PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
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	
11415943-9	2001	In addition, TNF-alpha-induced ROS production was inhibited by the acidic sphingomyelinase inhibitor desipramine (5 microM; -80%, n = 4, P < 0.01) and totally blocked by the ceramide-activated protein kinase (CAPK) inhibitor dimethylaminopurine (1 mM; n = 6, P < 0.05).	Desipramine	101-112	tumor necrosis factor	Homo sapiens	13-22	
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	
29169412-10	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	
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	
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	
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	
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	
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