1b KO mice when compared to their wild-type counterparts.	Desipramine	15-26	arginine vasopressin receptor 1B	Mus musculus	114-120
18310890-5	2008	Imipramine, desipramine, mazindol, and GBR12909 competitively inhibited PROG 21-hydroxylation mediated by CYP2D4 and/or CYP2D6, and all psychotropic drugs inhibited ALLO 21-hydroxylation mediated by CYP2D4 and/or CYP2D6.	Desipramine	12-23	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	106-112
18310890-5	2008	Imipramine, desipramine, mazindol, and GBR12909 competitively inhibited PROG 21-hydroxylation mediated by CYP2D4 and/or CYP2D6, and all psychotropic drugs inhibited ALLO 21-hydroxylation mediated by CYP2D4 and/or CYP2D6.	Desipramine	12-23	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	120-126
18310890-5	2008	Imipramine, desipramine, mazindol, and GBR12909 competitively inhibited PROG 21-hydroxylation mediated by CYP2D4 and/or CYP2D6, and all psychotropic drugs inhibited ALLO 21-hydroxylation mediated by CYP2D4 and/or CYP2D6.	Desipramine	12-23	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	199-205
18310890-5	2008	Imipramine, desipramine, mazindol, and GBR12909 competitively inhibited PROG 21-hydroxylation mediated by CYP2D4 and/or CYP2D6, and all psychotropic drugs inhibited ALLO 21-hydroxylation mediated by CYP2D4 and/or CYP2D6.	Desipramine	12-23	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	213-219
18310890-6	2008	The inhibition constants (Ki values) of imipramine, desipramine, and mazindol against the 21-hydroxylation of PROG and ALLO by CYP2D6 were lower than those by CYP2D4.	Desipramine	52-63	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	127-133
18310890-6	2008	The inhibition constants (Ki values) of imipramine, desipramine, and mazindol against the 21-hydroxylation of PROG and ALLO by CYP2D6 were lower than those by CYP2D4.	Desipramine	52-63	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	159-165
17981365-0	2008	Down-regulation of norepinephrine transporter expression on membrane surface induced by chronic administration of desipramine and the antagonism by co-administration of local anesthetics in mice.	Desipramine	114-125	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	19-45
17981365-1	2008	We have previously shown that chronic administration of the antidepressant desipramine, a norepinephrine transporter (NET) inhibitor to mice markedly enhanced convulsions induced by local anesthetics and that behavioral sensitization may be relevant to decreased [(3)H]norepinephrine uptake by the isolated hippocampus.	Desipramine	75-86	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	90-116
17981365-1	2008	We have previously shown that chronic administration of the antidepressant desipramine, a norepinephrine transporter (NET) inhibitor to mice markedly enhanced convulsions induced by local anesthetics and that behavioral sensitization may be relevant to decreased [(3)H]norepinephrine uptake by the isolated hippocampus.	Desipramine	75-86	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	118-121
17981365-2	2008	The co-administration of local anesthetics with desipramine reversed the behavioral sensitization and down-regulation of NET function induced by desipramine.	Desipramine	145-156	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	121-124
17981365-3	2008	The present study aimed to elucidate whether chronic treatment with desipramine regulates the expression of NET protein examined in membrane fractions in various brain regions and whether co-administration of local anesthetics affects the desipramine-induced alteration of NET expression.	Desipramine	68-79	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	108-111
17981365-3	2008	The present study aimed to elucidate whether chronic treatment with desipramine regulates the expression of NET protein examined in membrane fractions in various brain regions and whether co-administration of local anesthetics affects the desipramine-induced alteration of NET expression.	Desipramine	239-250	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	273-276
17981365-9	2008	However, administration of desipramine significantly reduced the amount of immunoreactive NET in the cell-surface protein fraction.	Desipramine	27-38	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	90-93
17981365-11	2008	These results indicate that the NET down-regulation indicated by the reduction of [(3)H]nisoxetine binding was induced by administration of desipramine via decrease of NET localization on the cell surface.	Desipramine	140-151	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	32-35
17981365-11	2008	These results indicate that the NET down-regulation indicated by the reduction of [(3)H]nisoxetine binding was induced by administration of desipramine via decrease of NET localization on the cell surface.	Desipramine	140-151	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	168-171
17981365-12	2008	The antagonistic actions of local anesthetics against NET down-regulation by desipramine were related to alterations of the cell-surface localization of NET.	Desipramine	77-88	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	54-57
17981365-12	2008	The antagonistic actions of local anesthetics against NET down-regulation by desipramine were related to alterations of the cell-surface localization of NET.	Desipramine	77-88	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	153-156
18171937-6	2008	Similar treatment with the norepinephrine transporter (NET) inhibitor, desipramine, did not adversely affect adult behavior, suggesting that 5-HT and norepinephrine (NE) do not share the same effects on brain development.	Desipramine	71-82	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	27-53
18028907-9	2008	GRK2/3 levels remained unchanged and increased, respectively, in the cortex and the hippocampus, after chronic exposure to desipramine.	Desipramine	123-134	beta-adrenergic receptor kinase 1	Cavia porcellus	0-6
18028907-11	2008	On the whole, the present data suggest that alpha(2)-adrenoceptor and mu-opioid receptor expression and transcription are similarly influenced by chronic treatment with desipramine, in the guinea pig cortex and hippocampus.	Desipramine	169-180	mu-type opioid receptor	Cavia porcellus	70-88
18048068-0	2008	The differential regulation of BDNF and TrkB levels in juvenile rats after four days of escitalopram and desipramine treatment.	Desipramine	105-116	brain-derived neurotrophic factor	Rattus norvegicus	31-35
18048068-0	2008	The differential regulation of BDNF and TrkB levels in juvenile rats after four days of escitalopram and desipramine treatment.	Desipramine	105-116	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	40-44
18974610-6	2008	In addition, the method was applied to the CYP2D6-mediated desipramine-quinidine interaction: the predicted 6.4-fold increase of desipramine AUC by quinidine was consistent with the observed 6.7-fold increase of AUC in the clinical drug-drug interaction study.	Desipramine	59-70	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	43-49
17356567-0	2007	The antidepressant desipramine requires the ABCB1 (Mdr1)-type p-glycoprotein to upregulate the glucocorticoid receptor in mice.	Desipramine	19-30	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	44-49
17356567-0	2007	The antidepressant desipramine requires the ABCB1 (Mdr1)-type p-glycoprotein to upregulate the glucocorticoid receptor in mice.	Desipramine	19-30	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	51-55
17356567-0	2007	The antidepressant desipramine requires the ABCB1 (Mdr1)-type p-glycoprotein to upregulate the glucocorticoid receptor in mice.	Desipramine	19-30	phosphoglycolate phosphatase	Mus musculus	62-76
17356567-0	2007	The antidepressant desipramine requires the ABCB1 (Mdr1)-type p-glycoprotein to upregulate the glucocorticoid receptor in mice.	Desipramine	19-30	nuclear receptor subfamily 3, group C, member 1	Mus musculus	95-118
17356567-4	2007	Here, the tricyclic antidepressant, desipramine (20 mg/kg/day, i.p., for seven days), was administered to abcb1ab MDR PGP knockout mice (congenic on the FVB/N background strain) and to FVB/N controls.	Desipramine	36-47	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	106-111
17356567-4	2007	Here, the tricyclic antidepressant, desipramine (20 mg/kg/day, i.p., for seven days), was administered to abcb1ab MDR PGP knockout mice (congenic on the FVB/N background strain) and to FVB/N controls.	Desipramine	36-47	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	114-117
17356567-4	2007	Here, the tricyclic antidepressant, desipramine (20 mg/kg/day, i.p., for seven days), was administered to abcb1ab MDR PGP knockout mice (congenic on the FVB/N background strain) and to FVB/N controls.	Desipramine	36-47	phosphoglycolate phosphatase	Mus musculus	118-121
17356567-6	2007	In FVB/N controls, desipramine induced a significant upregulation of GR mRNA in the CA1 region (+31%; p=0.045); in contrast, in abcb1ab (-/-) mice, desipramine induced a significant downregulation of GR mRNA in the CA1 region (-45%; p=0.004).	Desipramine	19-30	nuclear receptor subfamily 3, group C, member 1	Mus musculus	69-71
17356567-6	2007	In FVB/N controls, desipramine induced a significant upregulation of GR mRNA in the CA1 region (+31%; p=0.045); in contrast, in abcb1ab (-/-) mice, desipramine induced a significant downregulation of GR mRNA in the CA1 region (-45%; p=0.004).	Desipramine	19-30	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	128-133
17356567-6	2007	In FVB/N controls, desipramine induced a significant upregulation of GR mRNA in the CA1 region (+31%; p=0.045); in contrast, in abcb1ab (-/-) mice, desipramine induced a significant downregulation of GR mRNA in the CA1 region (-45%; p=0.004).	Desipramine	19-30	nuclear receptor subfamily 3, group C, member 1	Mus musculus	200-202
17356567-8	2007	Desipramine decreased corticosterone levels in both FVB/N controls and in abcb1ab (-/-) mice, but in abcb1ab (-/-) mice the effects were smaller.	Desipramine	0-11	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	74-79
17356567-10	2007	Finally, desipramine reduced Mdr1a mRNA expression across all hippocampus areas (-9 to -23%), but had no effect on 11beta-HSD1 mRNA expression.	Desipramine	9-20	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	29-34
17979223-5	2007	The NET blocker desipramine reduced the uptake of [ (131)I] 12a only to a small extent, further suggesting a limited role of NET in its binding and accumulation.	Desipramine	16-27	solute carrier family 6 member 2	Homo sapiens	4-7
18324519-5	2008	Pre-treatment with ROS scavenger NAC, ASMase inhibitor desipramine or JNK inhibitor SP600125 was found to effectively prohibit UVA-induced apoptosis and desipramine markedly blocked phosphorylation of JNK.	Desipramine	55-66	sphingomyelin phosphodiesterase 1	Homo sapiens	38-44
18324519-5	2008	Pre-treatment with ROS scavenger NAC, ASMase inhibitor desipramine or JNK inhibitor SP600125 was found to effectively prohibit UVA-induced apoptosis and desipramine markedly blocked phosphorylation of JNK.	Desipramine	55-66	mitogen-activated protein kinase 8	Homo sapiens	201-204
18324519-5	2008	Pre-treatment with ROS scavenger NAC, ASMase inhibitor desipramine or JNK inhibitor SP600125 was found to effectively prohibit UVA-induced apoptosis and desipramine markedly blocked phosphorylation of JNK.	Desipramine	153-164	synuclein alpha	Homo sapiens	33-36
18324519-5	2008	Pre-treatment with ROS scavenger NAC, ASMase inhibitor desipramine or JNK inhibitor SP600125 was found to effectively prohibit UVA-induced apoptosis and desipramine markedly blocked phosphorylation of JNK.	Desipramine	153-164	sphingomyelin phosphodiesterase 1	Homo sapiens	38-44
18324519-5	2008	Pre-treatment with ROS scavenger NAC, ASMase inhibitor desipramine or JNK inhibitor SP600125 was found to effectively prohibit UVA-induced apoptosis and desipramine markedly blocked phosphorylation of JNK.	Desipramine	153-164	mitogen-activated protein kinase 8	Homo sapiens	70-73
18324519-5	2008	Pre-treatment with ROS scavenger NAC, ASMase inhibitor desipramine or JNK inhibitor SP600125 was found to effectively prohibit UVA-induced apoptosis and desipramine markedly blocked phosphorylation of JNK.	Desipramine	153-164	mitogen-activated protein kinase 8	Homo sapiens	201-204
17166518-5	2008	They received desipramine for 6 weeks in order to simulate the length of time and dosing used previously to obtain an IR-1 down-regulation and a therapeutic response in depressed patients.	Desipramine	14-25	nischarin	Homo sapiens	118-122
17976922-9	2008	We conclude that pharmacological blockade of CB1 signaling shares antidepressant-like behavioral effects with desipramine, but reveals opposite effects on HPA axis activity.	Desipramine	110-121	cannabinoid receptor 1 (brain)	Mus musculus	45-48
17850785-5	2007	Competition binding studies using [(3)H]nisoxetine and [(3)H]citalopram showed desipramine to be 25 times more selective for the rat norepinephrine as compared to serotonin transporter (6.2 nM vs. 158 nM) whereas desmethyldesipramine is 12 times more selective for the serotonin over the norepinephrine transporter (12.8 nM vs. 153 nM).	Desipramine	79-90	solute carrier family 6 member 2	Rattus norvegicus	288-314
17850785-6	2007	Interestingly, the affinity of desmethyldesipramine for the serotonin transporter is similar to the affinity of desipramine for the norepinephrine transporter.	Desipramine	40-51	solute carrier family 6 member 4	Rattus norvegicus	60-81
17850785-8	2007	Thus, the pharmacological effects of desipramine in rats may be attributed not only to the inhibition of the norepinephrine transporter by desipramine but also to the inhibition of serotonin transporter by the active metabolite desmethyldesipramine.	Desipramine	37-48	solute carrier family 6 member 2	Rattus norvegicus	109-135
17850785-8	2007	Thus, the pharmacological effects of desipramine in rats may be attributed not only to the inhibition of the norepinephrine transporter by desipramine but also to the inhibition of serotonin transporter by the active metabolite desmethyldesipramine.	Desipramine	37-48	solute carrier family 6 member 4	Rattus norvegicus	181-202
17850785-8	2007	Thus, the pharmacological effects of desipramine in rats may be attributed not only to the inhibition of the norepinephrine transporter by desipramine but also to the inhibition of serotonin transporter by the active metabolite desmethyldesipramine.	Desipramine	139-150	solute carrier family 6 member 2	Rattus norvegicus	109-135
18974610-6	2008	In addition, the method was applied to the CYP2D6-mediated desipramine-quinidine interaction: the predicted 6.4-fold increase of desipramine AUC by quinidine was consistent with the observed 6.7-fold increase of AUC in the clinical drug-drug interaction study.	Desipramine	129-140	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	43-49
17584982-5	2007	We demonstrated that the LPS induced TNF-alpha response is in direct correlation with the biophase level of NE, as it is significantly higher when the release of NE of vesicular origin was completely inhibited in an animal model of depression (reserpine treatment) and it is significantly lower in the case of increasing biophase levels of NE by genetic (NET-KO) or chemical (desipramine) disruption of NE reuptake.	Desipramine	376-387	toll-like receptor 4	Mus musculus	25-28
17584982-5	2007	We demonstrated that the LPS induced TNF-alpha response is in direct correlation with the biophase level of NE, as it is significantly higher when the release of NE of vesicular origin was completely inhibited in an animal model of depression (reserpine treatment) and it is significantly lower in the case of increasing biophase levels of NE by genetic (NET-KO) or chemical (desipramine) disruption of NE reuptake.	Desipramine	376-387	tumor necrosis factor	Mus musculus	37-46
17584982-6	2007	IL-10 was changed inversely to TNF-alpha levels only in the desipramine-treated animals.	Desipramine	60-71	interleukin 10	Mus musculus	0-5
17584982-6	2007	IL-10 was changed inversely to TNF-alpha levels only in the desipramine-treated animals.	Desipramine	60-71	tumor necrosis factor	Mus musculus	31-40
17690258-3	2007	We determined the crystal structure at 2.9 angstroms of the bacterial leucine transporter (LeuT), a homolog of SERT, NET, and DAT, in complex with leucine and the antidepressant desipramine.	Desipramine	178-189	Leucine transport, high	Homo sapiens	70-89
17690258-3	2007	We determined the crystal structure at 2.9 angstroms of the bacterial leucine transporter (LeuT), a homolog of SERT, NET, and DAT, in complex with leucine and the antidepressant desipramine.	Desipramine	178-189	Leucine transport, high	Homo sapiens	91-95
17690258-3	2007	We determined the crystal structure at 2.9 angstroms of the bacterial leucine transporter (LeuT), a homolog of SERT, NET, and DAT, in complex with leucine and the antidepressant desipramine.	Desipramine	178-189	solute carrier family 6 member 4	Homo sapiens	111-115
17690258-3	2007	We determined the crystal structure at 2.9 angstroms of the bacterial leucine transporter (LeuT), a homolog of SERT, NET, and DAT, in complex with leucine and the antidepressant desipramine.	Desipramine	178-189	solute carrier family 6 member 3	Homo sapiens	126-129
17690258-7	2007	Mutagenesis experiments on human SERT and DAT indicate that both the desipramine-binding site and its inhibition mechanism are probably conserved in the human neurotransmitter transporters.	Desipramine	69-80	solute carrier family 6 member 4	Homo sapiens	33-37
17690258-7	2007	Mutagenesis experiments on human SERT and DAT indicate that both the desipramine-binding site and its inhibition mechanism are probably conserved in the human neurotransmitter transporters.	Desipramine	69-80	solute carrier family 6 member 3	Homo sapiens	42-45
17477857-16	2007	In vitro, desipramine and fluoxetine dose-dependently inhibited the release of TNF-alpha from LPS-treated monocytes.	Desipramine	10-21	tumor necrosis factor	Rattus norvegicus	79-88
17634380-3	2007	Here, we show that, at baseline, CREB(alpha delta) mutant mice exhibited increased hippocampal cell proliferation and neurogenesis compared with wild-type (WT) controls, effects similar to those observed in WT mice after chronic desipramine (DMI) administration.	Desipramine	229-240	cAMP responsive element binding protein 1	Mus musculus	33-37
17634380-3	2007	Here, we show that, at baseline, CREB(alpha delta) mutant mice exhibited increased hippocampal cell proliferation and neurogenesis compared with wild-type (WT) controls, effects similar to those observed in WT mice after chronic desipramine (DMI) administration.	Desipramine	242-245	cAMP responsive element binding protein 1	Mus musculus	33-37
17382299-3	2007	At nanomolar concentrations, CLOM and DMI increased expression of phospho-CREB (cyclic AMP response element binding protein).	Desipramine	38-41	cAMP responsive element binding protein 1	Homo sapiens	74-78
17540003-7	2007	We found that acidic sphingomyelinase activity was induced by acidic extracellular pH and that the specific acidic sphingomyelinase inhibitors (perhexiline and desipramine) and siRNA targeting aSMase/smpd1 could inhibit acidic extracellular pH-induced matrix metalloproteinase-9 expression.	Desipramine	160-171	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	193-199
17540003-7	2007	We found that acidic sphingomyelinase activity was induced by acidic extracellular pH and that the specific acidic sphingomyelinase inhibitors (perhexiline and desipramine) and siRNA targeting aSMase/smpd1 could inhibit acidic extracellular pH-induced matrix metalloproteinase-9 expression.	Desipramine	160-171	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	200-205
17540003-7	2007	We found that acidic sphingomyelinase activity was induced by acidic extracellular pH and that the specific acidic sphingomyelinase inhibitors (perhexiline and desipramine) and siRNA targeting aSMase/smpd1 could inhibit acidic extracellular pH-induced matrix metalloproteinase-9 expression.	Desipramine	160-171	matrix metallopeptidase 9	Mus musculus	252-278
17510525-0	2007	Desipramine activated Bcl-2 expression and inhibited lipopolysaccharide-induced apoptosis in hippocampus-derived adult neural stem cells.	Desipramine	0-11	BCL2, apoptosis regulator	Rattus norvegicus	22-27
17417877-4	2007	FCS-binding studies with the fluorescently labeled ligand Alexa532-noradrenaline (Alexa532-NA) binding to beta2-AR of C6 cells showed a significant reduction in total beta2-AR binding after preincubation with hyperforin and hyperoside for 3 days, respectively, which was also found for DMI.	Desipramine	286-289	adrenoceptor beta 2	Homo sapiens	106-114
17417877-4	2007	FCS-binding studies with the fluorescently labeled ligand Alexa532-noradrenaline (Alexa532-NA) binding to beta2-AR of C6 cells showed a significant reduction in total beta2-AR binding after preincubation with hyperforin and hyperoside for 3 days, respectively, which was also found for DMI.	Desipramine	286-289	adrenoceptor beta 2	Homo sapiens	167-175
17267168-0	2007	Desipramine-induced Ca2+ movement and cytotoxicity in PC3 human prostate cancer cells.	Desipramine	0-11	carbonic anhydrase 2	Homo sapiens	20-23
17267168-0	2007	Desipramine-induced Ca2+ movement and cytotoxicity in PC3 human prostate cancer cells.	Desipramine	0-11	chromobox 8	Homo sapiens	54-57
17267168-12	2007	Collectively, the data suggest that in PC3 cells, desipramine induced a [Ca(2+)](i) increase by causing Ca(2+) release from endoplasmic reticulum in a phospholipase C-independent fashion and by inducing Ca(2+) influx.	Desipramine	50-61	chromobox 8	Homo sapiens	39-42
17352382-5	2007	Both, hypoosmotic ROS generation and p47(phox) serine phosphorylation were sensitive to the acidic sphingomyelinase inhibitors AY9944 and desipramine, the protein kinase C (PKC)zeta-inhibitory pseudosubstrate peptide, the NMDA receptor antagonist MK-801 and the intracellular Ca(2+) chelator BAPTA-AM.	Desipramine	138-149	NSFL1 (p97) cofactor (p47)	Mus musculus	37-40
17510525-5	2007	First, we demonstrated that the expression of Bcl-2 mRNA and nestin in 2 microM DP-treated NSCs were up-regulated and detected by real-time reverse transcriptase polymerase chain reaction (RT-PCR).	Desipramine	80-82	BCL2, apoptosis regulator	Rattus norvegicus	46-51
17510525-6	2007	The results of Western blotting and immunofluorescent study confirmed that Bcl-2 protein expression was significantly increased in Day 3 DP-treated NSCs.	Desipramine	137-139	BCL2, apoptosis regulator	Rattus norvegicus	75-80
17510525-7	2007	Using the Bcl-2 small interfering RNA (siRNA) method, our results further showed that DP protects the lipopolysaccharide (LPS)-induced apoptosis in NSCs, in part by activating the expression of Bcl-2.	Desipramine	86-88	BCL2, apoptosis regulator	Rattus norvegicus	10-15
17510525-7	2007	Using the Bcl-2 small interfering RNA (siRNA) method, our results further showed that DP protects the lipopolysaccharide (LPS)-induced apoptosis in NSCs, in part by activating the expression of Bcl-2.	Desipramine	86-88	BCL2, apoptosis regulator	Rattus norvegicus	194-199
17510525-8	2007	Furthermore, DP treatment significantly inhibited the induction of proinflammatory factor interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha in the culture medium of LPS-treated NSCs mediated by Bcl-2 modulation.	Desipramine	13-15	interleukin 1 beta	Rattus norvegicus	90-112
17510525-8	2007	Furthermore, DP treatment significantly inhibited the induction of proinflammatory factor interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha in the culture medium of LPS-treated NSCs mediated by Bcl-2 modulation.	Desipramine	13-15	interleukin 6	Rattus norvegicus	114-151
17510525-8	2007	Furthermore, DP treatment significantly inhibited the induction of proinflammatory factor interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha in the culture medium of LPS-treated NSCs mediated by Bcl-2 modulation.	Desipramine	13-15	BCL2, apoptosis regulator	Rattus norvegicus	206-211
17510525-9	2007	The results of high performance liquid chromatography coupled to electrochemical detection further confirmed that DP significantly increased the functional production of serotonin (26+/-3.5 microM, DP-treated 96 h) and noradrenaline (50+/-8.9 microM, DP-treated 96 h) in NSCs through activation of the MAPK/ERK pathway and partially mediated by Bcl-2.	Desipramine	114-116	Eph receptor B1	Rattus norvegicus	307-310
17510525-9	2007	The results of high performance liquid chromatography coupled to electrochemical detection further confirmed that DP significantly increased the functional production of serotonin (26+/-3.5 microM, DP-treated 96 h) and noradrenaline (50+/-8.9 microM, DP-treated 96 h) in NSCs through activation of the MAPK/ERK pathway and partially mediated by Bcl-2.	Desipramine	114-116	BCL2, apoptosis regulator	Rattus norvegicus	345-350
17510525-10	2007	In conclusion, the present results indicate that DP can increase neuroprotection ability by inhibiting the LPS-induced inflammatory process in NSCs via the modulation of Bcl-2 expression, as confirmed by the siRNA method.	Desipramine	49-51	BCL2, apoptosis regulator	Rattus norvegicus	170-175
16680561-2	2007	The purpose of this study was to evaluate the effect of cinacalcet on CYP2D6 activity, using desipramine as a probe substrate, in healthy subjects.	Desipramine	93-104	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	70-76
17121970-10	2007	Alpha-amylase supplementation increased DMI (P = 0.05) and ADG (P = 0.03) during the initial 28 d on feed and carcass-adjusted ADG (P = 0.04) across corn processing methods.	Desipramine	40-43	alpha-amylase	Zea mays	0-13
17194442-4	2007	Paroxetine increased the interaction of GluR1 with Rab4A, and desipramine markedly increased the interaction of GluR1 with SAP97.	Desipramine	62-73	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	112-117
17194442-4	2007	Paroxetine increased the interaction of GluR1 with Rab4A, and desipramine markedly increased the interaction of GluR1 with SAP97.	Desipramine	62-73	discs large MAGUK scaffold protein 1	Rattus norvegicus	123-128
17055479-8	2006	Levels of G protein-coupled receptor kinase 2/3 and of inhibitory G(i/o) proteins were significantly reduced in the myenteric plexus after chronic treatment with desipramine.	Desipramine	162-173	beta-adrenergic receptor kinase 1	Cavia porcellus	10-47
16697351-5	2007	We also demonstrate that loss of BDNF in both male and female mice attenuates the actions of the antidepressant desipramine in the forced swim test.	Desipramine	112-123	brain derived neurotrophic factor	Mus musculus	33-37
17071817-7	2007	Other TCAs, such as amitriptyline, desipramine, and imipramine, also inhibited Kir4.1 currents in a similar voltage-dependent fashion.	Desipramine	35-46	potassium inwardly rectifying channel subfamily J member 10	Homo sapiens	79-85
19356015-2	2007	The CYP form with the lowest in vitro K(i) is evaluated first clinically, employing a suitable probe drug like midazolam (CYP3A4), theophylline (CYP1A2), (S)-warfarin (CYP2C9) and desipramine (CYP2D6), and the NCE is classified as a "none", "weak", "moderate", or "strong" inhibitor.	Desipramine	180-191	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	4-7
17069850-11	2007	The survival signal was further confirmed by increased phosphorylation of AKT and enhanced induction of expression of Bcl-2 during adaptation and its reversal with desipramine.	Desipramine	164-175	AKT serine/threonine kinase 1	Rattus norvegicus	74-77
17069850-11	2007	The survival signal was further confirmed by increased phosphorylation of AKT and enhanced induction of expression of Bcl-2 during adaptation and its reversal with desipramine.	Desipramine	164-175	BCL2, apoptosis regulator	Rattus norvegicus	118-123
16388933-7	2006	Interestingly, exposure to a lower concentration (1 microM) of the antidepressants tended to increase T-cell-derived IL-10 production, with significant effects elicited by the noradrenaline reuptake inhibitors reboxetine and desipramine.	Desipramine	225-236	interleukin 10	Homo sapiens	117-122
16710317-4	2006	Furthermore, chronic desipramine treatment resulted in a reduction in both secretion of corticosterone and the induction of the immediate early gene c-fos in the medial dorsal parvocellular region of the paraventricular nucleus of the hypothalamus (PVN) following a 5 min exposure to swim stress.	Desipramine	21-32	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	149-154
16710317-5	2006	Acute treatment with the CB(1) receptor antagonist, AM251 (1 mg/kg), before exposure to swim stress, completely occluded the ability of desipramine to reduce both corticosterone secretion and induction of c-fos expression in the PVN.	Desipramine	136-147	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	205-210
16941481-0	2006	Desipramine prevents the sustained increase in corticotropin-releasing hormone-like immunoreactivity induced by repeated immobilization stress in the rat central extended amygdala.	Desipramine	0-11	corticotropin releasing hormone	Rattus norvegicus	47-78
16941481-6	2006	The concomitant administration of desipramine (DMI), a specific noradrenaline uptake inhibitor, fully prevented the RIS-induced increase in CRH expression.	Desipramine	34-45	corticotropin releasing hormone	Rattus norvegicus	140-143
16941481-6	2006	The concomitant administration of desipramine (DMI), a specific noradrenaline uptake inhibitor, fully prevented the RIS-induced increase in CRH expression.	Desipramine	47-50	corticotropin releasing hormone	Rattus norvegicus	140-143
16941481-7	2006	RIS also induced an increase of CRH-LI expression in the PVN that was prevented by the concomitant DMI administration.	Desipramine	99-102	corticotropin releasing hormone	Rattus norvegicus	32-35
16803890-7	2006	The amphiphilic compound desipramine, a frequently employed inhibitor of acid sphingomyelinase (ASMase), blocked PGE(2) production.	Desipramine	25-36	sphingomyelin phosphodiesterase 1	Homo sapiens	73-94
16926120-6	2006	Cotreatment of Ad-GFPApoptin-infected cells with the ASMase inhibitor desipramine (2.5 muM) attenuated (30%; P&lt;0.01) apoptin-induced cell death.	Desipramine	70-81	sphingomyelin phosphodiesterase 1	Homo sapiens	53-59
16844100-12	2006	The highest potency at Ca(v)2.2 tricyclic antidepressant identified was desipramine.	Desipramine	72-83	calcium voltage-gated channel subunit alpha1 B	Homo sapiens	23-31
16842762-6	2006	Following an acute injection, all three drugs tested: fluoxetine, desipramine and TCP decreased total BDNF mRNA (exon V) as well as exon IV mRNA, while no significant effect was recorded for exons I and III mRNAs.	Desipramine	66-77	brain-derived neurotrophic factor	Rattus norvegicus	102-106
16803890-7	2006	The amphiphilic compound desipramine, a frequently employed inhibitor of acid sphingomyelinase (ASMase), blocked PGE(2) production.	Desipramine	25-36	sphingomyelin phosphodiesterase 1	Homo sapiens	96-102
16803890-9	2006	Further investigations revealed that desipramine down-regulated acid ceramidase (AC), but not sphingosine kinase, at the protein level.	Desipramine	37-48	N-acylsphingosine amidohydrolase 1	Homo sapiens	64-79
16803890-14	2006	In addition, the results of this study warrant careful reconsideration of desipramine as a specific inhibitor for ASMase.	Desipramine	74-85	sphingomyelin phosphodiesterase 1	Homo sapiens	114-120
16725121-0	2006	Down-regulation of norepinephrine transporter function induced by chronic administration of desipramine linking to the alteration of sensitivity of local-anesthetics-induced convulsions and the counteraction by co-administration with local anesthetics.	Desipramine	92-103	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	19-45
16901483-0	2006	New insights on the use of desipramine as an inhibitor for acid ceramidase.	Desipramine	27-38	N-acylsphingosine amidohydrolase 1	Homo sapiens	59-74
16901483-1	2006	Treatment of different cancer cell lines with desipramine induced a time- and dose-dependent downregulation of acid ceramidase.	Desipramine	46-57	N-acylsphingosine amidohydrolase 1	Homo sapiens	111-126
16901483-2	2006	Desipramine"s effect on acid ceramidase appeared specific for amphiphilic agents (desipramine, chlorpromazine, and chloroquine) but not other lysomotropic agents such as ammonium chloride and bafilomycin A1, and was not transcriptionally regulated.	Desipramine	0-11	N-acylsphingosine amidohydrolase 1	Homo sapiens	24-39
16901483-2	2006	Desipramine"s effect on acid ceramidase appeared specific for amphiphilic agents (desipramine, chlorpromazine, and chloroquine) but not other lysomotropic agents such as ammonium chloride and bafilomycin A1, and was not transcriptionally regulated.	Desipramine	82-93	N-acylsphingosine amidohydrolase 1	Homo sapiens	24-39
16901483-3	2006	The cathepsin B/L inhibitor, CA074ME, but not the cathepsin D inhibitor, pepstatin A, blocked desipramine"s effect on acid ceramidase.	Desipramine	94-105	cathepsin B	Homo sapiens	4-15
16901483-3	2006	The cathepsin B/L inhibitor, CA074ME, but not the cathepsin D inhibitor, pepstatin A, blocked desipramine"s effect on acid ceramidase.	Desipramine	94-105	N-acylsphingosine amidohydrolase 1	Homo sapiens	118-133
16901483-4	2006	Desipramine led to a more pronounced downregulation of sphingosine compared to ceramide suggesting acid ceramidase inhibition is important to desipramine"s mechanism of action.	Desipramine	0-11	N-acylsphingosine amidohydrolase 1	Homo sapiens	99-114
16901483-4	2006	Desipramine led to a more pronounced downregulation of sphingosine compared to ceramide suggesting acid ceramidase inhibition is important to desipramine"s mechanism of action.	Desipramine	142-153	N-acylsphingosine amidohydrolase 1	Homo sapiens	99-114
16730340-3	2006	In mouse hippocampus and cerebral cortex, the effects of repeated treatment with the antidepressants desipramine and fluoxetine or the PDE4 inhibitor rolipram on the expression of PDE4D was compared to that of PDE4A and PDE4B, the other two subtypes expressed in the brain.	Desipramine	101-112	phosphodiesterase 4D, cAMP specific	Mus musculus	180-185
16278342-5	2005	We showed that 1) after 1 h of reoxygenation, fluorescence had risen and that ROS production was inhibited by desipramine, an inhibitor of sphingomyelinase, an enzyme responsible for ceramide production (126 +/- 7% vs. 48 +/- 12%, P &lt; 0.05); 2) administration of ceramide (N-acetylsphingosine) per se (i.e., in the absence of H/R) induced ROS production (65 +/- 3%), which was inhibited by complex III inhibitor: antimycin A (24 +/- 3%, P &lt; 0.0001), or stigmatellin (31 +/- 2%, P &lt; 0.0001); 3) hypoxia/reoxygenation-induced ROS production was not affected by either ceramide-activated protein kinase inhibitor dimethyl aminopurine or mitochondrial permeability transition inhibitor cyclosporin A but was significantly inhibited by the antiapoptotic protein Bcl-2 (82 +/- 8%, P &lt; 0.05); 4) ceramide-induced ROS production was also inhibited by Bcl-2 (41 +/- 4%, P &lt; 0.0001).	Desipramine	110-121	BCL2 apoptosis regulator	Homo sapiens	766-771
16845218-4	2006	Desipramine, a classic antidepressant, increased BDNF mRNA level in both examined brain regions.	Desipramine	0-11	brain derived neurotrophic factor	Homo sapiens	49-53
16460696-5	2006	The most consistent effect, observed with pronoradrenergic drugs (desipramine and reboxetine), was a decrease of GluR3 expression both in P/FC and HI.	Desipramine	66-77	glutamate ionotropic receptor AMPA type subunit 3	Rattus norvegicus	113-118
16460696-6	2006	Interestingly, in HI, the same drugs also decreased the editing levels of either the flip (desipramine) or flop (reboxetine) form of GluR3.	Desipramine	91-102	glutamate ionotropic receptor AMPA type subunit 3	Rattus norvegicus	133-138
16478969-14	2006	The RFIM (DMI - DMR) was moderately correlated with DMI and ADG (0.37 and -0.38; respectively), suggesting that selecting for low RFI(M) would decrease DMI and increase ADG in this database.	Desipramine	10-13	RFI	Bos taurus	4-7
16478969-14	2006	The RFIM (DMI - DMR) was moderately correlated with DMI and ADG (0.37 and -0.38; respectively), suggesting that selecting for low RFI(M) would decrease DMI and increase ADG in this database.	Desipramine	52-55	RFI	Bos taurus	4-7
16478969-14	2006	The RFIM (DMI - DMR) was moderately correlated with DMI and ADG (0.37 and -0.38; respectively), suggesting that selecting for low RFI(M) would decrease DMI and increase ADG in this database.	Desipramine	52-55	RFI	Bos taurus	4-7
16293366-10	2006	Chronic citalopram and desipramine treatments also increased the somatostatin levels by 83+/-32% and 40+/-6% of basal, respectively.	Desipramine	23-34	somatostatin	Rattus norvegicus	65-77
16753142-5	2006	Further studies showed that desipramine caused the apoptotic cell death, which could be prevented by neither catalase, reduced-form glutathione (GSH), nor N-acetylcysteine (NAC), without accompanying the disruption of mitochondrial membrane potential within the cells and the release of cytochrome c into the cell cytoplasm.	Desipramine	28-39	cytochrome c, somatic	Homo sapiens	287-299
16386803-6	2006	We found that propranolol blocked the IL-1beta response to footshock in both the hypothalamus and the spleen, while the noradrenergic reuptake inhibitor desipramine significantly augmented the footshock-induced IL-1beta response in both of these sites.	Desipramine	153-164	interleukin 1 beta	Rattus norvegicus	211-219
16140280-9	2006	Also, rats treated simultaneously with sertraline plus desipramine exhibited reductions in both SERT and NET binding.	Desipramine	55-66	solute carrier family 6 member 4	Rattus norvegicus	96-100
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.	Desipramine	117-128	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.	Desipramine	15-26	brain-derived neurotrophic factor	Rattus norvegicus	135-168
16278342-5	2005	We showed that 1) after 1 h of reoxygenation, fluorescence had risen and that ROS production was inhibited by desipramine, an inhibitor of sphingomyelinase, an enzyme responsible for ceramide production (126 +/- 7% vs. 48 +/- 12%, P &lt; 0.05); 2) administration of ceramide (N-acetylsphingosine) per se (i.e., in the absence of H/R) induced ROS production (65 +/- 3%), which was inhibited by complex III inhibitor: antimycin A (24 +/- 3%, P &lt; 0.0001), or stigmatellin (31 +/- 2%, P &lt; 0.0001); 3) hypoxia/reoxygenation-induced ROS production was not affected by either ceramide-activated protein kinase inhibitor dimethyl aminopurine or mitochondrial permeability transition inhibitor cyclosporin A but was significantly inhibited by the antiapoptotic protein Bcl-2 (82 +/- 8%, P &lt; 0.05); 4) ceramide-induced ROS production was also inhibited by Bcl-2 (41 +/- 4%, P &lt; 0.0001).	Desipramine	110-121	BCL2 apoptosis regulator	Homo sapiens	855-860
16330572-11	2005	11C-mHED accumulation could be inhibited by desipramine, a potent inhibitor of hNET.	Desipramine	44-55	solute carrier family 6 member 2	Homo sapiens	79-83
16338282-9	2005	CONCLUSIONS: Low-dose ritonavir (100 mg twice daily) exerts a modest inhibitory effect on the activity of CYP2D6 in extensive metabolizers, as assessed with desipramine as the index substrate.	Desipramine	157-168	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	106-112
16143352-7	2005	On the contrary, the effect of DMI on BDNF mRNA was neither dose- nor time-dependent.	Desipramine	31-34	brain-derived neurotrophic factor	Rattus norvegicus	38-42
16143352-3	2005	Here we looked for the time course of the effect of different doses of two antidepressants, desipramine (DMI) and paroxetine (PAR), which differentially affect monoamine reuptake, on BDNF mRNA expression in hippocampal subfields (CA1, CA3 and dentate gyrus) and levels of AMPAR subunits in total and membrane-enriched extracts from rat hippocampus.	Desipramine	92-103	brain-derived neurotrophic factor	Rattus norvegicus	183-187
16143352-3	2005	Here we looked for the time course of the effect of different doses of two antidepressants, desipramine (DMI) and paroxetine (PAR), which differentially affect monoamine reuptake, on BDNF mRNA expression in hippocampal subfields (CA1, CA3 and dentate gyrus) and levels of AMPAR subunits in total and membrane-enriched extracts from rat hippocampus.	Desipramine	105-108	brain-derived neurotrophic factor	Rattus norvegicus	183-187
16359723-6	2005	Furthermore, as with selective serotonin reuptake inhibitors such as fluvoxamine and paroxetine, SIV was also reduced by the serotonin and noradrenaline reuptake inhibitor milnacipran and the metabotropic glutamate receptor 5 antagonist MPEP, while desipramine was without effect.	Desipramine	249-260	glutamate metabotropic receptor 5	Rattus norvegicus	192-225
16337960-10	2006	Ceramide plays a crucial role in this process, because prevention of ceramide formation either by myocardial adaptation to ischemia or with desipramine results in the inhibition of eNOS association with caveolin-1 thereby reducing myocardial ischemic reperfusion injury.	Desipramine	140-151	nitric oxide synthase 3	Rattus norvegicus	181-185
16337960-10	2006	Ceramide plays a crucial role in this process, because prevention of ceramide formation either by myocardial adaptation to ischemia or with desipramine results in the inhibition of eNOS association with caveolin-1 thereby reducing myocardial ischemic reperfusion injury.	Desipramine	140-151	caveolin 1	Rattus norvegicus	203-213
15894065-5	2005	On the other hand, desipramine and mazindol inhibited the increase in wet-dog shakes in ACTH-treated rats.	Desipramine	19-30	proopiomelanocortin	Canis lupus familiaris	88-92
16111724-5	2005	We show that agents with antidepressant activity, namely the antidepressants fluoxetine and desipramine, the atypical antipsychotic clozapine, and the mood stabilizer lithium increased VGLUT1 mRNA expression in neurons of the cerebral cortex and the hippocampus and in concert enhanced VGLUT1 protein expression in their projection fields.	Desipramine	92-103	solute carrier family 17 member 7	Homo sapiens	185-191
16111724-5	2005	We show that agents with antidepressant activity, namely the antidepressants fluoxetine and desipramine, the atypical antipsychotic clozapine, and the mood stabilizer lithium increased VGLUT1 mRNA expression in neurons of the cerebral cortex and the hippocampus and in concert enhanced VGLUT1 protein expression in their projection fields.	Desipramine	92-103	solute carrier family 17 member 7	Homo sapiens	286-292
15983795-7	2005	In contrast, complexin II was significantly induced by desipramine and tranylcypromine, but not fluoxetine, in several brain regions.	Desipramine	55-66	complexin 2	Rattus norvegicus	13-25
15922009-3	2005	The different CYPs involved in IMI demethylation to the pharmacologically active metabolite desipramine (DES) were CYP2C19 &gt; CYP1A2 &gt; CYP3A4.	Desipramine	92-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	115-122
15922009-3	2005	The different CYPs involved in IMI demethylation to the pharmacologically active metabolite desipramine (DES) were CYP2C19 &gt; CYP1A2 &gt; CYP3A4.	Desipramine	92-103	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	128-134
15922009-3	2005	The different CYPs involved in IMI demethylation to the pharmacologically active metabolite desipramine (DES) were CYP2C19 &gt; CYP1A2 &gt; CYP3A4.	Desipramine	92-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	140-146
15922009-3	2005	The different CYPs involved in IMI demethylation to the pharmacologically active metabolite desipramine (DES) were CYP2C19 &gt; CYP1A2 &gt; CYP3A4.	Desipramine	105-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	115-122
15922009-3	2005	The different CYPs involved in IMI demethylation to the pharmacologically active metabolite desipramine (DES) were CYP2C19 &gt; CYP1A2 &gt; CYP3A4.	Desipramine	105-108	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	128-134
15922009-3	2005	The different CYPs involved in IMI demethylation to the pharmacologically active metabolite desipramine (DES) were CYP2C19 &gt; CYP1A2 &gt; CYP3A4.	Desipramine	105-108	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	140-146
15705795-4	2005	Desipramine and imipramine, inhibitors of acid sphingomyelinase (ASMase), suppressed RGDfV-induced ceramide increase.	Desipramine	0-11	sphingomyelin phosphodiesterase 1	Homo sapiens	42-63
15705795-4	2005	Desipramine and imipramine, inhibitors of acid sphingomyelinase (ASMase), suppressed RGDfV-induced ceramide increase.	Desipramine	0-11	sphingomyelin phosphodiesterase 1	Homo sapiens	65-71
15705795-5	2005	Importantly, desipramine, imipramine, and a third ASMase inhibitor, SR33557, but not inhibitors of neutral sphingomyelinase, suppressed RGDfV-induced apoptosis, suggesting that ASMase was required for integrin-mediated apoptosis.	Desipramine	13-24	sphingomyelin phosphodiesterase 1	Homo sapiens	177-183
15885359-8	2005	Co-incubation with tricyclic antidepressants (desipramine) or serotonin reuptake inhibitors (fluoxetine) attenuated the effect of IFN-alpha on GR or 5-HTR1A.	Desipramine	46-57	interferon alpha 1	Homo sapiens	130-139
15885359-8	2005	Co-incubation with tricyclic antidepressants (desipramine) or serotonin reuptake inhibitors (fluoxetine) attenuated the effect of IFN-alpha on GR or 5-HTR1A.	Desipramine	46-57	nuclear receptor subfamily 3 group C member 1	Homo sapiens	143-145
15885359-8	2005	Co-incubation with tricyclic antidepressants (desipramine) or serotonin reuptake inhibitors (fluoxetine) attenuated the effect of IFN-alpha on GR or 5-HTR1A.	Desipramine	46-57	5-hydroxytryptamine receptor 1A	Homo sapiens	151-156
15885359-12	2005	These levels of GR and 5-HTR1A, following IFN-alpha-induced downregulation, recovered after withdrawal of IFN-alpha or addition of desipramine or fluoxetine.	Desipramine	131-142	5-hydroxytryptamine receptor 1A	Homo sapiens	25-30
15901772-5	2005	Chronic fluoxetine did not influence activin betaA expression, but fluoxetine as well as desipramine did increase Smad2 phosphorylation in the frontal cortex.	Desipramine	89-100	SMAD family member 2	Rattus norvegicus	114-119
15814154-1	2005	Previous research has shown that exposure of norepinephrine transporter (NET)-expressing cells to desipramine (DMI) downregulates the norepinephrine transporter, although changes in the several transporter parameters do not demonstrate the same time course.	Desipramine	98-109	solute carrier family 6 member 2	Rattus norvegicus	45-71
15814154-1	2005	Previous research has shown that exposure of norepinephrine transporter (NET)-expressing cells to desipramine (DMI) downregulates the norepinephrine transporter, although changes in the several transporter parameters do not demonstrate the same time course.	Desipramine	98-109	solute carrier family 6 member 2	Rattus norvegicus	73-76
15814154-1	2005	Previous research has shown that exposure of norepinephrine transporter (NET)-expressing cells to desipramine (DMI) downregulates the norepinephrine transporter, although changes in the several transporter parameters do not demonstrate the same time course.	Desipramine	98-109	solute carrier family 6 member 2	Rattus norvegicus	134-160
15814154-1	2005	Previous research has shown that exposure of norepinephrine transporter (NET)-expressing cells to desipramine (DMI) downregulates the norepinephrine transporter, although changes in the several transporter parameters do not demonstrate the same time course.	Desipramine	111-114	solute carrier family 6 member 2	Rattus norvegicus	45-71
15814154-1	2005	Previous research has shown that exposure of norepinephrine transporter (NET)-expressing cells to desipramine (DMI) downregulates the norepinephrine transporter, although changes in the several transporter parameters do not demonstrate the same time course.	Desipramine	111-114	solute carrier family 6 member 2	Rattus norvegicus	73-76
15814154-1	2005	Previous research has shown that exposure of norepinephrine transporter (NET)-expressing cells to desipramine (DMI) downregulates the norepinephrine transporter, although changes in the several transporter parameters do not demonstrate the same time course.	Desipramine	111-114	solute carrier family 6 member 2	Rattus norvegicus	134-160
15814154-3	2005	Recent demonstration of persistent drug retention in cells following desipramine exposures raises the possibility that previous reported changes in the norepinephrine transporter may be partly accountable by residual drug.	Desipramine	69-80	solute carrier family 6 member 2	Rattus norvegicus	152-178
16220339-6	2005	Chronic bupropion and desipramine significantly decreased BDNF expression in the dentate gyrus of the hippocampus, while fluoxetine had no effect in any brain region.	Desipramine	22-33	brain-derived neurotrophic factor	Rattus norvegicus	58-62
21180171-6	2005	Norepinephrine and dopamine could not induce the transporter current while the 5-HT induced current could be specifically inhibited by 5-HTT blocker, desipramine.	Desipramine	150-161	solute carrier family 6 member 4	Homo sapiens	135-140
16036225-4	2005	This effect of DMI was not dependent upon activity at the levels of the beta2 receptor, cAMP accumulation or phosphorylation of the transcription factor, cAMP response element binding protein (CREB).	Desipramine	15-18	cAMP responsive element binding protein 1	Homo sapiens	193-197
16036225-8	2005	The results suggest a molecular target for DMI that lies downstream of CREB phosphorylation.	Desipramine	43-46	cAMP responsive element binding protein 1	Homo sapiens	71-75
15992385-4	2005	Repeated treatment with fluoxetine, paroxetine or desipramine increased VGLUT1 mRNA abundance in frontal, orbital, cingulate and parietal cortices, and regions of the hippocampus.	Desipramine	50-61	solute carrier family 17 member 7	Rattus norvegicus	72-78
15946644-4	2005	Here, intrinsic tryptophan fluorescence spectroscopy is used to document the binding of desipramine, a member of the tricyclic antidepressant family, to a well-defined extracellular glutamate binding domain (S1S2) of the GluR2 subunit of the amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor.	Desipramine	88-99	glutamate ionotropic receptor AMPA type subunit 2	Homo sapiens	221-226
15726116-1	2005	Previous studies demonstrated that Gsalpha migrates from a Triton X-100 (TTX-100) insoluble membrane domain to a TTX-100 soluble membrane domain in response to chronic treatment with the antidepressants desipramine and fluoxetine.	Desipramine	203-214	GNAS complex locus	Homo sapiens	35-42
15726116-4	2005	Chronic treatment of C6 cells with two fuctionally and structurally distinct antidepressants, desipramine and fluoxetine, decreased the Gsalpha content of TTX-100 insoluble membrane domains by as much as 60%, while the inactive fluoxetine analog LY368514 had no effect.	Desipramine	94-105	GNAS complex locus	Homo sapiens	136-143
15617725-7	2005	Based on a possible correlation between the onset of 5HT2C receptor-mediated inhibition and the behavioral effects of desipramine and nefazodone treatment that was described in our previous studies, we suggest that 5HT2C receptor activation may be important for the onset of the behavioral effects of antidepressant treatment.	Desipramine	118-129	5-hydroxytryptamine receptor 2C	Rattus norvegicus	215-220
15802801-3	2005	When either rat liver microsomes or recombinant CYP2D2 was employed, the preincubation with DMI (0.3 microM) caused a greater inhibition of BF 1""-hydroxylation than the co-incubation did, whereas BF 1""-hydroxylation by rat CYP2D1 was not markedly affected under the same conditions.	Desipramine	92-95	cytochrome P450, family 2, subfamily d, polypeptide 2	Rattus norvegicus	48-54
15802801-3	2005	When either rat liver microsomes or recombinant CYP2D2 was employed, the preincubation with DMI (0.3 microM) caused a greater inhibition of BF 1""-hydroxylation than the co-incubation did, whereas BF 1""-hydroxylation by rat CYP2D1 was not markedly affected under the same conditions.	Desipramine	92-95	forkhead box G1	Rattus norvegicus	140-144
15802801-3	2005	When either rat liver microsomes or recombinant CYP2D2 was employed, the preincubation with DMI (0.3 microM) caused a greater inhibition of BF 1""-hydroxylation than the co-incubation did, whereas BF 1""-hydroxylation by rat CYP2D1 was not markedly affected under the same conditions.	Desipramine	92-95	forkhead box G1	Rattus norvegicus	197-201
15802801-3	2005	When either rat liver microsomes or recombinant CYP2D2 was employed, the preincubation with DMI (0.3 microM) caused a greater inhibition of BF 1""-hydroxylation than the co-incubation did, whereas BF 1""-hydroxylation by rat CYP2D1 was not markedly affected under the same conditions.	Desipramine	92-95	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	225-231
15802801-4	2005	The inhibitory effect of DMI on BF 1""-hydroxylation by human liver microsomal fractions or recombinant CYP2D6 was much lower than that on the hydroxylation by rat liver microsomes or CYP2D2.	Desipramine	25-28	forkhead box G1	Rattus norvegicus	32-36
15802801-4	2005	The inhibitory effect of DMI on BF 1""-hydroxylation by human liver microsomal fractions or recombinant CYP2D6 was much lower than that on the hydroxylation by rat liver microsomes or CYP2D2.	Desipramine	25-28	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	104-110
15802801-7	2005	Binding experiments employing the recombinant enzymes and [(3)H]-DMI revealed that CYP2D2 and CYP2D6 were the only prominent proteins to which considerable radioactive DMI metabolite(s) bound.	Desipramine	65-68	cytochrome P450, family 2, subfamily d, polypeptide 2	Rattus norvegicus	83-89
15802801-7	2005	Binding experiments employing the recombinant enzymes and [(3)H]-DMI revealed that CYP2D2 and CYP2D6 were the only prominent proteins to which considerable radioactive DMI metabolite(s) bound.	Desipramine	65-68	cytochrome P450, family 2, subfamily d, polypeptide 3	Rattus norvegicus	94-100
15802801-8	2005	These results indicate that rat CYP2D2 biotransforms DMI into reactive metabolite(s), which covalently bind to CYP2D2, resulting in inactivation of the enzyme.	Desipramine	53-56	cytochrome P450, family 2, subfamily d, polypeptide 2	Rattus norvegicus	32-38
15802801-8	2005	These results indicate that rat CYP2D2 biotransforms DMI into reactive metabolite(s), which covalently bind to CYP2D2, resulting in inactivation of the enzyme.	Desipramine	53-56	cytochrome P450, family 2, subfamily d, polypeptide 2	Rattus norvegicus	111-117
15802801-9	2005	In contrast, human CYP2D6 may also biotransform DMI into some metabolite(s) that covalently bind to CYP2D6, but that do not inactivate the enzyme.	Desipramine	48-51	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	19-25
15802801-9	2005	In contrast, human CYP2D6 may also biotransform DMI into some metabolite(s) that covalently bind to CYP2D6, but that do not inactivate the enzyme.	Desipramine	48-51	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	100-106
15814105-9	2005	Furthermore, with the exception of "grooming", the effects of desipramine on behaviour of NK1-/- mice could be explained by the effects of this antidepressant on locomotor activity.	Desipramine	62-73	tachykinin 1	Mus musculus	90-93
15652409-6	2005	Consistent with expression of a functional SERT, specific uptake of (3)H-serotonin in macrophages was sodium dependent and inhibited by fluoxetine (IC(50) 6.9 nM) and desipramine (IC(50) 32 nM) but not by nisoxetine or reserpine.	Desipramine	167-178	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	43-47
15617725-6	2005	However, only 14-day treatment with desipramine or 7-day treatment with nefazodone, but not 7-day treatment with desipramine, decreased 5HT2C receptor-mediated inhibition of accumbal dopamine release.	Desipramine	36-47	5-hydroxytryptamine receptor 2C	Rattus norvegicus	136-141
15617725-7	2005	Based on a possible correlation between the onset of 5HT2C receptor-mediated inhibition and the behavioral effects of desipramine and nefazodone treatment that was described in our previous studies, we suggest that 5HT2C receptor activation may be important for the onset of the behavioral effects of antidepressant treatment.	Desipramine	118-129	5-hydroxytryptamine receptor 2C	Rattus norvegicus	53-58
15802801-2	2005	Inhibition was examined under the following two conditions: 1) DMI was co-incubated with BF and NADPH in the reaction mixture containing rat or human liver microsomes or yeast cell microsomes expressing rat CYP2D1, CYP2D2 or human CYP2D6 (co-incubation); 2) DMI was preincubated with NADPH and the same enzyme sources prior to adding the substrate (preincubation).	Desipramine	63-66	cytochrome P450, family 2, subfamily d, polypeptide 2	Rattus norvegicus	215-221
15802801-2	2005	Inhibition was examined under the following two conditions: 1) DMI was co-incubated with BF and NADPH in the reaction mixture containing rat or human liver microsomes or yeast cell microsomes expressing rat CYP2D1, CYP2D2 or human CYP2D6 (co-incubation); 2) DMI was preincubated with NADPH and the same enzyme sources prior to adding the substrate (preincubation).	Desipramine	63-66	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	231-237
15710233-0	2005	Effects of desipramine treatment on tyrosine hydroxylase gene expression in cultured neuroblastoma cells and rat brain tissue.	Desipramine	11-22	tyrosine hydroxylase	Rattus norvegicus	36-56
15710233-5	2005	In contrast, 500 nM DMI led to an initial slight increase, followed by a continuous and sustained decrease in TH protein level by up to 53%, from day 3 to day 14.	Desipramine	20-23	tyrosine hydroxylase	Rattus norvegicus	110-112
15710233-9	2005	These findings indicate that DMI exerts complex, typically opposite and perhaps compensatory, gradually evolving effects on the expression of TH protein (decreases) and its message (increases), possibly in response to increased synaptic availability of NE.	Desipramine	29-32	tyrosine hydroxylase	Rattus norvegicus	142-144
15878644-0	2005	An antidepressant mechanism of desipramine is to decrease tumor necrosis factor-alpha production culminating in increases in noradrenergic neurotransmission.	Desipramine	31-42	tumor necrosis factor	Homo sapiens	58-85
15878644-7	2005	Desipramine administration results in a virtual ablation of neuron-derived tumor necrosis factor-alpha (TNF), thus implicating an essential role of TNF in the therapeutic efficacy of this antidepressant.	Desipramine	0-11	tumor necrosis factor	Homo sapiens	75-102
15878644-7	2005	Desipramine administration results in a virtual ablation of neuron-derived tumor necrosis factor-alpha (TNF), thus implicating an essential role of TNF in the therapeutic efficacy of this antidepressant.	Desipramine	0-11	tumor necrosis factor	Homo sapiens	104-107
15878644-7	2005	Desipramine administration results in a virtual ablation of neuron-derived tumor necrosis factor-alpha (TNF), thus implicating an essential role of TNF in the therapeutic efficacy of this antidepressant.	Desipramine	0-11	tumor necrosis factor	Homo sapiens	148-151
15878644-8	2005	Additionally, following chronic administration of desipramine, TNF-regulation of NE release is transformed, from inhibition to facilitation.	Desipramine	50-61	tumor necrosis factor	Homo sapiens	63-66
15878644-11	2005	Thus, the efficacy of desipramine is due to decreased levels of TNF in the brain induced by this drug, ultimately modifying noradrenergic neurotransmission.	Desipramine	22-33	tumor necrosis factor	Homo sapiens	64-67
15150531-8	2004	Furthermore, GIRK current responses activated by the cloned A1 adenosine receptor were similarly inhibited by the tricyclic antidepressant desipramine.	Desipramine	139-150	potassium inwardly rectifying channel subfamily J member 3 S homeolog	Xenopus laevis	13-17
15451381-3	2004	In the present study we performed parallel measurements of BDNF mRNA and protein expression in the frontal cortex and hippocampus of the rat after chronic treatment with electroconvulsive seizures (ECS), lithium, desipramine or escitalopram.	Desipramine	213-224	brain-derived neurotrophic factor	Rattus norvegicus	59-63
15451381-5	2004	Desipramine moderately increased BDNF mRNA expression in the dentate gyrus but did not change BDNF protein in neither region.	Desipramine	0-11	brain-derived neurotrophic factor	Rattus norvegicus	33-37
15138445-4	2004	We investigated how different drugs (fluoxetine (FLX), desipramine (DMI), reboxetine (RBX)) affect CREB expression and phosphorylation of Ser(133) in the hippocampus and prefrontal/frontal cortex (PFCX).	Desipramine	55-66	cAMP responsive element binding protein 1	Homo sapiens	99-103
15138445-4	2004	We investigated how different drugs (fluoxetine (FLX), desipramine (DMI), reboxetine (RBX)) affect CREB expression and phosphorylation of Ser(133) in the hippocampus and prefrontal/frontal cortex (PFCX).	Desipramine	68-71	cAMP responsive element binding protein 1	Homo sapiens	99-103
15150531-10	2004	The GIRK currents induced by ethanol were also attenuated in the presence of desipramine.	Desipramine	77-88	potassium inwardly rectifying channel subfamily J member 3 S homeolog	Xenopus laevis	4-8
15150531-4	2004	Here, we report the inhibitory effects of various antidepressants: imipramine, desipramine, amitriptyline, nortriptyline, clomipramine, maprotiline, and citalopram, on GIRK channels.	Desipramine	79-90	potassium inwardly rectifying channel subfamily J member 3 S homeolog	Xenopus laevis	168-172
15337319-4	2004	The obtained results indicate that transcriptional activity of dopamine D2 receptor gene promoter was dose-dependently increased by retinoic acid, forskolin, rolipram and phorbol 12 myristate 13-acetate, as well as by DMI, CIT and MIA.	Desipramine	218-221	dopamine receptor D2	Mus musculus	63-83
15262904-6	2004	Blockade of norepinephrine transporter or alpha2-adrenoceptors using desipramine or rauwolscine reduced the losartan-induced shifts in the ED50 values of noradrenaline by 63% and 21%, respectively.	Desipramine	69-80	solute carrier family 6 member 2	Rattus norvegicus	12-38
15082752-1	2004	The present study documents a role for brain-derived tumor necrosis factor-alpha (TNF) in the mechanism of action of the antidepressant drug desmethylimipramine (desipramine).	Desipramine	141-160	tumor necrosis factor	Rattus norvegicus	82-85
15082752-1	2004	The present study documents a role for brain-derived tumor necrosis factor-alpha (TNF) in the mechanism of action of the antidepressant drug desmethylimipramine (desipramine).	Desipramine	162-173	tumor necrosis factor	Rattus norvegicus	82-85
15082752-3	2004	Chronic desipramine administration transforms TNF-mediated inhibition of NE release to facilitation, dependent upon alpha2-adrenergic receptor activation.	Desipramine	8-19	tumor necrosis factor	Rattus norvegicus	46-49
15082752-6	2004	To determine whether this transformation is due to desipramine-induced inhibition of TNF bioactivity in the brain, rats were i.c.v.	Desipramine	51-62	tumor necrosis factor	Rattus norvegicus	85-88
15082752-10	2004	Although simultaneous microinfusion of rrTNF with chronic desipramine administration prevents the transformation induced by desipramine, microinfusion of rrTNF enhances TNF inhibition of NE release.	Desipramine	124-135	tumor necrosis factor	Rattus norvegicus	41-44
15082752-17	2004	microinfusion of rrTNF with concomitant desipramine administration opposes decreases in neuron-associated TNF levels, required to transform presynaptic sensitivity to TNF, which is necessary for the drug to be efficacious.	Desipramine	40-51	tumor necrosis factor	Rattus norvegicus	106-109
15219272-5	2004	Fluoxetine and desipramine, both are psychotropics and specific SERT ligands and decreased the affinity of [(123)I]ADAM, while p-chloroamphetamine (PCA), a narcotic, destroyed most of serotonergic neurons, as well as reducing the concentration of serotonin and the number of SERT in the brain as shown by the biodistribution of [(123)I]ADAM.	Desipramine	15-26	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	64-68
15261759-1	2004	High concentration of corticosterone (Cort) 0.2 mM was incubated with PC12 cells to simulate the lesion state of brain neurons in depressive illness, it was found that the inulin-type oligosaccharides extracted from Morinda officinalis, inulin-type hexasaccharide (IHS) at the doses of 0.625, 1.25 microM or desipramine (DIM) 0.25, 1 microM protected the PC12 cells from the lesion induced by Cort.	Desipramine	308-319	cortistatin	Rattus norvegicus	38-42
15249684-5	2004	We also demonstrate that the loss of forebrain BDNF attenuates the actions of desipramine, an antidepressant, in the forced swim test, suggesting the involvement of BDNF in antidepressant efficacy.	Desipramine	78-89	brain derived neurotrophic factor	Mus musculus	47-51
15249684-5	2004	We also demonstrate that the loss of forebrain BDNF attenuates the actions of desipramine, an antidepressant, in the forced swim test, suggesting the involvement of BDNF in antidepressant efficacy.	Desipramine	78-89	brain derived neurotrophic factor	Mus musculus	165-169
15219272-5	2004	Fluoxetine and desipramine, both are psychotropics and specific SERT ligands and decreased the affinity of [(123)I]ADAM, while p-chloroamphetamine (PCA), a narcotic, destroyed most of serotonergic neurons, as well as reducing the concentration of serotonin and the number of SERT in the brain as shown by the biodistribution of [(123)I]ADAM.	Desipramine	15-26	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	275-279
15219272-8	2004	In addition, the inhibition effect on binding ability of [(123)I]ADAM to SERT by the psychotropics and the narcotic was found to have the order of: PCA &gt; fluoxetine &gt; desipramine.	Desipramine	173-184	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	73-77
14735130-6	2004	It was found that imipramine, amitryptyline, desipramine, fluoxetine, and mianserin, present in the culture medium for 5 days, in a concentration-dependent manner inhibited basal hCRH gene promoter activity in undifferentiated Neuro-2A cells, while other drugs under study (citalopram, tianeptine, moclobemide, venlafaxine, reboxetine, mirtazapine, and milnacipram) were inactive.	Desipramine	45-56	corticotropin releasing hormone	Homo sapiens	179-183
15110811-7	2004	The cardioprotective abilities of PC were abolished with desipramine, which also downregulated a PC-mediated increase in antiapoptotic protein Bcl-2.	Desipramine	57-68	BCL2 apoptosis regulator	Homo sapiens	143-148
15115913-0	2004	Impact of CYP2D6 intermediate metabolizer alleles on single-dose desipramine pharmacokinetics.	Desipramine	65-76	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	10-16
15115913-1	2004	This study utilized cytochrome P450 2D6 (CYP2D6) genotypes to explain variability of desipramine pharmacokinetics in a cohort of non-poor metabolizer individuals.	Desipramine	85-96	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	20-39
15115913-1	2004	This study utilized cytochrome P450 2D6 (CYP2D6) genotypes to explain variability of desipramine pharmacokinetics in a cohort of non-poor metabolizer individuals.	Desipramine	85-96	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	41-47
15132707-1	2004	Interactions of two amphiphilic antidepressant drugs, imipramine and desipramine hydrochlorides, with the blood protein human serum albumin (HSA) were investigated to gain an understanding of the effects of drug molecular structure on the complex formation of drug-protein molecules.	Desipramine	69-95	albumin	Homo sapiens	126-139
16680870-1	2004	Clinically, cimetidine therapy impairs the clearance of various drugs metabolized by CYP2D6, such as desipramine and sparteine.	Desipramine	101-112	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	85-91
15033385-5	2004	These results indicate that the blockade of 5-HT(1B) rather than 5-HT(1A) receptors may facilitate the anti-immobility effect of imipramine, desipramine or moclobemide in the forced swimming test.	Desipramine	141-152	5-hydroxytryptamine receptor 1B	Rattus norvegicus	44-51
14985439-5	2004	Here we establish that both subchronic and chronic desipramine (DMI) treatments upregulate hypothalamic ICER expression in wild-type mice.	Desipramine	51-62	cAMP responsive element modulator	Mus musculus	104-108
14730412-0	2004	Effect of the novel anxiolytic drug deramciclane on cytochrome P(450) 2D6 activity as measured by desipramine pharmacokinetics.	Desipramine	98-109	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	52-73
14730412-1	2004	BACKGROUND: In vitro findings have indicated that the novel anxiolytic drug, deramciclane, is an inhibitor of the cytochrome P(450) (CYP) 2D6 enzyme and co-administration of deramciclane and the CYP2D6 probe drug desipramine is possible in clinical practice.	Desipramine	213-224	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	114-131
14730412-1	2004	BACKGROUND: In vitro findings have indicated that the novel anxiolytic drug, deramciclane, is an inhibitor of the cytochrome P(450) (CYP) 2D6 enzyme and co-administration of deramciclane and the CYP2D6 probe drug desipramine is possible in clinical practice.	Desipramine	213-224	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	133-136
14960314-0	2004	Interactions of acid sphingomyelinase and lipid bilayers in the presence of the tricyclic antidepressant desipramine.	Desipramine	105-116	sphingomyelin phosphodiesterase 1	Homo sapiens	16-37
14960314-1	2004	The tricyclic antidepressant desipramine causes a decrease in cellular acid sphingomyelinase (A-SMase, EC 3.1.4.12) activity when added to culture medium of human fibroblasts.	Desipramine	29-40	sphingomyelin phosphodiesterase 1	Homo sapiens	71-92
14960314-1	2004	The tricyclic antidepressant desipramine causes a decrease in cellular acid sphingomyelinase (A-SMase, EC 3.1.4.12) activity when added to culture medium of human fibroblasts.	Desipramine	29-40	sphingomyelin phosphodiesterase 1	Homo sapiens	94-101
14960314-6	2004	Our findings indicate that desipramine interferes with the binding of A-SMase to the lipid bilayers and thereby displaces the enzyme from its membrane-bound substrate.	Desipramine	27-38	sphingomyelin phosphodiesterase 1	Homo sapiens	70-77
14960314-8	2004	We hypothesize that the displacement of the glycoprotein A-SMase from the inner membranes of late endosomes and lysosomes by desipramine renders it susceptible to proteolytic cleavage by lysosomal proteases.	Desipramine	125-136	sphingomyelin phosphodiesterase 1	Homo sapiens	57-64
14985439-5	2004	Here we establish that both subchronic and chronic desipramine (DMI) treatments upregulate hypothalamic ICER expression in wild-type mice.	Desipramine	64-67	cAMP responsive element modulator	Mus musculus	104-108
14985439-6	2004	Behavioral responses to DMI in the forced swim and tail suspension tests are unchanged in mice lacking ICER.	Desipramine	24-27	cAMP responsive element modulator	Mus musculus	103-107
14610241-5	2004	Based on the potential of interaction from the in vitro experiments, drug interaction studies in healthy subjects were conducted using probe substrates for CYP2D6 (desipramine) in CYP2D6 extensive metabolizer subjects and CYP3A (midazolam) in CYP2D6 poor metabolizer subjects.	Desipramine	164-175	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	156-162
14985439-7	2004	However, the ability of DMI to suppress an acute corticosterone response after swim stress is compromised in ICER-deficient mice, suggesting that increased hypothalamic ICER mRNA after DMI treatment may be required for suppression of corticosterone release.	Desipramine	185-188	cAMP responsive element modulator	Mus musculus	109-113
14610241-5	2004	Based on the potential of interaction from the in vitro experiments, drug interaction studies in healthy subjects were conducted using probe substrates for CYP2D6 (desipramine) in CYP2D6 extensive metabolizer subjects and CYP3A (midazolam) in CYP2D6 poor metabolizer subjects.	Desipramine	164-175	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	180-186
14985439-7	2004	However, the ability of DMI to suppress an acute corticosterone response after swim stress is compromised in ICER-deficient mice, suggesting that increased hypothalamic ICER mRNA after DMI treatment may be required for suppression of corticosterone release.	Desipramine	185-188	cAMP responsive element modulator	Mus musculus	169-173
14610241-5	2004	Based on the potential of interaction from the in vitro experiments, drug interaction studies in healthy subjects were conducted using probe substrates for CYP2D6 (desipramine) in CYP2D6 extensive metabolizer subjects and CYP3A (midazolam) in CYP2D6 poor metabolizer subjects.	Desipramine	164-175	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	180-186
14985439-11	2004	These data indicate that ICER is required for DMI to reduce stress-induced corticosterone release through regulation of hypothalamic CRF expression, revealing a novel role for ICER in antidepressant regulation of the hypothalamic-pituitary adrenal axis.	Desipramine	46-49	cAMP responsive element modulator	Mus musculus	25-29
14985439-11	2004	These data indicate that ICER is required for DMI to reduce stress-induced corticosterone release through regulation of hypothalamic CRF expression, revealing a novel role for ICER in antidepressant regulation of the hypothalamic-pituitary adrenal axis.	Desipramine	46-49	cAMP responsive element modulator	Mus musculus	176-180
14515337-9	2003	After inhibition of the DA and NA transporter, by perfusing 100 microM desmethyl-imipramine into the mPFC, clonidine perfusion into the LC reduced extracellular NA and DA in the mPFC by about 50%.	Desipramine	71-91	complement factor properdin	Mus musculus	101-105
14716709-6	2004	A study on the relative influence of CYP1A2 and 3A4 only revealed minor changes in the presence of desipramine.	Desipramine	99-110	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	37-43
14640711-5	2003	The system was used both to yield the Michaelis constant (K(m)) of the P450 biotransformation of imipramine into desipramine and to determine the IC50 value of a chemical inhibitor (tranylcypromine) for this CYP2C19-mediated reaction.	Desipramine	113-124	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	71-75
14640711-5	2003	The system was used both to yield the Michaelis constant (K(m)) of the P450 biotransformation of imipramine into desipramine and to determine the IC50 value of a chemical inhibitor (tranylcypromine) for this CYP2C19-mediated reaction.	Desipramine	113-124	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	208-215
14515337-9	2003	After inhibition of the DA and NA transporter, by perfusing 100 microM desmethyl-imipramine into the mPFC, clonidine perfusion into the LC reduced extracellular NA and DA in the mPFC by about 50%.	Desipramine	71-91	complement factor properdin	Mus musculus	178-182
14623141-6	2003	This result suggests that MAP-4 and drebrin may be involved in the antidepressant like effects of desipramine and fluoxetine.	Desipramine	98-109	microtubule-associated protein 4	Rattus norvegicus	26-31
14623141-6	2003	This result suggests that MAP-4 and drebrin may be involved in the antidepressant like effects of desipramine and fluoxetine.	Desipramine	98-109	drebrin 1	Rattus norvegicus	36-43
14623141-5	2003	cDNA homology analysis revealed that desipramine up-regulated the expression of microtubule-associated protein 4 (MAP-4) mRNA and fluoxetine up-regulated the expression of drebrin A mRNA in the rat hippocampus compared with the chronically stressed group.	Desipramine	37-48	microtubule-associated protein 4	Rattus norvegicus	80-112
14623141-5	2003	cDNA homology analysis revealed that desipramine up-regulated the expression of microtubule-associated protein 4 (MAP-4) mRNA and fluoxetine up-regulated the expression of drebrin A mRNA in the rat hippocampus compared with the chronically stressed group.	Desipramine	37-48	microtubule-associated protein 4	Rattus norvegicus	114-119
12837768-0	2003	chi-Conopeptide MrIA partially overlaps desipramine and cocaine binding sites on the human norepinephrine transporter.	Desipramine	40-51	solute carrier family 6 member 2	Homo sapiens	91-117
12750385-12	2003	Desipramine (a sphingomyelinase inhibitor) prevented the increase in ceramide and inhibited apoptosis after M-CSF deprivation.	Desipramine	0-11	colony stimulating factor 1	Homo sapiens	108-113
14499328-5	2003	Pretreatment with the NET ligand, desipramine, decreased the specific binding of (S,S)-[(11)C]MeNER.	Desipramine	34-45	solute carrier family 6 member 2	Homo sapiens	22-25
14555335-9	2003	The secondary amines nisoxetine (NIS), and especially, desipramine (DES) and nortriptyline (NOR), also inhibited CYP2C11 and generated MI complexes with microsomal CYP.	Desipramine	55-66	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	113-120
14555335-9	2003	The secondary amines nisoxetine (NIS), and especially, desipramine (DES) and nortriptyline (NOR), also inhibited CYP2C11 and generated MI complexes with microsomal CYP.	Desipramine	55-66	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	113-116
14555335-9	2003	The secondary amines nisoxetine (NIS), and especially, desipramine (DES) and nortriptyline (NOR), also inhibited CYP2C11 and generated MI complexes with microsomal CYP.	Desipramine	68-71	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	113-120
14555335-9	2003	The secondary amines nisoxetine (NIS), and especially, desipramine (DES) and nortriptyline (NOR), also inhibited CYP2C11 and generated MI complexes with microsomal CYP.	Desipramine	68-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	113-116
12782200-6	2003	Acute treatment of both wild-type and NET-KO mice with desipramine significantly decreased the TNF-alpha response and significantly increased interleukin-10 production, indicating the role of an intact noradrenaline transporter in anti-inflammatory responses.	Desipramine	55-66	tumor necrosis factor	Mus musculus	95-104
12849931-4	2003	Under the conditions of the assays, [(3)H]paroxetine binding in the LC was specific for the SERT, based on the rank order of affinity of compounds for inhibiting [(3)H]paroxetine binding in the LC, i.e. citalopram &gt; imipramine &gt; desipramine &gt; mazindol.	Desipramine	235-246	solute carrier family 6 member 4	Homo sapiens	92-96
12782200-6	2003	Acute treatment of both wild-type and NET-KO mice with desipramine significantly decreased the TNF-alpha response and significantly increased interleukin-10 production, indicating the role of an intact noradrenaline transporter in anti-inflammatory responses.	Desipramine	55-66	interleukin 10	Mus musculus	142-156
12757900-3	2003	Desipramine, clomiplamine, fluoxetine, milnacipran and clorgyline all induced rapid and sustained translocation of GR into the nucleus of human lymphocytes.	Desipramine	0-11	nuclear receptor subfamily 3 group C member 1	Homo sapiens	115-117
12700702-0	2003	Impact of maternal deprivation on brain corticotropin-releasing hormone circuits: prevention of CRH receptor-2 mRNA changes by desipramine treatment.	Desipramine	127-138	corticotropin releasing hormone	Homo sapiens	40-71
12694379-4	2003	We first showed that the nonspecific adrenergic agonist noradrenaline, the alpha- or beta-adrenergic agonists phenylephrine or dobutamine, or the noradrenergic uptake inhibitor desipramine, all significantly stimulated ACTH secretion by freely moving, nonanaesthetized rats.	Desipramine	177-188	proopiomelanocortin	Homo sapiens	219-223
12700702-0	2003	Impact of maternal deprivation on brain corticotropin-releasing hormone circuits: prevention of CRH receptor-2 mRNA changes by desipramine treatment.	Desipramine	127-138	corticotropin releasing hormone	Homo sapiens	96-99
12700702-11	2003	One week of desipramine (DES) administration preceding the maternal deprivation event prevented all the deprivation-induced changes in CRHr2 mRNA, regardless of the direction of the original change.	Desipramine	12-23	corticotropin releasing hormone receptor 2	Homo sapiens	135-140
12700702-11	2003	One week of desipramine (DES) administration preceding the maternal deprivation event prevented all the deprivation-induced changes in CRHr2 mRNA, regardless of the direction of the original change.	Desipramine	25-28	corticotropin releasing hormone receptor 2	Homo sapiens	135-140
12657510-5	2003	The SERT inhibitors desipramine and fluoxetine also inhibited (3)H-MPP(+) specific uptake (with IC(50)s of 189 and 0.92 microM, respectively).	Desipramine	20-31	solute carrier family 6 member 4	Homo sapiens	4-8
12751629-6	2003	The hepatic metabolism of lidocaine was inhibited by a CYP2D6 substrate desipramine, not by a CYP3A4 inhibitor ketoconazole.	Desipramine	72-83	cytochrome P450, family 2, subfamily d, polypeptide 3	Rattus norvegicus	55-61
12499385-7	2003	We show that ASP(+) (4-(4-(dimethylamino)styrl)-N-methylpyridinium) has micromolar potency for the human norepinephrine transporter, that ASP(+) accumulation is Na(+)-, Cl(-)-, cocaine-, and desipramine-sensitive and temperature-dependent, and that ASP(+) competes with norepinephrine uptake.	Desipramine	191-202	solute carrier family 6 member 2	Homo sapiens	105-131
12644358-0	2003	Regulation of GAP-43 expression by chronic desipramine treatment in rat cultured hippocampal cells.	Desipramine	43-54	growth associated protein 43	Rattus norvegicus	14-20
12644358-7	2003	In situ hybridization revealed that desipramine increased GAP-43 gene expression in dentate gyrus but not other brain regions.	Desipramine	36-47	growth associated protein 43	Rattus norvegicus	58-64
12644358-8	2003	Northern and immunoblotting analysis revealed that desipramine increased GAP-43 mRNA and protein levels.	Desipramine	51-62	growth associated protein 43	Rattus norvegicus	73-79
12493574-5	2003	In the presence of P(6), or tricyclic antidepressant desipramine (DIM), the apoptosis induced by Cort in the three measurements above was significantly inhibited.	Desipramine	53-64	cortistatin	Rattus norvegicus	97-101
12493574-5	2003	In the presence of P(6), or tricyclic antidepressant desipramine (DIM), the apoptosis induced by Cort in the three measurements above was significantly inhibited.	Desipramine	66-69	cortistatin	Rattus norvegicus	97-101
12464448-11	2002	In contrast, 5-HTT-/- mice retained sensitivity to the anti-immobility effects of the norepinephrine reuptake inhibitor, desipramine (20 mg/kg), and the mixed serotonin/norepinephrine reuptake inhibitor, imipramine (25 mg/kg).	Desipramine	121-132	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	13-18
12644358-10	2003	CONCLUSIONS: Because GAP-43 regulates growth of axons and modulates the formation of new connections, our findings suggest that desipramine may have an effect on neuronal plasticity in the central nervous system.	Desipramine	128-139	growth associated protein 43	Rattus norvegicus	21-27
12464451-5	2002	Finally, rolipram potently augmented GR enhancement by the antidepressant, desipramine.	Desipramine	75-86	nuclear receptor subfamily 3, group C, member 1	Mus musculus	37-39
12613867-4	2003	During the hot period, the THI 2 d earlier and mean air temperature 2 d earlier had the greatest impact on milk yield and DMI, respectively.	Desipramine	122-125	alcohol dehydrogenase iron containing 1	Bos taurus	11-14
12228186-8	2002	The secondary amine TCAs, nortriptyline and desipramine, however, showed minimal inhibition of CYP2C19 (estimated IC(50) of 600 and 685 micro M, respectively).	Desipramine	44-55	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	95-102
12527472-2	2002	Here we studied the acute and chronic effect of the antidepressants desipramine and paroxetine, which differentially affect monoamine reuptake, on the expression of the AMPAR subunits GluR1 and GluR2/3, analyzed by Western blot, both in total and in membrane-enriched extracts from rat hippocampus.	Desipramine	68-79	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	184-189
12527472-2	2002	Here we studied the acute and chronic effect of the antidepressants desipramine and paroxetine, which differentially affect monoamine reuptake, on the expression of the AMPAR subunits GluR1 and GluR2/3, analyzed by Western blot, both in total and in membrane-enriched extracts from rat hippocampus.	Desipramine	68-79	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	194-199
12527474-2	2002	This study was designed to assess the in vivo indirect activation of adrenoceptors or 5-HT receptors by the reuptake blocker desipramine or fluoxetine on the cellular distribution of GRK 2/3 in rat brain.	Desipramine	125-136	G protein-coupled receptor kinase 2	Rattus norvegicus	183-190
12527474-11	2002	The results indicate that the in vivo activation of adrenoceptors by desipramine is associated with a time-dependent modulation of membrane-associated GRK 2/3 (i.e. an acute increase in the kinase content which is followed by a return to the basal expression upon repeated treatment).	Desipramine	69-80	G protein-coupled receptor kinase 2	Rattus norvegicus	151-158
12412819-0	2002	Effect of terbinafine on the pharmacokinetics and pharmacodynamics of desipramine in healthy volunteers identified as cytochrome P450 2D6 (CYP2D6) extensive metabolizers.	Desipramine	70-81	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	118-137
12412819-0	2002	Effect of terbinafine on the pharmacokinetics and pharmacodynamics of desipramine in healthy volunteers identified as cytochrome P450 2D6 (CYP2D6) extensive metabolizers.	Desipramine	70-81	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	139-145
12412819-1	2002	Terbinafine-CYP2D6 inhibition was evaluated by assessing 48-hour concentration-time profiles of the tricyclic antidepressant desipramine in 12 healthy volunteers identified as extensive cytochrome P450 2D6 (CYP2D6) metabolizers by genotyping and phenotyping.	Desipramine	125-136	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	12-18
12084721-6	2002	Heparin or heparan sulfate displaces FGF3 from binding sites on the cell surface inhibiting the growth of DMI cells and reverts the transformed phenotype ().	Desipramine	106-109	fibroblast growth factor 3	Mus musculus	37-41
12230948-0	2002	Caspase 3 gene expression and [Ca2+]i homeostasis underlying desipramine-induced C6 glioma cell apoptosis.	Desipramine	61-72	caspase 3	Rattus norvegicus	0-9
12230948-1	2002	AIM: To study desipramine (Des)-induced apoptosis and regulation of caspase 3 gene expression and [Ca2+]i homeostasis in rat glioma C6 cells.	Desipramine	14-25	caspase 3	Rattus norvegicus	68-77
12230948-1	2002	AIM: To study desipramine (Des)-induced apoptosis and regulation of caspase 3 gene expression and [Ca2+]i homeostasis in rat glioma C6 cells.	Desipramine	27-30	caspase 3	Rattus norvegicus	68-77
12230948-6	2002	Apoptotic DNA breaks were further confirmed by a typical "DNA ladder" on agarose gel electrophoresis after exposure to Des 40 micromol/L for 24 h. Meanwhile, expression of caspase 3 gene was observed following Des 20 micromol/L treatment.	Desipramine	119-122	caspase 3	Rattus norvegicus	172-181
12162636-8	2002	In animals challenged with clonidine, there was a significant age by treatment interaction effect for the prepubertal group pretreated with high doses of desipramine (less growth hormone secretion) but not for the peri- or postpubertal groups.	Desipramine	154-165	gonadotropin releasing hormone receptor	Rattus norvegicus	172-186
12070759-0	2002	Inhibition of transport function and desipramine binding at the human noradrenaline transporter by N-ethylmaleimide and protection by substrate analogs.	Desipramine	37-48	solute carrier family 6 member 2	Homo sapiens	70-95
12137927-0	2002	Regulation of norepinephrine transporter abundance by catecholamines and desipramine in vivo.	Desipramine	73-84	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	14-40
12144933-0	2002	Inhibition of SK3 channels in the TE671 human medulloblastoma cell line by desipramine and imipramine.	Desipramine	75-86	potassium calcium-activated channel subfamily N member 3	Homo sapiens	14-17
12144933-4	2002	The interaction of desipramine with the selective SK3 blocker, apamin, was studied in more detail.	Desipramine	19-30	potassium calcium-activated channel subfamily N member 3	Homo sapiens	50-53
12091475-0	2002	Effects of desipramine treatment on norepinephrine transporter gene expression in the cultured SK-N-BE(2)M17 cells and rat brain tissue.	Desipramine	11-22	solute carrier family 6 member 2	Rattus norvegicus	36-62
12091475-1	2002	The antidepressant desipramine (DMI) is a selective inhibitor of norepinephrine (NE) transport that down-regulates the norepinephrine transporter (NET) protein in a concentration- and time-dependent manner in vitro.	Desipramine	19-30	solute carrier family 6 member 2	Rattus norvegicus	119-145
12091475-1	2002	The antidepressant desipramine (DMI) is a selective inhibitor of norepinephrine (NE) transport that down-regulates the norepinephrine transporter (NET) protein in a concentration- and time-dependent manner in vitro.	Desipramine	19-30	solute carrier family 6 member 2	Rattus norvegicus	147-150
12091475-1	2002	The antidepressant desipramine (DMI) is a selective inhibitor of norepinephrine (NE) transport that down-regulates the norepinephrine transporter (NET) protein in a concentration- and time-dependent manner in vitro.	Desipramine	32-35	solute carrier family 6 member 2	Rattus norvegicus	119-145
12091475-1	2002	The antidepressant desipramine (DMI) is a selective inhibitor of norepinephrine (NE) transport that down-regulates the norepinephrine transporter (NET) protein in a concentration- and time-dependent manner in vitro.	Desipramine	32-35	solute carrier family 6 member 2	Rattus norvegicus	147-150
12091475-2	2002	In this study, possible regulatory effects of DMI on NET mRNA and protein levels were investigated with the NET-expressing SK-N-BE(2)M17 cell line and rat brain tissue.	Desipramine	46-49	solute carrier family 6 member 2	Rattus norvegicus	53-56
12091475-3	2002	Northern blot analysis showed that incubation of the cultured cells with DMI (5-500 nm) for 3 days reduced levels of NET mRNA in both its 5.8-kb (by up to 58%) and 3.6-kb forms (to 68%), whereas incubation for 14 days increased both levels (to 40% and 100%) in a concentration-dependent manner.	Desipramine	73-76	solute carrier family 6 member 2	Rattus norvegicus	117-120
12091475-4	2002	In contrast, NET protein levels decreased after 3-14 days of exposure of the cells to DMI, as determined by western blotting.	Desipramine	86-89	solute carrier family 6 member 2	Rattus norvegicus	13-16
12091475-6	2002	Thus, in situ hybridization demonstrated initially decreased, and later increased, NET mRNA levels in locus coeruleus (LC) tissue of rats treated with DMI; whereas NET protein levels in the LC were reduced after 14 days, but unchanged after three daily DMI treatments.	Desipramine	151-154	solute carrier family 6 member 2	Rattus norvegicus	83-86
12091475-6	2002	Thus, in situ hybridization demonstrated initially decreased, and later increased, NET mRNA levels in locus coeruleus (LC) tissue of rats treated with DMI; whereas NET protein levels in the LC were reduced after 14 days, but unchanged after three daily DMI treatments.	Desipramine	151-154	solute carrier family 6 member 2	Rattus norvegicus	164-167
12091475-7	2002	Thus, DMI had similar effects on NET expression in vitro and in vivo, with opposite changes in NET mRNA and protein levels, suggesting that the regulatory mechanisms involved are complex and non-congruent.	Desipramine	6-9	solute carrier family 6 member 2	Rattus norvegicus	33-36
12070759-6	2002	These compounds as well as methamphetamine, methcathinone, and desipramine also protected the hNET from NEM inactivation of [(3)H]desipramine binding.	Desipramine	63-74	solute carrier family 6 member 2	Homo sapiens	94-98
12070759-6	2002	These compounds as well as methamphetamine, methcathinone, and desipramine also protected the hNET from NEM inactivation of [(3)H]desipramine binding.	Desipramine	130-141	solute carrier family 6 member 2	Homo sapiens	94-98
11996893-5	2002	Likewise, attenuation of antidepressant-induced NF-kappa B activity by elevation of the intracellular cAMP concentration or by retroviral driven expression of the non-degradable superrepressor I kappa B alpha S32A/S36A demonstrated that the elevation of NF-kappa B activity by amitriptyline, desipramine and fluoxetine is not an integral part of the apoptotic signaling cascade triggered by these compounds.	Desipramine	292-303	NFKB inhibitor alpha	Rattus norvegicus	193-208
11943827-6	2002	Furthermore, the ability of DMI to suppress an acute corticosterone response after swim stress is maintained in CREB-deficient mice.	Desipramine	28-31	cAMP responsive element binding protein 1	Mus musculus	112-116
11943827-7	2002	However, upregulation of a molecular target of CREB, BDNF, is abolished in the CREB-deficient mice after chronic administration of DMI.	Desipramine	131-134	cAMP responsive element binding protein 1	Mus musculus	47-51
11943827-7	2002	However, upregulation of a molecular target of CREB, BDNF, is abolished in the CREB-deficient mice after chronic administration of DMI.	Desipramine	131-134	brain derived neurotrophic factor	Mus musculus	53-57
11943827-7	2002	However, upregulation of a molecular target of CREB, BDNF, is abolished in the CREB-deficient mice after chronic administration of DMI.	Desipramine	131-134	cAMP responsive element binding protein 1	Mus musculus	79-83
12020742-5	2002	The objective of the present experiment was to determine whether two commonly used antidepressants (desipramine and fluoxetine) were effective in ameliorating IFN-alpha-induced anhedonia in rats.	Desipramine	100-111	interferon alpha 1	Homo sapiens	159-168
11704655-2	2001	Previous data demonstrate that the tricyclic antidepressant, desipramine, induces glucocorticoid receptor (GR) translocation from the cytoplasm to the nucleus in L929 cells and increases dexamethasone-induced GR-mediated gene transcription in L929 cells stably transfected with the mouse mammary tumour virus-chloramphenicol acetyltransferase (MMTV-CAT) reporter gene (LMCAT cells) (Pariante et al., 1997).	Desipramine	61-72	nuclear receptor subfamily 3, group C, member 1	Mus musculus	82-105
11916794-0	2002	Tramadol inhibits norepinephrine transporter function at desipramine-binding sites in cultured bovine adrenal medullary cells.	Desipramine	57-68	solute carrier family 6 member 2	Bos taurus	18-44
11916794-9	2002	These findings indicate that tramadol competitively inhibits NET function at desipramine-binding sites.	Desipramine	77-88	solute carrier family 6 member 2	Bos taurus	61-64
11916794-10	2002	IMPLICATIONS: Tramadol competitively inhibits norepinephrine transporter function at desipramine-binding sites in the adrenal medullary cells and probably the noradrenergic neurons of the descending inhibitory system.	Desipramine	85-96	solute carrier family 6 member 2	Bos taurus	46-72
11738543-4	2001	Patients on desipramine showed more diffuse rCBF reductions in frontal and temporal regions, more so in the left side.	Desipramine	12-23	CCAAT/enhancer binding protein zeta	Rattus norvegicus	44-48
11704655-2	2001	Previous data demonstrate that the tricyclic antidepressant, desipramine, induces glucocorticoid receptor (GR) translocation from the cytoplasm to the nucleus in L929 cells and increases dexamethasone-induced GR-mediated gene transcription in L929 cells stably transfected with the mouse mammary tumour virus-chloramphenicol acetyltransferase (MMTV-CAT) reporter gene (LMCAT cells) (Pariante et al., 1997).	Desipramine	61-72	nuclear receptor subfamily 3, group C, member 1	Mus musculus	107-109
11704655-2	2001	Previous data demonstrate that the tricyclic antidepressant, desipramine, induces glucocorticoid receptor (GR) translocation from the cytoplasm to the nucleus in L929 cells and increases dexamethasone-induced GR-mediated gene transcription in L929 cells stably transfected with the mouse mammary tumour virus-chloramphenicol acetyltransferase (MMTV-CAT) reporter gene (LMCAT cells) (Pariante et al., 1997).	Desipramine	61-72	nuclear receptor subfamily 3, group C, member 1	Mus musculus	209-211
11704655-7	2001	Twenty-four hours coincubation of cells with desipramine, clomipramine or paroxetine, also enhanced GR function in the presence of cortisol, but not of corticosterone.	Desipramine	45-56	nuclear receptor subfamily 3, group C, member 1	Mus musculus	100-102
11556901-0	2001	Chronic desipramine treatment selectively potentiates somatostatin-induced dopamine release in the nucleus accumbens.	Desipramine	8-19	somatostatin	Rattus norvegicus	54-66
11504807-12	2001	The immobility of 5-HT(1B) receptor mutant mice was decreased similarly by desipramine (5.0--20.0 mg/kg i.p.).	Desipramine	75-86	5-hydroxytryptamine (serotonin) receptor 1B	Mus musculus	18-35
11838318-6	2001	Desipramine (10 mg/kg), a tricycle antidepressant, or fluoxetine (10 mg/kg), a serotonin reuptake inhibitor, significantly reversed the LPS-induced increase in immobility time.	Desipramine	0-11	toll-like receptor 4	Mus musculus	136-139
11556901-4	2001	Chronic desipramine treatment resulted in an exaggerated somatostatin-induced increase of dopamine levels, specifically in the nucleus accumbens (3542% compared with 564% of basal in the striatum), whereas acute desipramine treatment had no effect (582% of basal) compared with saline treated rats.	Desipramine	8-19	somatostatin	Rattus norvegicus	57-69
11415943-9	2001	In addition, TNF-alpha-induced ROS production was inhibited by the acidic sphingomyelinase inhibitor desipramine (5 microM; -80%, n = 4, P &lt; 0.01) and totally blocked by the ceramide-activated protein kinase (CAPK) inhibitor dimethylaminopurine (1 mM; n = 6, P &lt; 0.05).	Desipramine	101-112	tumor necrosis factor	Homo sapiens	13-22
11454927-7	2001	In addition, desipramine significantly reduced immobility in the Dbh(-/-) mice following pretreatment with the synthetic NE precursor L-threo-3,4-dihydroxyphenylserine, but not saline.	Desipramine	13-24	dopamine beta hydroxylase	Mus musculus	65-68
11417443-0	2001	Duplication of CYP2D6 predicts high clearance of desipramine but high clearance does not predict duplication of CYP2D6.	Desipramine	49-60	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	15-21
11353802-1	2001	Previous studies have demonstrated that chronic treatment of C6 glioma cells with the antidepressants desipramine and fluoxetine increases the Triton X-100 solubility of the G protein Gsalpha (Toki et al., 1999).	Desipramine	102-113	GNAS complex locus	Homo sapiens	184-191
11353802-6	2001	Desipramine- or fluoxetine-treated cells show a more centralized clustering of Gsalpha in the Golgi region of the cell and a drastic reduction of Gsalpha in the cellular processes.	Desipramine	0-11	GNAS complex locus	Homo sapiens	79-86
11353802-6	2001	Desipramine- or fluoxetine-treated cells show a more centralized clustering of Gsalpha in the Golgi region of the cell and a drastic reduction of Gsalpha in the cellular processes.	Desipramine	0-11	GNAS complex locus	Homo sapiens	146-153
11417443-1	2001	OBJECTIVE: Duplication of CYP2D6 causes very rapid metabolism of CYP2D6 substrates such as desipramine.	Desipramine	91-102	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	26-32
11417443-1	2001	OBJECTIVE: Duplication of CYP2D6 causes very rapid metabolism of CYP2D6 substrates such as desipramine.	Desipramine	91-102	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	65-71
11106872-1	2001	The present study investigated the effect of long-term (15 mg/kg for 15 days) and acute (15 mg/kg, single administration) treatment with desmethylimipramine, a tricyclic antidepressant drug, on calcium/calmodulin-dependent protein kinase II (CaMKII), a kinase implicated in the mechanism of antidepressant drug action.	Desipramine	137-156	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	194-240
11303058-3	2001	Immunohistochemical analysis and in situ hybridization reveal that administration of the antidepressant drug desipramine decreases the accumulation of constitutively expressed TNF mRNA in neurons of the rat brain.	Desipramine	109-120	tumor necrosis factor	Rattus norvegicus	176-179
11246093-0	2001	Prolonged desipramine treatment increases the production of interleukin-10, an anti-inflammatory cytokine, in C57BL/6 mice subjected to the chronic mild stress model of depression.	Desipramine	10-21	interleukin 10	Mus musculus	60-74
11246093-5	2001	RESULTS: Prolonged treatment of C57BL/6 mice subjected to CMS with desipramine increases the ability of T cells to produce IL-10 and the ability of B cells to proliferate after stimulation with LPS; and significantly decreases the cytotoxic activity of NK cells and the proliferative responses of lymphocytes after stimulation with Con-A, PHA and anti-CD3 monoclonal antibodies.	Desipramine	67-78	interleukin 10	Mus musculus	123-128
11246093-6	2001	Repeated administration of desipramine to non-stressed mice increases the activity of T lymphocytes, lowers that of B lymphocytes, increases the production of IL-10 by T cells and has no significant effect on the activity of NK cells.	Desipramine	27-38	interleukin 10	Mus musculus	159-164
11246093-7	2001	CONCLUSION: Prolonged desipramine treatment of stressed and non-stressed C57BL/6 mice induces an increase in the production of IL-10, an anti-inflammatory cytokine.	Desipramine	22-33	interleukin 10	Mus musculus	127-132
11354249-9	2001	Inhibition of ceramide production by desipramine (25-50 microM) reduced UV-induced JNK activation in both 293 and Jurkat cells; and protects 293 cells from UV-induced apoptosis.	Desipramine	37-48	mitogen-activated protein kinase 8	Homo sapiens	83-86
11106872-2	2001	Similar to selective and non-selective serotonin reuptake inhibitors, long-term, but not acute, treatment with desmethylimipramine markedly increased the activity of CaMKII in the hippocampal synaptic vesicle fraction (+51.9%).	Desipramine	111-130	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	166-172
11106872-1	2001	The present study investigated the effect of long-term (15 mg/kg for 15 days) and acute (15 mg/kg, single administration) treatment with desmethylimipramine, a tricyclic antidepressant drug, on calcium/calmodulin-dependent protein kinase II (CaMKII), a kinase implicated in the mechanism of antidepressant drug action.	Desipramine	137-156	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	242-248
10951284-8	2000	Furthermore, both palmitoyldihydrosphingosine and desipramine, a chemically and mechanically unrelated acid-sphingomyelinase inhibitor, significantly delay barrier recovery both 2 and 4 h after acute barrier abrogation.	Desipramine	50-61	sphingomyelin phosphodiesterase 1	Homo sapiens	103-124
11082428-3	2000	We previously described down-regulation of the NET in cultured cells after continuous exposure to the tricyclic antidepressant desipramine.	Desipramine	127-138	solute carrier family 6 member 2	Homo sapiens	47-50
11080533-9	2000	Desipramine decreased epidermal growth factor (EGF) levels in all age groups, but increased the secretion of peroxidase and lysozyme.	Desipramine	0-11	epidermal growth factor like 1	Rattus norvegicus	22-45
11080533-9	2000	Desipramine decreased epidermal growth factor (EGF) levels in all age groups, but increased the secretion of peroxidase and lysozyme.	Desipramine	0-11	epidermal growth factor like 1	Rattus norvegicus	47-50
11037800-2	2000	Desipramine is extensively metabolized by cytochrome P450 2D6 (CYP2D6), and kinetics of this compound are altered in poor metabolizers.	Desipramine	0-11	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	42-61
11037800-2	2000	Desipramine is extensively metabolized by cytochrome P450 2D6 (CYP2D6), and kinetics of this compound are altered in poor metabolizers.	Desipramine	0-11	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	63-69
10913689-8	2001	Chronic treatment with desipramine or trimipramine, which do not directly inhibit 5-HT uptake, compared to fluoxetine and venlafaxine, lead to increases in 5-HT transporter densities in cingulate, agranular insular and perirhinal cortices.	Desipramine	23-34	solute carrier family 6 member 4	Rattus norvegicus	156-172
10996474-3	2000	One and two weeks administration of desipramine significantly reduces the secretion of IL-4, an anti-inflammatory cytokine.	Desipramine	36-47	interleukin 4	Mus musculus	87-91
10996474-5	2000	Prolonged desipramine administration (seven and 28 days) significantly increased the bioactivity of IL-1.	Desipramine	10-21	interleukin 1 complex	Mus musculus	100-104
10996474-6	2000	Four weeks of prolonged administration of amitriptyline and desipramine induces a significant increase in the secretion of IL-10, a cytokine with immunosuppressive and anti-inflammatory activities.	Desipramine	60-71	interleukin 10	Mus musculus	123-128
10792576-7	2000	Desmethylimipramine (DMI) treatment for 24 days did not affect basal plasma concentrations of corticosterone or insulin, or arcuate nucleus NPY mRNA expressions, but significantly decreased basal levels of locus coeruleus NPY mRNA compared to saline-treated rats.	Desipramine	0-19	neuropeptide Y	Rattus norvegicus	222-225
12516468-3	2000	Furthermore, using RT-PCR mediated cross-species partial cDNA cloning, it was found that MW-97 and desipramine(DIM) increased NGF, BDNF mRNA in the frontal cortex after chronic administration for 21 days, meanwhile, BDNF mRNA in hippocampus was also increased.	Desipramine	99-110	brain-derived neurotrophic factor	Rattus norvegicus	131-135
12516468-3	2000	Furthermore, using RT-PCR mediated cross-species partial cDNA cloning, it was found that MW-97 and desipramine(DIM) increased NGF, BDNF mRNA in the frontal cortex after chronic administration for 21 days, meanwhile, BDNF mRNA in hippocampus was also increased.	Desipramine	99-110	brain-derived neurotrophic factor	Rattus norvegicus	216-220
10871295-3	2000	In situ hybridization to rat brain sections revealed that ICER mRNA expression was significantly increased by uncompetitive NMDA receptor antagonists (MK-801, phencyclidine, ketamine, memantine) but not by the competitive antagonist CPP [(+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid] or other psychotropic agents (clozapine, haloperidol, desipramine).	Desipramine	352-363	cAMP responsive element modulator	Rattus norvegicus	58-62
10895986-0	2000	Metabolism of desipramine in Japanese psychiatric patients: the impact of CYP2D6 genotype on the hydroxylation of desipramine.	Desipramine	114-125	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	74-80
10895986-1	2000	We investigated the impact of the genotype of CYP2D6 on the hydroxylation of desipramine in eighteen patients who were administered desipramine hydrochloride per os.	Desipramine	77-88	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	46-52
10895986-1	2000	We investigated the impact of the genotype of CYP2D6 on the hydroxylation of desipramine in eighteen patients who were administered desipramine hydrochloride per os.	Desipramine	132-157	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	46-52
10895986-4	2000	The genotyping of CYP2D6 only grossly predicts the steady state concentration of desipramine, mainly predicts the risk of getting very high plasma levels.	Desipramine	81-92	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	18-24
10808050-6	2000	Chronic (14 days) administration of the antidepressant drugs desipramine or zimelidine transforms alpha(2)-adrenergic receptor-dependent decreases in TNF levels to increases in levels of TNF in the locus coeruleus.	Desipramine	61-72	tumor necrosis factor	Rattus norvegicus	150-153
10808050-6	2000	Chronic (14 days) administration of the antidepressant drugs desipramine or zimelidine transforms alpha(2)-adrenergic receptor-dependent decreases in TNF levels to increases in levels of TNF in the locus coeruleus.	Desipramine	61-72	tumor necrosis factor	Rattus norvegicus	187-190
10837797-14	2000	Treatment of rats with 6-OHDA resulted in a 52% decrease in the PDE4B3 and 58% decrease in 78 kDa PDE4B variant in hypothalamus; administration of desipramine attenuated the 6-OHDA-induced down-regulation of both PDE4B variants.	Desipramine	147-158	phosphodiesterase 4B	Rattus norvegicus	64-70
10837797-14	2000	Treatment of rats with 6-OHDA resulted in a 52% decrease in the PDE4B3 and 58% decrease in 78 kDa PDE4B variant in hypothalamus; administration of desipramine attenuated the 6-OHDA-induced down-regulation of both PDE4B variants.	Desipramine	147-158	phosphodiesterase 4B	Rattus norvegicus	64-69
10837797-14	2000	Treatment of rats with 6-OHDA resulted in a 52% decrease in the PDE4B3 and 58% decrease in 78 kDa PDE4B variant in hypothalamus; administration of desipramine attenuated the 6-OHDA-induced down-regulation of both PDE4B variants.	Desipramine	147-158	phosphodiesterase 4B	Rattus norvegicus	98-103
10837797-16	2000	In contrast, cerebellar PDE4B3 variant is up-regulated by 6-OHDA treatment and were partially normalized to control values by desipramine pretreatment.	Desipramine	126-137	phosphodiesterase 4B	Rattus norvegicus	24-30
10792576-7	2000	Desmethylimipramine (DMI) treatment for 24 days did not affect basal plasma concentrations of corticosterone or insulin, or arcuate nucleus NPY mRNA expressions, but significantly decreased basal levels of locus coeruleus NPY mRNA compared to saline-treated rats.	Desipramine	21-24	neuropeptide Y	Rattus norvegicus	222-225
10792576-8	2000	After repeated immobilization (2 h daily, for 4 days), DMI significantly reduced the stress-induced rise in locus coeruleus NPY mRNA levels, but potentiated the stress-induced rise in arcuate nucleus NPY mRNA expression.	Desipramine	55-58	neuropeptide Y	Rattus norvegicus	124-127
10792576-8	2000	After repeated immobilization (2 h daily, for 4 days), DMI significantly reduced the stress-induced rise in locus coeruleus NPY mRNA levels, but potentiated the stress-induced rise in arcuate nucleus NPY mRNA expression.	Desipramine	55-58	neuropeptide Y	Rattus norvegicus	200-203
10792576-9	2000	These results demonstrate that: (1) the increase in arcuate nucleus NPY mRNA expressions in stressed rats closely follows the decrease in plasma concentrations of insulin; (2) increases in NPY mRNA expressions occur in the absence of changes in plasma corticosterone; and (3) desipramine treatment potentiated the effect of stress on arcuate nucleus NPY mRNA expressions, but blocked the repeated stress-induced increase in locus coeruleus NPY mRNA expressions.	Desipramine	276-287	neuropeptide Y	Rattus norvegicus	189-192
10792576-9	2000	These results demonstrate that: (1) the increase in arcuate nucleus NPY mRNA expressions in stressed rats closely follows the decrease in plasma concentrations of insulin; (2) increases in NPY mRNA expressions occur in the absence of changes in plasma corticosterone; and (3) desipramine treatment potentiated the effect of stress on arcuate nucleus NPY mRNA expressions, but blocked the repeated stress-induced increase in locus coeruleus NPY mRNA expressions.	Desipramine	276-287	neuropeptide Y	Rattus norvegicus	189-192
10792576-9	2000	These results demonstrate that: (1) the increase in arcuate nucleus NPY mRNA expressions in stressed rats closely follows the decrease in plasma concentrations of insulin; (2) increases in NPY mRNA expressions occur in the absence of changes in plasma corticosterone; and (3) desipramine treatment potentiated the effect of stress on arcuate nucleus NPY mRNA expressions, but blocked the repeated stress-induced increase in locus coeruleus NPY mRNA expressions.	Desipramine	276-287	neuropeptide Y	Rattus norvegicus	189-192
10792576-10	2000	Thus, NPY mRNA expression in the arcuate nucleus and the locus coeruleus is sensitive to the effects of stress and to the antidepressant drug desipramine, but the arcuate nucleus NPY system is regulated by different mechanisms than the locus coeruleus NPY system.	Desipramine	142-153	neuropeptide Y	Rattus norvegicus	6-9
10706994-3	2000	The current study examined the effect of long-term administration, up to 6 weeks, of fluvoxamine, desipramine or saline on MAO-A and MAO-B activities in rat striatum, frontal cortex and liver.	Desipramine	98-109	monoamine oxidase A	Rattus norvegicus	123-128
11343573-4	2000	in desipramine- and citalopram-treated rats was abolished, indicating a desensitization of 5-HT1A receptors.	Desipramine	3-14	5-hydroxytryptamine receptor 1A	Rattus norvegicus	91-97
10706994-3	2000	The current study examined the effect of long-term administration, up to 6 weeks, of fluvoxamine, desipramine or saline on MAO-A and MAO-B activities in rat striatum, frontal cortex and liver.	Desipramine	98-109	monoamine oxidase B	Rattus norvegicus	133-138
10693959-1	2000	In a previous study, an up-regulation of rolipram-sensitive, low-Km, cyclic AMP phosphodiesterase (PDE4) subtype PDE4A in rat cerebral cortex following repeated treatment of desipramine was observed.	Desipramine	174-185	phosphodiesterase 4A	Rattus norvegicus	113-118
10693959-2	2000	To determine whether this effect is shared by antidepressants from different pharmacological classes, PDE4A expression was examined using immunoblot analyses following repeated treatment with the norepinephrine re-uptake inhibitor desipramine, the monoamine oxidase inhibitor phenelzine, the atypical antidepressant trazodone, and the serotonin reuptake inhibitor fluoxetine.	Desipramine	231-242	phosphodiesterase 4A	Rattus norvegicus	102-107
10693959-3	2000	Desipramine, phenelzine, and fluoxetine all increased the intensities of the PDE4A bands in hippocampal preparations; trazodone did not.	Desipramine	0-11	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.	Desipramine	96-107	phosphodiesterase 4A	Rattus norvegicus	59-64
10633490-2	2000	Coadministration of rolipram or Ro 20-1724 with an antidepressant (either desipramine or Org 4428) for 21 d resulted in a significant induction of BDNF mRNA in hippocampus relative to administration of vehicle.	Desipramine	74-85	brain-derived neurotrophic factor	Rattus norvegicus	147-151
10854034-5	2000	The induction of BDNF mRNA by MK-801 was attenuated by pre-treatment (1 h prior to MK-801 administration) with the antipsychotics, clozapine (25 mg/kg) and haloperidol (2 mg/kg), but not with the antidepressant desipramine (15 mg/kg).	Desipramine	211-222	brain-derived neurotrophic factor	Rattus norvegicus	17-21
10718121-2	2000	The formation of metabolite intermediate (MI)-complexes between cytochrome P450 (CYP) and the alkylamine-substituted drugs diltiazem (DTZ) and desipramine (DES) and their effect on CYP activities was investigated in rat liver.	Desipramine	143-154	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-79
10718121-2	2000	The formation of metabolite intermediate (MI)-complexes between cytochrome P450 (CYP) and the alkylamine-substituted drugs diltiazem (DTZ) and desipramine (DES) and their effect on CYP activities was investigated in rat liver.	Desipramine	143-154	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-84
10718121-2	2000	The formation of metabolite intermediate (MI)-complexes between cytochrome P450 (CYP) and the alkylamine-substituted drugs diltiazem (DTZ) and desipramine (DES) and their effect on CYP activities was investigated in rat liver.	Desipramine	156-159	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-79
10718121-2	2000	The formation of metabolite intermediate (MI)-complexes between cytochrome P450 (CYP) and the alkylamine-substituted drugs diltiazem (DTZ) and desipramine (DES) and their effect on CYP activities was investigated in rat liver.	Desipramine	156-159	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-84
10718121-2	2000	The formation of metabolite intermediate (MI)-complexes between cytochrome P450 (CYP) and the alkylamine-substituted drugs diltiazem (DTZ) and desipramine (DES) and their effect on CYP activities was investigated in rat liver.	Desipramine	156-159	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	181-184
10718121-10	2000	By comparison, inhibition of CYP activity by DES was less pronounced than in control liver.	Desipramine	45-48	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-32
10601816-9	2000	Vehicle treated OB rats displayed a significant impairment in LPS-induced IL-1beta (54%) and TNF-alpha (70%) secretion compared to their sham operated controls, an effect that was potentiated following chronic desipramine treatment.	Desipramine	210-221	interleukin 1 beta	Rattus norvegicus	74-82
10601816-9	2000	Vehicle treated OB rats displayed a significant impairment in LPS-induced IL-1beta (54%) and TNF-alpha (70%) secretion compared to their sham operated controls, an effect that was potentiated following chronic desipramine treatment.	Desipramine	210-221	tumor necrosis factor	Rattus norvegicus	93-102
10601816-10	2000	Furthermore, sham animals that were chronically treated with desipramine displayed decreases in LPS-provoked IL-1beta (51%) and TNF-alpha (49%) secretion compared to vehicle treated counterparts.	Desipramine	61-72	interleukin 1 beta	Rattus norvegicus	109-117
10601816-10	2000	Furthermore, sham animals that were chronically treated with desipramine displayed decreases in LPS-provoked IL-1beta (51%) and TNF-alpha (49%) secretion compared to vehicle treated counterparts.	Desipramine	61-72	tumor necrosis factor	Rattus norvegicus	128-137
10601816-13	2000	Whilst chronic treatment with desipramine normalized the behavioural hyperactivity observed in OB rats, such treatment further impaired LPS-induced IL-1beta and TNF-alpha secretion in bulbectomized rats.	Desipramine	30-41	tumor necrosis factor	Rattus norvegicus	161-170
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.	Desipramine	245-248	solute carrier family 6 member 4	Rattus norvegicus	0-4
11015030-3	2000	We investigated the effect of 21 days administration, followed by 7 days withdrawal, of fluvoxamine (10 mg/kg), desipramine (10 mg/kg) and lithium carbonate (25 mg/kg) on PBR and CBR binding characteristics in male Sprague-Dawley rats.	Desipramine	112-123	translocator protein	Rattus norvegicus	171-174
10520140-4	1999	The time course of the effects of the tricyclic antidepressants desipramine and amitriptyline on GR binding, as assessed by [3H]dexamethasone binding using RU 28362, a specific agonist for GR, showed a biphasic mode of stimulation: desipramine significantly increased the GR binding with 2-day exposure by 36% over that in controls and by 99% and 60% with 10- and 14-day exposures, respectively.	Desipramine	64-75	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	97-99
10520140-7	1999	Northern blot analysis demonstrated that the GR mRNA level was significantly increased by 14-day treatment with desipramine (+142% over control), amitriptyline (+108%), mianserin (+124%), paroxetine (+42%) and sulpiride (+92%), but not with haloperidol.	Desipramine	112-123	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	45-47
10520140-8	1999	Immunocytochemistry for GR revealed that 2- or 14-day treatment with desipramine significantly increased the number of GR-positive cells with dominant immunoreactivity in the nuclei of granule cell-like neurones or in perikarya of pyramidal cell- and granule cell-like neurones.	Desipramine	69-80	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	24-26
10520140-8	1999	Immunocytochemistry for GR revealed that 2- or 14-day treatment with desipramine significantly increased the number of GR-positive cells with dominant immunoreactivity in the nuclei of granule cell-like neurones or in perikarya of pyramidal cell- and granule cell-like neurones.	Desipramine	69-80	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	119-121
10424850-0	1999	Desipramine treatment decreases 3H-nisoxetine binding and norepinephrine transporter mRNA in SK-N-SHSY5Y cells.	Desipramine	0-11	solute carrier family 6 member 2	Homo sapiens	58-84
11015030-6	2000	After withdrawal, PBR density remained decreased in the liver in all three groups and in the kidneys of the desipramine- and lithium-treated animals.	Desipramine	108-119	translocator protein	Rattus norvegicus	18-21
11015030-7	2000	In the cerebral cortex, CBR density increased in response to all three agents, whereas PBR density decreased significantly in response to desipramine and lithium carbonate.	Desipramine	138-149	translocator protein	Rattus norvegicus	87-90
11015030-8	2000	Chronic treatment with fluvoxamine, desipramine and lithium carbonate is apparently associated with a modulation in PBR expression in the testes, adrenals, kidneys, liver and brain, and in CBR expression in brain.	Desipramine	36-47	translocator protein	Rattus norvegicus	116-119
10424850-1	1999	The antidepressant desipramine has been shown to decrease synaptic membrane concentrations of the norepinephrine re-uptake transporter (NET) in vivo and in vitro, on both an acute and a chronic basis.	Desipramine	19-30	solute carrier family 6 member 2	Homo sapiens	98-134
10424850-1	1999	The antidepressant desipramine has been shown to decrease synaptic membrane concentrations of the norepinephrine re-uptake transporter (NET) in vivo and in vitro, on both an acute and a chronic basis.	Desipramine	19-30	solute carrier family 6 member 2	Homo sapiens	136-139
10424850-3	1999	In this study, we treated SK-N-SHSY5Y cells with 100 nM desipramine for 24 or 72 h, and measured 3H-nisoxetine binding (as an estimate of NETs) and NET mRNA by quantitative reverse transcription polymerase chain reaction.	Desipramine	56-67	solute carrier family 6 member 2	Homo sapiens	138-141
10424850-6	1999	We conclude that decreased NET synthesis may contribute to the chronic, but not acute, effect of desipramine to downregulate the NET.	Desipramine	97-108	solute carrier family 6 member 2	Homo sapiens	27-30
10424850-6	1999	We conclude that decreased NET synthesis may contribute to the chronic, but not acute, effect of desipramine to downregulate the NET.	Desipramine	97-108	solute carrier family 6 member 2	Homo sapiens	129-132
10201278-0	1999	Different effect of desipramine on protein kinase C in platelets between bipolar and major depressive disorders.	Desipramine	20-31	proline rich transmembrane protein 2	Homo sapiens	35-51
10408227-7	1999	SKF 525-A, an inhibitor of cytochrome P450 (CYP), markedly suppressed DMI formation at both pH points.	Desipramine	70-73	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	27-42
10408227-7	1999	SKF 525-A, an inhibitor of cytochrome P450 (CYP), markedly suppressed DMI formation at both pH points.	Desipramine	70-73	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	44-47
10408227-9	1999	These results suggest that CYP enzyme(s) are mainly responsible for DMI formation at pH 8.5 and 7.5, and FMO enzyme(s) also are involved in IMI N-demethylation at a higher pH range in rat liver microsomes, at least in part.	Desipramine	68-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	27-30
10218774-9	1999	This presynaptic modulation requires SNARE proteins because cleavage of SNAP-25 with the botulinum neurotoxin A strongly reduced the desipramine-induced glutamate release.	Desipramine	133-144	synaptosome associated protein 25	Rattus norvegicus	72-79
9989935-6	1999	On the other hand, AST-RB2 efficiently catalyzed sulfonation of desipramine and DHEA, but had no activity toward 2-naphthol.	Desipramine	64-75	sulfotransferase 2A1	Oryctolagus cuniculus	19-26
10201278-2	1999	The PKC activity of platelets incubated with desipramine was determined in vitro.	Desipramine	45-56	proline rich transmembrane protein 2	Homo sapiens	4-7
10201278-3	1999	The PKC activity of the major depressive disorder subjects and healthy volunteers was inhibited by desipramine, whereas that of the bipolar disorder subjects showed both inhibition and activation.	Desipramine	99-110	proline rich transmembrane protein 2	Homo sapiens	4-7
9861783-5	1998	Desipramine (DESI), another tricyclic antidepressant, also decreased the TRH content (from 63.6 +/- 2.5, at 10(-9) mol/L, to 12.6 +/- 0.4, at 10(-5) mol/L, fmol/well; P &lt; 0.05).	Desipramine	0-11	thyrotropin releasing hormone	Rattus norvegicus	73-76
9987205-10	1999	In vitro experiments also showed that desipramine increased glucocorticoid receptor mRNA.	Desipramine	38-49	nuclear receptor subfamily 3, group C, member 1	Mus musculus	60-83
10374896-4	1999	After chronic desipramine but not after chronic clorgyline treatments, the density (Bmax) of alpha2-adrenoceptors was increased (46%).	Desipramine	14-25	adrenoceptor alpha 2A	Rattus norvegicus	93-113
10374896-7	1999	The selective upregulation of the alpha2A-adrenoceptor subtype following chronic desipramine administration is compatible with a differential location and function of the alpha2-adrenoceptor subtypes in the rat kidney.	Desipramine	81-92	adrenoceptor alpha 2A	Rattus norvegicus	34-54
10435604-7	1999	Depressed patients showed a significant decrease in 5-HT2 receptor binding as measured by setoperone binding in frontal, temporal, parietal, and occipital cortical regions following desipramine treatment.	Desipramine	182-193	5-hydroxytryptamine receptor 2A	Homo sapiens	52-66
9877326-7	1998	The beta1-antagonist atenolol (1.0 micromol/l) potentiated the facilitatory effects of isoprenaline in the presence of DMI and corticosterone.	Desipramine	119-122	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	4-9
9861783-5	1998	Desipramine (DESI), another tricyclic antidepressant, also decreased the TRH content (from 63.6 +/- 2.5, at 10(-9) mol/L, to 12.6 +/- 0.4, at 10(-5) mol/L, fmol/well; P &lt; 0.05).	Desipramine	13-17	thyrotropin releasing hormone	Rattus norvegicus	73-76
9930326-6	1998	Transfection of H441 cells in the presence of 0.1-1 microgram/ml DMI-2 caused: (1) 10-fold enhancement of CAT activity when the bacterial plasmid was complexed with either surfactant protein A-poly-lysine or transferrin-poly-lysine; (2) 1.5- to two-fold enhancement of CAT activity in cells exposed to lipofectin-DNA complexes: (3) no effect on transfection via calcium phosphate co-precipitation.	Desipramine	65-68	transferrin	Homo sapiens	208-219
9758674-0	1998	Inhibition of desipramine hydroxylation (Cytochrome P450-2D6) in vitro by quinidine and by viral protease inhibitors: relation to drug interactions in vivo.	Desipramine	14-25	cytochrome P450 2D6	Homo sapiens	41-60
9758674-3	1998	Biotransformation of desipramine (DMI) to hydroxydesipramine (OH-DMI), an index reaction used to profile activity of human cytochrome P450-2D6, was studied in vitro using human liver microsomes.	Desipramine	34-37	cytochrome P450 2D6	Homo sapiens	123-142
9724254-6	1998	min-1), Na+-dependent mechanism that was inhibited by chlorimipramine &gt; imipramine &gt; fluoxetine &gt; desipramine &gt; zimelidine.	Desipramine	107-118	CD59 molecule (CD59 blood group)	Homo sapiens	0-5
9669506-2	1998	The selective 5-HT reuptake inhibitors paroxetine, indalpine and fluvoxamine displayed a high affinity for the 5-HT transporter, whereas the norepinephrine reuptake inhibitor desipramine had a high affinity for the norepinephrine transporter.	Desipramine	175-186	solute carrier family 6 member 2	Rattus norvegicus	215-241
9778103-3	1998	injection of 10 mg/kg desipramine to naive mice increased the relative weight of their spleens, the response of their splenocytes to the mitogen concavaline-A and their ability to produce IL-10, as compared to saline controls.	Desipramine	22-33	interleukin 10	Mus musculus	188-193
9778103-4	1998	Exposing the desipramine-treated mice to a swimming stress significantly reduced these parameters, as well as the levels of IL-2 and IFN-gamma, as compared to desipramine-treated mice.	Desipramine	13-24	interleukin 2	Mus musculus	124-128
9778103-4	1998	Exposing the desipramine-treated mice to a swimming stress significantly reduced these parameters, as well as the levels of IL-2 and IFN-gamma, as compared to desipramine-treated mice.	Desipramine	13-24	interferon gamma	Mus musculus	133-142
9723120-14	1998	Since chronic desipramine, and not fluoxetine, is able to increase hippocampal glucocorticoid receptor (GR) expression, interactions of GR with CREB and SP1 may determine the lack of effect of desipramine on binding activity of the two latter transcription factors in this brain region.	Desipramine	14-25	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	79-102
9723120-14	1998	Since chronic desipramine, and not fluoxetine, is able to increase hippocampal glucocorticoid receptor (GR) expression, interactions of GR with CREB and SP1 may determine the lack of effect of desipramine on binding activity of the two latter transcription factors in this brain region.	Desipramine	14-25	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	104-106
9723124-0	1998	Bupropion and desipramine increase dopamine transporter mRNA expression in the ventral tegmental area/substantia nigra of rat brain.	Desipramine	14-25	solute carrier family 6 member 3	Rattus norvegicus	35-55
9595891-18	1998	DISCUSSION: Treatment with either desipramine or ECT modified noradrenergic functioning in patients with depression, as assessed by growth hormone response to the clonidine challenge.	Desipramine	34-45	growth hormone 1	Homo sapiens	132-146
9523572-10	1998	The present findings imply that down-regulation of the hNET in 293-hNET cells induced by desipramine results from a selective reduction in hNET protein levels, presumably a consequence of either a reduction in the translation of hNET mRNA or from an enhanced degradation of hNET protein.	Desipramine	89-100	solute carrier family 6 member 2	Homo sapiens	55-59
9564441-10	1998	The decreases in 5-HT1A mRNA and binding, as well as the MR/GR alterations, were prevented in animals that received imipramine or desipramine antidepressant treatment.	Desipramine	130-141	5-hydroxytryptamine receptor 1A	Rattus norvegicus	17-23
9523560-9	1998	Scatchard analysis of [3H]desipramine binding revealed that IFN-alpha decreased the maximal binding (Bmax) values without any change in the dissociation constant (K(D)) values.	Desipramine	26-37	interferon alpha-A	Bos taurus	60-69
9625487-8	1998	These findings indicate that the extent of increases in imipramine and desipramine serum and brain levels are greater during elevated serum AAG states than during normal AAG states when imipramine is co-administered with fluoxetine.	Desipramine	71-82	nitrogen permease regulator-like 3	Mus musculus	140-143
9625487-8	1998	These findings indicate that the extent of increases in imipramine and desipramine serum and brain levels are greater during elevated serum AAG states than during normal AAG states when imipramine is co-administered with fluoxetine.	Desipramine	71-82	nitrogen permease regulator-like 3	Mus musculus	170-173
9523572-10	1998	The present findings imply that down-regulation of the hNET in 293-hNET cells induced by desipramine results from a selective reduction in hNET protein levels, presumably a consequence of either a reduction in the translation of hNET mRNA or from an enhanced degradation of hNET protein.	Desipramine	89-100	solute carrier family 6 member 2	Homo sapiens	67-71
9523572-10	1998	The present findings imply that down-regulation of the hNET in 293-hNET cells induced by desipramine results from a selective reduction in hNET protein levels, presumably a consequence of either a reduction in the translation of hNET mRNA or from an enhanced degradation of hNET protein.	Desipramine	89-100	solute carrier family 6 member 2	Homo sapiens	67-71
9523572-10	1998	The present findings imply that down-regulation of the hNET in 293-hNET cells induced by desipramine results from a selective reduction in hNET protein levels, presumably a consequence of either a reduction in the translation of hNET mRNA or from an enhanced degradation of hNET protein.	Desipramine	89-100	solute carrier family 6 member 2	Homo sapiens	67-71
9523572-10	1998	The present findings imply that down-regulation of the hNET in 293-hNET cells induced by desipramine results from a selective reduction in hNET protein levels, presumably a consequence of either a reduction in the translation of hNET mRNA or from an enhanced degradation of hNET protein.	Desipramine	89-100	solute carrier family 6 member 2	Homo sapiens	67-71
9495547-4	1997	Heterologous expression of rNET in HEK293 cells revealed that uptake of [3H]norepinephrine is sodium- and chloride-dependent and highly sensitive to the selective norepinephrine transporter inhibitors desipramine and nisoxetine.	Desipramine	201-212	solute carrier family 6 member 2	Rattus norvegicus	27-31
9523572-0	1998	Down-regulation of the human norepinephrine transporter in intact 293-hNET cells exposed to desipramine.	Desipramine	92-103	solute carrier family 6 member 2	Homo sapiens	29-55
9523572-0	1998	Down-regulation of the human norepinephrine transporter in intact 293-hNET cells exposed to desipramine.	Desipramine	92-103	solute carrier family 6 member 2	Homo sapiens	70-74
9523572-1	1998	The effects of continuous exposure of cultured cells expressing the human norepinephrine transporter (hNET) to the hNET inhibitor desipramine on hNET expression and function were studied.	Desipramine	130-141	solute carrier family 6 member 2	Homo sapiens	115-119
9523572-1	1998	The effects of continuous exposure of cultured cells expressing the human norepinephrine transporter (hNET) to the hNET inhibitor desipramine on hNET expression and function were studied.	Desipramine	130-141	solute carrier family 6 member 2	Homo sapiens	115-119
9523572-2	1998	Exposure of HEK-293 cells transfected stably with the hNET cDNA (293-hNET cells) to desipramine for 3 days reduced the specific binding of [3H]nisoxetine in membrane homogenates in a concentration-dependent manner.	Desipramine	84-95	solute carrier family 6 member 2	Homo sapiens	54-58
9523572-2	1998	Exposure of HEK-293 cells transfected stably with the hNET cDNA (293-hNET cells) to desipramine for 3 days reduced the specific binding of [3H]nisoxetine in membrane homogenates in a concentration-dependent manner.	Desipramine	84-95	solute carrier family 6 member 2	Homo sapiens	69-73
9523572-3	1998	The magnitude of the reductions in [3H]nisoxetine binding to hNET was dependent on the length of time of the exposure to desipramine, reaching 77% after a 21-day exposure.	Desipramine	121-132	solute carrier family 6 member 2	Homo sapiens	61-65
9523572-6	1998	Similar to binding, hNET protein levels returned to control levels 72 h after cessation of desipramine exposure.	Desipramine	91-102	solute carrier family 6 member 2	Homo sapiens	20-24
9523572-7	1998	Northern blotting indicated that exposure of 293-hNET cells to desipramine did not significantly alter hNET mRNA levels.	Desipramine	63-74	solute carrier family 6 member 2	Homo sapiens	49-53
9523572-8	1998	Uptake of [3H]norepinephrine by 293-hNET cells was markedly reduced after a 3-day exposure to desipramine.	Desipramine	94-105	solute carrier family 6 member 2	Homo sapiens	36-40
9495547-4	1997	Heterologous expression of rNET in HEK293 cells revealed that uptake of [3H]norepinephrine is sodium- and chloride-dependent and highly sensitive to the selective norepinephrine transporter inhibitors desipramine and nisoxetine.	Desipramine	201-212	solute carrier family 6 member 2	Bos taurus	163-189
9205822-1	1997	AIMS: In order to anticipate drug-interactions of potential clinical significance the ability of the novel antidepressant, venlafaxine, to inhibit CYP2D6 dependent imipramine and desipramine 2-hydroxylation was investigated in human liver microsomes.	Desipramine	179-190	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	147-153
9462878-7	1997	Only DMI (5 mg/kg) suppressed AS at P11.	Desipramine	5-8	S100 calcium binding protein A10	Rattus norvegicus	36-39
9428594-0	1997	Synthesis of 11C-labeled desipramine and its metabolite 2-hydroxydesipramine: potential radiotracers for PET studies of the norepinephrine transporter.	Desipramine	25-36	solute carrier family 6 member 2	Homo sapiens	124-150
9428594-5	1997	[11C]DMI and [11C]HDMI have potential utility as PET radiotracers for the norepinephrine transporter.	Desipramine	5-8	solute carrier family 6 member 2	Homo sapiens	74-100
9357451-7	1997	After administration of the tricyclic antidepressant desipramine, tissue sections obtained from the rat hippocampus and locus coeruleus are devoid of neuronal-associated TNF alpha immunoreactivity.	Desipramine	53-64	tumor necrosis factor	Rattus norvegicus	170-179
9380019-0	1997	Steroid-independent translocation of the glucocorticoid receptor by the antidepressant desipramine.	Desipramine	87-98	nuclear receptor subfamily 3, group C, member 1	Mus musculus	41-64
9380019-5	1997	To examine this latter possibility, we evaluated translocation of the GR from the cytoplasm to the nucleus after 24-hr in vitro treatment of L929 cells (mouse fibroblasts) with the tricyclic antidepressant desipramine (0.1-10 microM) in the presence or absence of the synthetic steroid dexamethasone.	Desipramine	206-217	nuclear receptor subfamily 3, group C, member 1	Mus musculus	70-72
9380019-7	1997	Desipramine was found to (i) induce GR translocation from the cytoplasm to the nucleus in the absence of steroids (with no effect alone on GR-mediated gene transcription) and (ii) potentiate dexamethasone-induced GR translocation and dexamethasone-induced GR-mediated gene transcription.	Desipramine	0-11	nuclear receptor subfamily 3, group C, member 1	Mus musculus	36-38
9380019-7	1997	Desipramine was found to (i) induce GR translocation from the cytoplasm to the nucleus in the absence of steroids (with no effect alone on GR-mediated gene transcription) and (ii) potentiate dexamethasone-induced GR translocation and dexamethasone-induced GR-mediated gene transcription.	Desipramine	0-11	nuclear receptor subfamily 3, group C, member 1	Mus musculus	139-141
9380019-7	1997	Desipramine was found to (i) induce GR translocation from the cytoplasm to the nucleus in the absence of steroids (with no effect alone on GR-mediated gene transcription) and (ii) potentiate dexamethasone-induced GR translocation and dexamethasone-induced GR-mediated gene transcription.	Desipramine	0-11	nuclear receptor subfamily 3, group C, member 1	Mus musculus	139-141
9380019-7	1997	Desipramine was found to (i) induce GR translocation from the cytoplasm to the nucleus in the absence of steroids (with no effect alone on GR-mediated gene transcription) and (ii) potentiate dexamethasone-induced GR translocation and dexamethasone-induced GR-mediated gene transcription.	Desipramine	0-11	nuclear receptor subfamily 3, group C, member 1	Mus musculus	139-141
9276071-3	1997	This report demonstrates that a single dose of desipramine (10 or 25 mg/kg), a classical tricyclic antidepressant drug acting on the adrenergic system, induced c-fos and zif268 expression in rat hippocampus without affecting c-jun.	Desipramine	47-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
9276071-3	1997	This report demonstrates that a single dose of desipramine (10 or 25 mg/kg), a classical tricyclic antidepressant drug acting on the adrenergic system, induced c-fos and zif268 expression in rat hippocampus without affecting c-jun.	Desipramine	47-58	early growth response 1	Rattus norvegicus	170-176
9314045-2	1997	We have investigated the effects of long-term treatment with desipramine on the phosphorylation state of microtubule-associated protein 2 (MAP2) and microtubule assembly in the rat cerebral cortex.	Desipramine	61-72	microtubule-associated protein 2	Rattus norvegicus	105-137
9314045-2	1997	We have investigated the effects of long-term treatment with desipramine on the phosphorylation state of microtubule-associated protein 2 (MAP2) and microtubule assembly in the rat cerebral cortex.	Desipramine	61-72	microtubule-associated protein 2	Rattus norvegicus	139-143
9314045-4	1997	The degree of phosphorylation of serine residues of MAP2 was significantly increased after chronic administration of desipramine without changes in the total concentration of MAP2.	Desipramine	117-128	microtubule-associated protein 2	Rattus norvegicus	52-56
9314045-8	1997	These results raise the possibility that the changes in the degree of phosphorylation of MAP2 and microtubule assembly represent intracellular modifications involved in functional changes elicited by long-term treatment with desipramine.	Desipramine	225-236	microtubule-associated protein 2	Rattus norvegicus	89-93
9220124-3	1997	This review article will focus on basic pharmacokinetic considerations for elderly patients when psychotropics metabolized by CYP2D6, such as nortriptyline and desipramine, are prescribed.	Desipramine	160-171	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	126-132
9220124-12	1997	Significant correlations have been reported between individual CYP2D6 activity and plasma concentrations of nortriptyline and desipramine.	Desipramine	126-137	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	63-69
9651108-0	1998	Influence of the antidepressants desipramine and fluoxetine on tryptophan-2,3-dioxygenase in the presence of exogenous melatonin.	Desipramine	33-44	tryptophan 2,3-dioxygenase	Rattus norvegicus	63-89
9651108-4	1998	Desipramine reduced basal hepatic tryptophan-2,3-dioxygenase activity in the liver while fluoxetine had no observable effect.	Desipramine	0-11	tryptophan 2,3-dioxygenase	Rattus norvegicus	34-60
9256169-6	1997	The binding of [3H]GBR-12935 to CYP2D6 was decreased partially by substrates or inhibitors of CYP2D isoforms (quinine, quinidine, propranolol, bufuralol, imipramine, and desipramine).	Desipramine	170-181	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-38
9256169-6	1997	The binding of [3H]GBR-12935 to CYP2D6 was decreased partially by substrates or inhibitors of CYP2D isoforms (quinine, quinidine, propranolol, bufuralol, imipramine, and desipramine).	Desipramine	170-181	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-37
9205822-5	1997	The inhibitory effect of imipramine and desipramine on liver microsomal CYP2D6 dependent venlafaxine O-demethylation was determined similarly.	Desipramine	40-51	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	72-78
9205822-10	1997	Imipramine and desipramine gave marked inhibition of CYP2D6 dependent venlafaxine O-demethylase activity (Ki values of 3.9 +/- 1.7 and 1.7 +/- 0.9 microM, respectively).	Desipramine	15-26	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	53-59
9169301-3	1997	In this study, the influence of the selective beta 1- (CGP 20712A) and beta 2- (ICI 118551) adrenergic blockers on the antinociceptive effect of desipramine and nortriptyline was studied in mice using physical and chemical nociceptive tests that implicate different levels of sensory-motor integration in the central nervous system (CNS).	Desipramine	145-156	hemoglobin, beta adult major chain	Mus musculus	46-52
9169301-3	1997	In this study, the influence of the selective beta 1- (CGP 20712A) and beta 2- (ICI 118551) adrenergic blockers on the antinociceptive effect of desipramine and nortriptyline was studied in mice using physical and chemical nociceptive tests that implicate different levels of sensory-motor integration in the central nervous system (CNS).	Desipramine	145-156	hemoglobin, beta adult minor chain	Mus musculus	71-77
9063880-6	1997	It has the same specificity as wild type SERT for the antidepressants paroxetine and desipramine.	Desipramine	85-96	solute carrier family 6 member 4	Homo sapiens	41-45
9084457-2	1997	At least three different P450s appear to be responsible for the N-demethylation of imipramine to desipramine in vivo: CYP1A2, CYP2C19, and CYP3A4.	Desipramine	97-108	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	118-124
9084457-2	1997	At least three different P450s appear to be responsible for the N-demethylation of imipramine to desipramine in vivo: CYP1A2, CYP2C19, and CYP3A4.	Desipramine	97-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	126-133
9084457-2	1997	At least three different P450s appear to be responsible for the N-demethylation of imipramine to desipramine in vivo: CYP1A2, CYP2C19, and CYP3A4.	Desipramine	97-108	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	139-145
9049581-0	1997	Relationship between plasma desipramine levels, CYP2D6 phenotype and clinical response to desipramine: a prospective study.	Desipramine	90-101	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	48-54
9049581-1	1997	OBJECTIVE: The clinical relevance of the CYP2D6 oxidation polymorphism in the treatment of depression with desipramine (DMI) was studied prospectively in depressed outpatients.	Desipramine	107-118	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	41-47
9049581-1	1997	OBJECTIVE: The clinical relevance of the CYP2D6 oxidation polymorphism in the treatment of depression with desipramine (DMI) was studied prospectively in depressed outpatients.	Desipramine	120-123	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	41-47
9503270-3	1997	DMI, as previously reported, significantly increased hippocampal glucocorticoid receptor (GR) mRNA while the equipotent NE uptake inhibitor (+)-oxaprotiline like the inactive (-)-oxaprotiline did not alter hippocampal levels of GR mRNA.	Desipramine	0-3	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	65-88
9503270-3	1997	DMI, as previously reported, significantly increased hippocampal glucocorticoid receptor (GR) mRNA while the equipotent NE uptake inhibitor (+)-oxaprotiline like the inactive (-)-oxaprotiline did not alter hippocampal levels of GR mRNA.	Desipramine	0-3	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	90-92
9503270-3	1997	DMI, as previously reported, significantly increased hippocampal glucocorticoid receptor (GR) mRNA while the equipotent NE uptake inhibitor (+)-oxaprotiline like the inactive (-)-oxaprotiline did not alter hippocampal levels of GR mRNA.	Desipramine	0-3	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	228-230
9395259-0	1997	Interaction mechanisms of imipramine and desipramine with enkephalin-degrading aminopeptidases in vitro.	Desipramine	41-52	proenkephalin	Rattus norvegicus	58-68
9395259-4	1997	The present work shows the effects in vitro of imipramine and its active metabolite desipramine on the activities of two membrane-bound enkephalin-degrading aminopeptidases present in rat brain.	Desipramine	84-95	proenkephalin	Rattus norvegicus	136-146
8832768-7	1996	Basal and DMI-induced GH levels, on the other hand, did not differ in PTSD versus normal subjects.	Desipramine	10-13	growth hormone 1	Homo sapiens	22-24
8893267-1	1996	PURPOSE: The effect of elevated serum alpha-1-acid glycoprotein (AAG) concentrations on the steady-state serum and brain levels of imipramine and its metabolite desipramine was assessed.	Desipramine	161-172	nitrogen permease regulator-like 3	Mus musculus	38-63
8893267-1	1996	PURPOSE: The effect of elevated serum alpha-1-acid glycoprotein (AAG) concentrations on the steady-state serum and brain levels of imipramine and its metabolite desipramine was assessed.	Desipramine	161-172	nitrogen permease regulator-like 3	Mus musculus	65-68
8893267-11	1996	CONCLUSIONS: Elevated serum AAG impedes the transport of imipramine and desipramine into the brain.	Desipramine	72-83	nitrogen permease regulator-like 3	Mus musculus	28-31
8835703-6	1996	In conclusion, by taking into account that the incidence of the PMs of CYP2C19 is much greater (18-23%) than that of CYP2D6 (&lt; 1%) in Japanese population, the individually predetermined assessment of the CYP2C19-mediated metabolic capacity of imipramine would be more valuable than that of the CYP2D6-mediated capacity for forecasting the steady-state concentrations of imipramine and desipramine in Japanese depressive patients, thereby attaining an individualized optimization of imipramine therapy.	Desipramine	388-399	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
9178363-2	1997	The purpose of this study was to examine the phosphorylation of a major PKC substrate involved in modulation of neurotransmitter release, GAP-43, in a synaptosomal preparation from rat cerebral cortex after repeated administration of fluxetine (FL) and desipramine (DMI).	Desipramine	253-264	protein kinase C, gamma	Rattus norvegicus	72-75
9178363-2	1997	The purpose of this study was to examine the phosphorylation of a major PKC substrate involved in modulation of neurotransmitter release, GAP-43, in a synaptosomal preparation from rat cerebral cortex after repeated administration of fluxetine (FL) and desipramine (DMI).	Desipramine	253-264	growth associated protein 43	Rattus norvegicus	138-144
9178363-2	1997	The purpose of this study was to examine the phosphorylation of a major PKC substrate involved in modulation of neurotransmitter release, GAP-43, in a synaptosomal preparation from rat cerebral cortex after repeated administration of fluxetine (FL) and desipramine (DMI).	Desipramine	266-269	protein kinase C, gamma	Rattus norvegicus	72-75
9178363-2	1997	The purpose of this study was to examine the phosphorylation of a major PKC substrate involved in modulation of neurotransmitter release, GAP-43, in a synaptosomal preparation from rat cerebral cortex after repeated administration of fluxetine (FL) and desipramine (DMI).	Desipramine	266-269	growth associated protein 43	Rattus norvegicus	138-144
9178363-8	1997	The extent of phosphorylation of GAP-43 protein by native PKC in synaptosomes of rats treated with either FL or DMI was not significantly different from that observed in control animals.	Desipramine	112-115	growth associated protein 43	Rattus norvegicus	33-39
9178363-8	1997	The extent of phosphorylation of GAP-43 protein by native PKC in synaptosomes of rats treated with either FL or DMI was not significantly different from that observed in control animals.	Desipramine	112-115	protein kinase C, gamma	Rattus norvegicus	58-61
9178363-9	1997	The previously observed suppression of basal PKC activity in rat cortical synaptosomes by FL and DMI treatment was thus not reflected in altered GAP-43 phosphorylation.	Desipramine	97-100	protein kinase C, gamma	Rattus norvegicus	45-48
8938825-2	1996	The authors studied the effects of coadministration of desipramine, which is a substrate of CYP2D6, on plasma concentrations of bromperidol and its reduced metabolite (reduced bromperidol).	Desipramine	55-66	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	92-98
8710929-6	1996	These events are stimulated by NE and by guanethidine, an hNET substrate, and they are blocked by cocaine and the antidepressant desipramine.	Desipramine	129-140	solute carrier family 6 member 2	Homo sapiens	58-62
8667208-6	1996	Desipramine blocked the toxicity of MPP+ toward the noradrenaline transporter, but not the dopamine transporter expressing cells.	Desipramine	0-11	solute carrier family 6 member 2	Homo sapiens	52-77
8627519-5	1996	Chronic treatment with imipramine and desipramine alone induced Fos-LI in the central nucleus of the amygdala and the dorsolateral bed nucleus of the stria terminalis.	Desipramine	38-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
8627519-8	1996	Chronic administration of imipramine, desipramine and nisoxetine antagonized the swim induced expression of Fos-LI in the PVN and in limbic cortical regions, including the medial prefrontal ventrolateral orbital and cingulate cortices.	Desipramine	38-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
8627519-10	1996	Thus, only antidepressant drugs that affect norepinephrine uptake (i.e., imipramine, desipramine and nisoxetine) antagonized swim stress-induced Fos-LI.	Desipramine	85-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
8737449-0	1996	Effect of desipramine on spontaneous activity of hippocampal CA1 neuron after transient cerebral ischemia in rats.	Desipramine	10-21	carbonic anhydrase 1	Rattus norvegicus	61-64
8730743-0	1996	Desipramine administration in the olfactory bulbectomized rat: changes in brain beta-adrenoceptor and 5-HT2A binding sites and their relationship to behaviour.	Desipramine	0-11	5-hydroxytryptamine receptor 2A	Rattus norvegicus	102-108
8730743-16	1996	DMI administration for up to 21 days produced a progressive reduction in the number of 5-HT2A receptors in frontal cortex, without significant alterations in occipital cortex.	Desipramine	0-3	5-hydroxytryptamine receptor 2A	Rattus norvegicus	87-93
8730743-20	1996	The present results suggest that the action of DMI in this animal model is unlikely to be directly related to a reduction in beta-adrenoceptors but may be related to a reduction in frontal cortical 5-HT2A receptors.	Desipramine	47-50	5-hydroxytryptamine receptor 2A	Rattus norvegicus	198-204
8848823-6	1996	These results suggest that PB is an inducer of the 2-hydroxylation of DMI, a reaction primarily catalyzed by CYP2D6, but do not provide further information on the specific P450 isoenzyme(s) being induced.	Desipramine	70-73	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	109-115
8724644-8	1996	The reduction of NA levels induced by DSP-4 was prevented by the concomitant administration of the NA uptake inhibitor desipramine.	Desipramine	119-130	dual specificity phosphatase 26	Homo sapiens	38-43
8883917-5	1996	When the 6-OHDA treatment was preceded by administration of desmethylimipramine which prevents NE depletion, IL-1 treatment increased Fos in the PVN, suggesting that the effect of 6-OHDA was indeed related to the depletion of NE.	Desipramine	60-79	interleukin 1 complex	Mus musculus	109-113
8883917-5	1996	When the 6-OHDA treatment was preceded by administration of desmethylimipramine which prevents NE depletion, IL-1 treatment increased Fos in the PVN, suggesting that the effect of 6-OHDA was indeed related to the depletion of NE.	Desipramine	60-79	FBJ osteosarcoma oncogene	Mus musculus	134-137
8741184-3	1996	beta-Adrenoceptor subtypes, beta 1 and beta 2, which coexist in neurons and astrocytes, are differently distributed in the brain and differently modified by desipramine administration which down-regulates beta 1-adrenoceptor in forebrain neurons and astrocytes and beta 2-adrenoceptor in cerebellum neurons.	Desipramine	157-168	adrenoceptor beta 1	Rattus norvegicus	205-224
8741184-3	1996	beta-Adrenoceptor subtypes, beta 1 and beta 2, which coexist in neurons and astrocytes, are differently distributed in the brain and differently modified by desipramine administration which down-regulates beta 1-adrenoceptor in forebrain neurons and astrocytes and beta 2-adrenoceptor in cerebellum neurons.	Desipramine	157-168	adrenoceptor beta 2	Rattus norvegicus	265-284
8845222-14	1996	These data suggest that NO production attributable to constitutive NOS (cNOS) activity aggravates the hypotension associated with DMI toxicity in the anesthetized rat, and contributes to the pathophysiology of this overdose.	Desipramine	130-133	nitric oxide synthase 3	Rattus norvegicus	54-70
8845222-14	1996	These data suggest that NO production attributable to constitutive NOS (cNOS) activity aggravates the hypotension associated with DMI toxicity in the anesthetized rat, and contributes to the pathophysiology of this overdose.	Desipramine	130-133	nitric oxide synthase 3	Rattus norvegicus	72-76
8737449-1	1996	AIM: To study the spontaneous firing of CA1 neurons in rat hippocampus after transient cerebral ischemia and the effect of desipramine (Des) on the post-ischemic electric activity of CA1 neurons.	Desipramine	123-134	carbonic anhydrase 1	Rattus norvegicus	183-186
8737449-1	1996	AIM: To study the spontaneous firing of CA1 neurons in rat hippocampus after transient cerebral ischemia and the effect of desipramine (Des) on the post-ischemic electric activity of CA1 neurons.	Desipramine	136-139	carbonic anhydrase 1	Rattus norvegicus	183-186
8848002-5	1995	In contrast, all chimeras containing dopamine transporter sequences from this region resemble the dopamine transporter, which demonstrates higher affinity for psychomotor stimulants compared with antidepressants (e.g., Ki = 391 +/- 39 nM cocaine compared with 9365 +/- 1260 nM desipramine).	Desipramine	277-288	solute carrier family 6 member 3	Homo sapiens	37-57
8848002-5	1995	In contrast, all chimeras containing dopamine transporter sequences from this region resemble the dopamine transporter, which demonstrates higher affinity for psychomotor stimulants compared with antidepressants (e.g., Ki = 391 +/- 39 nM cocaine compared with 9365 +/- 1260 nM desipramine).	Desipramine	277-288	solute carrier family 6 member 3	Homo sapiens	98-118
8848002-6	1995	A region including transmembrane domains 1-3 of the norepinephrine transporter also contributes to the interaction of desipramine and nisoxetine, whereas the analogous region of the dopamine transporter influences the affinity for piperazine derivatives (e.g., GBR12909 and LR1111) that are selective for the dopamine transporter.	Desipramine	118-129	solute carrier family 6 member 3	Homo sapiens	309-329
7472505-7	1995	Chronic (21 d), but not acute (1 d), administration of several different antidepressant drugs, including tranylcypromine, sertraline, desipramine, or mianserin, significantly increased BDNF mRNA and all but mianserin increased trkB mRNA in hippocampus.	Desipramine	134-145	brain-derived neurotrophic factor	Rattus norvegicus	185-189
8617667-10	1995	Increased DMI played a major role in the compensatory gain response in both CL-CA and FA-CA groups.	Desipramine	10-13	FA complementation group A	Homo sapiens	86-91
8564731-7	1995	The serine but not threonine or tyrosine phosphorylation of MAP2 was significantly increased after chronic treatment with DMI, MPR or CTR.	Desipramine	122-125	microtubule-associated protein 2	Rattus norvegicus	60-64
7589222-0	1995	Chronic fluoxetine or desmethylimipramine treatment alters 5-HT2 receptor mediated c-fos gene expression.	Desipramine	22-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
7582477-0	1995	Protein kinase C in rat brain cortex and hippocampus: effect of repeated administration of fluoxetine and desipramine.	Desipramine	106-117	protein kinase C, gamma	Rattus norvegicus	0-16
7582477-3	1995	The aim of this study was to investigate the effect of repeated administration of fluoxetine (FL) and desipramine (DMI) on the distribution and activity of protein kinase C (PKC) in subcellular fractions of rat cortex (Cx) and hippocampus (Hc) under basal conditions and in response to a single in vivo administration of 5-HT2A/2C agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI).	Desipramine	102-113	protein kinase C, gamma	Rattus norvegicus	156-172
7582477-3	1995	The aim of this study was to investigate the effect of repeated administration of fluoxetine (FL) and desipramine (DMI) on the distribution and activity of protein kinase C (PKC) in subcellular fractions of rat cortex (Cx) and hippocampus (Hc) under basal conditions and in response to a single in vivo administration of 5-HT2A/2C agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI).	Desipramine	102-113	protein kinase C, gamma	Rattus norvegicus	174-177
7582477-3	1995	The aim of this study was to investigate the effect of repeated administration of fluoxetine (FL) and desipramine (DMI) on the distribution and activity of protein kinase C (PKC) in subcellular fractions of rat cortex (Cx) and hippocampus (Hc) under basal conditions and in response to a single in vivo administration of 5-HT2A/2C agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI).	Desipramine	115-118	protein kinase C, gamma	Rattus norvegicus	156-172
7582477-3	1995	The aim of this study was to investigate the effect of repeated administration of fluoxetine (FL) and desipramine (DMI) on the distribution and activity of protein kinase C (PKC) in subcellular fractions of rat cortex (Cx) and hippocampus (Hc) under basal conditions and in response to a single in vivo administration of 5-HT2A/2C agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI).	Desipramine	115-118	protein kinase C, gamma	Rattus norvegicus	174-177
7582477-15	1995	The activity of PKC in subcellular fractions of Cx and Hc was significantly (by 40-50%) decreased in rats given repeated doses of FL or DMI.	Desipramine	136-139	protein kinase C, gamma	Rattus norvegicus	16-19
7582477-20	1995	The results indicate that repeated administration of FL and DMI produced similar changes in basal PKC activity but differentially affected the PKC response to the 5-HT2A/2c receptor agonist, DOI.	Desipramine	60-63	protein kinase C, gamma	Rattus norvegicus	98-101
7582477-20	1995	The results indicate that repeated administration of FL and DMI produced similar changes in basal PKC activity but differentially affected the PKC response to the 5-HT2A/2c receptor agonist, DOI.	Desipramine	60-63	protein kinase C, gamma	Rattus norvegicus	143-146
7582477-20	1995	The results indicate that repeated administration of FL and DMI produced similar changes in basal PKC activity but differentially affected the PKC response to the 5-HT2A/2c receptor agonist, DOI.	Desipramine	60-63	5-hydroxytryptamine receptor 2A	Rattus norvegicus	163-169
7883833-4	1995	In rats, DMI reduces the activity of the locus ceruleus, a major source of NE innervation of the hypothalamic paraventricular nucleus, the site of CRH neurons.	Desipramine	9-12	corticotropin releasing hormone	Rattus norvegicus	147-150
7667349-0	1995	Chronic desipramine alters stress-induced behaviors and regional expression of the immediate early gene, c-fos.	Desipramine	8-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
7667349-1	1995	This experiment examined the effects of acute or chronic administration of the antidepressant drug desipramine on conditioned stress-induced behaviors and regional c-fos expression in the brain.	Desipramine	99-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
7667349-7	1995	Similarly, Fos immunohistochemistry revealed that the chronic desipramine group showing positive behavioral effects was the only group in which there were significant reductions in the number of stress-induced Fos-positive neurons in five of 60 structures surveyed.	Desipramine	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
7667349-7	1995	Similarly, Fos immunohistochemistry revealed that the chronic desipramine group showing positive behavioral effects was the only group in which there were significant reductions in the number of stress-induced Fos-positive neurons in five of 60 structures surveyed.	Desipramine	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-213
7603449-8	1995	Upon membrane depolarization, desipramine reduced the phosphorylation of CREB at Ser-119 and also blocked the depolarization-induced increase in the intracellular free Ca2+ concentration in HIT cells.	Desipramine	30-41	cAMP responsive element binding protein 1	Rattus norvegicus	73-77
7612155-5	1995	Moreover, chronic administration of desipramine or sertraline, selective re-uptake inhibitors of norepinephrine, or serotonin, respectively, also significantly down-regulated the induction of c-fos mRNA in response to restraint stress.	Desipramine	36-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
7883833-13	1995	In summary, DMI increased basal cortisol levels consistent with facilitation of NE neurotransmission and, hence, hypothalamic CRH release.	Desipramine	12-15	corticotropin releasing hormone	Homo sapiens	126-129
7891324-2	1995	To delineate the pharmacokinetic mechanisms, we studied the effects of a high-affinity, drug-specific Fab fragment on desipramine (DMI) disposition in rats and on DMI kinetics in the isolated, perfused rat liver.	Desipramine	118-129	FA complementation group B	Homo sapiens	102-105
7891324-2	1995	To delineate the pharmacokinetic mechanisms, we studied the effects of a high-affinity, drug-specific Fab fragment on desipramine (DMI) disposition in rats and on DMI kinetics in the isolated, perfused rat liver.	Desipramine	131-134	FA complementation group B	Homo sapiens	102-105
7891324-4	1995	Rats received 20 mg/kg DMI intravenously over 30 min followed in 10 min by DMI-specific ovine polyclonal Fab (DMI-Fab) or nonspecific human Fab (control-Fab) (1.1 g/kg; molar Fab-to-DMI ratio, 0.34) intravenously over 20 min.	Desipramine	75-78	FA complementation group B	Homo sapiens	105-108
7891324-4	1995	Rats received 20 mg/kg DMI intravenously over 30 min followed in 10 min by DMI-specific ovine polyclonal Fab (DMI-Fab) or nonspecific human Fab (control-Fab) (1.1 g/kg; molar Fab-to-DMI ratio, 0.34) intravenously over 20 min.	Desipramine	75-78	FA complementation group B	Homo sapiens	105-108
7891324-5	1995	The serum DMI concentration increased by 50-fold 5 min after DMI-Fab administration.	Desipramine	10-13	FA complementation group B	Homo sapiens	65-68
7891324-8	1995	Renal clearance increased by 72% after DMI-Fab and total renal excretion of DMI increased by 7-fold due to the much higher serum DMI concentration.	Desipramine	39-42	FA complementation group B	Homo sapiens	43-46
7891324-9	1995	Ninety-four percent of DMI-Fab excretion and 87% of DMI excretion occurred in the first 12 h. The percent of DMI bound in urine was markedly increased by DMI-Fab (87.1 vs. 19.1%), as was the molar ratio of DMI to DMI-Fab in urine (0.75 vs. 0.08).	Desipramine	23-26	FA complementation group B	Homo sapiens	27-30
7891324-9	1995	Ninety-four percent of DMI-Fab excretion and 87% of DMI excretion occurred in the first 12 h. The percent of DMI bound in urine was markedly increased by DMI-Fab (87.1 vs. 19.1%), as was the molar ratio of DMI to DMI-Fab in urine (0.75 vs. 0.08).	Desipramine	23-26	FA complementation group B	Homo sapiens	158-161
7891324-9	1995	Ninety-four percent of DMI-Fab excretion and 87% of DMI excretion occurred in the first 12 h. The percent of DMI bound in urine was markedly increased by DMI-Fab (87.1 vs. 19.1%), as was the molar ratio of DMI to DMI-Fab in urine (0.75 vs. 0.08).	Desipramine	52-55	FA complementation group B	Homo sapiens	158-161
7891324-9	1995	Ninety-four percent of DMI-Fab excretion and 87% of DMI excretion occurred in the first 12 h. The percent of DMI bound in urine was markedly increased by DMI-Fab (87.1 vs. 19.1%), as was the molar ratio of DMI to DMI-Fab in urine (0.75 vs. 0.08).	Desipramine	52-55	FA complementation group B	Homo sapiens	158-161
7550552-1	1995	The tricyclic antidepressant desipramine impaired shuttle-box avoidance acquisition in mice of the CD-1 strain.	Desipramine	29-40	CD1 antigen complex	Mus musculus	99-103
7898321-0	1994	Desipramine-induced increase in norepinephrine transporter mRNA is not mediated via alpha 2 receptors.	Desipramine	0-11	solute carrier family 6 member 2	Rattus norvegicus	32-58
7898321-1	1994	In situ hybridization for the norepinephrine transporter (NET) was performed in rats receiving short-term (2 days) treatment with either an alpha-2 (alpha 2) receptor agonist (clonidine) or antagonist (yohimbine) followed by saline or desipramine (DMI).	Desipramine	235-246	solute carrier family 6 member 2	Rattus norvegicus	58-61
7898321-1	1994	In situ hybridization for the norepinephrine transporter (NET) was performed in rats receiving short-term (2 days) treatment with either an alpha-2 (alpha 2) receptor agonist (clonidine) or antagonist (yohimbine) followed by saline or desipramine (DMI).	Desipramine	248-251	solute carrier family 6 member 2	Rattus norvegicus	58-61
7898321-6	1994	In the "DMI" group an attentuation of the DMI-induced increase in NET mRNA was observed in the clonidine/DMI animals compared to the saline/DMI animals.	Desipramine	8-11	solute carrier family 6 member 2	Rattus norvegicus	66-69
7898321-6	1994	In the "DMI" group an attentuation of the DMI-induced increase in NET mRNA was observed in the clonidine/DMI animals compared to the saline/DMI animals.	Desipramine	42-45	solute carrier family 6 member 2	Rattus norvegicus	66-69
7898321-6	1994	In the "DMI" group an attentuation of the DMI-induced increase in NET mRNA was observed in the clonidine/DMI animals compared to the saline/DMI animals.	Desipramine	42-45	solute carrier family 6 member 2	Rattus norvegicus	66-69
7898321-6	1994	In the "DMI" group an attentuation of the DMI-induced increase in NET mRNA was observed in the clonidine/DMI animals compared to the saline/DMI animals.	Desipramine	42-45	solute carrier family 6 member 2	Rattus norvegicus	66-69
7898321-8	1994	These findings suggest that the DMI-induced increase in NET mRNA is not mediated via alpha 2 receptors for, although clonidine attenuates DMI"s effect, there is no reciprocal enhancement with the alpha 2 antagonist yohimbine.	Desipramine	32-35	solute carrier family 6 member 2	Rattus norvegicus	56-59
7898321-10	1994	Additional studies are needed to clarify the mechanism of the DMI-induced increase in NET mRNA and to correlate changes in NET mRNA with transporter expression at the synaptic membrane.	Desipramine	62-65	solute carrier family 6 member 2	Rattus norvegicus	86-89
7816863-0	1994	Beta 2- but not beta 1-adrenoceptors are involved in desipramine enhancement of aggressive behavior in long-term isolated mice.	Desipramine	53-64	hemoglobin, beta adult minor chain	Mus musculus	0-6
7816863-4	1994	ICI118,551 HCl (1.25-5 mg/kg, IP), a selective beta 2-adrenoceptor antagonist, also blocked the desipramine-induced enhancement of aggressive behavior in a dose-dependent manner, whereas metoprolol tartrate (5-20 mg/kg, IP), a selective beta 1-adrenoceptor antagonist, did not affect it.	Desipramine	96-107	adrenergic receptor, beta 2	Mus musculus	47-66
7816863-4	1994	ICI118,551 HCl (1.25-5 mg/kg, IP), a selective beta 2-adrenoceptor antagonist, also blocked the desipramine-induced enhancement of aggressive behavior in a dose-dependent manner, whereas metoprolol tartrate (5-20 mg/kg, IP), a selective beta 1-adrenoceptor antagonist, did not affect it.	Desipramine	96-107	adrenergic receptor, beta 1	Mus musculus	237-256
7816863-6	1994	Taken together with our previous finding that the desipramine-induced enhancement of aggressive behavior can be blocked by yohimbine, an alpha 2-adrenoceptor antagonist, the present results indicate that not only alpha 2- but also beta 2-adrenoceptor stimulation plays important roles in modulation of aggressive behavior in long-term isolated mice.	Desipramine	50-61	adrenergic receptor, beta 2	Mus musculus	231-250
7604141-4	1995	These findings suggest that CBZ induces the 2-hydroxylation of DMI, a reaction primarily catalyzed by the polymorphic CYP2D6 isozyme.	Desipramine	63-66	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	118-124
7895065-2	1994	Antidepressant administration of desipramine to rats twice-daily for 2 weeks increased hippocampal TNF levels and transformed the presynaptic TNF response.	Desipramine	33-44	tumor necrosis factor	Rattus norvegicus	99-102
7895065-2	1994	Antidepressant administration of desipramine to rats twice-daily for 2 weeks increased hippocampal TNF levels and transformed the presynaptic TNF response.	Desipramine	33-44	tumor necrosis factor	Rattus norvegicus	142-145
7895065-3	1994	One day of desipramine administration resulted in increased locus coeruleus TNF mRNA accumulation and, simultaneously, hippocampal TNF levels escalated.	Desipramine	11-22	tumor necrosis factor	Rattus norvegicus	76-79
7895065-3	1994	One day of desipramine administration resulted in increased locus coeruleus TNF mRNA accumulation and, simultaneously, hippocampal TNF levels escalated.	Desipramine	11-22	tumor necrosis factor	Rattus norvegicus	131-134
7895065-6	1994	In addition, TNF potentiation of [3H]norepinephrine release after chronic desipramine administration was reversed in the presence of idazoxan to a greater inhibition than in control slices exposed to idazoxan.	Desipramine	74-85	tumor necrosis factor	Rattus norvegicus	13-16
7810621-6	1994	In the absence and presence of desipramine, catechol-O-methyltransferase inhibition had no effect on the clearance of NE, Epi, and DA and decreased Iso clearance by 25%.	Desipramine	31-42	catechol O-methyltransferase	Oryctolagus cuniculus	44-72
7945993-2	1994	Desipramine induced rapid intracellular degradation of mature acid sphingomyelinase when added to the cells in the micromolar range, concomitantly abolishing the enzyme activity.	Desipramine	0-11	sphingomyelin phosphodiesterase 1	Homo sapiens	62-83
7945993-5	1994	From these results we conclude that desipramine and possibly also similarly acting tricyclic antidepressants induce proteolytic degradation of acid sphingomyelinase.	Desipramine	36-47	sphingomyelin phosphodiesterase 1	Homo sapiens	143-164
8052414-1	1994	The effect of castration combined with either long-term treatment with the tricyclic antidepressant drug desipramine or the sex steroid 17 beta-estradiol on serotonin responses in area CA1 of the hippocampus of male and female rats was examined.	Desipramine	105-116	carbonic anhydrase 1	Rattus norvegicus	185-188
8032878-9	1994	Addition of DMI to the CSF significantly increased perfusate NE levels, but produced no change in LH release.	Desipramine	12-15	colony stimulating factor 2	Rattus norvegicus	23-26