PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28398601-0	2017	Antidepressant Imipramine Protects Bupivacaine-Induced Neurotoxicity in Dorsal Root Ganglion Neurons Through Coactivation of TrkA and TrkB.	Imipramine	15-25	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	134-138	
28398601-11	2017	Imipramine protected bupivacaine-induced neurotoxicity in DRG, likely via the co-activation of TrkA and TrkB signaling pathways.	Imipramine	0-10	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	104-108	
27127489-0	2016	Imipramine protects retinal ganglion cells from oxidative stress through the tyrosine kinase receptor B signaling pathway.	Imipramine	0-10	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	77-103	
27127489-2	2016	In this study, we attempted to examine whether imipramine, a tricyclic antidepressant, may protect hydrogen peroxide (H2O2)-induced RGC degeneration through the activation of the TrkB pathway in RGC-5 cell lines.	Imipramine	47-57	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	179-183	
27127489-4	2016	Western blot assay showed that in H2O2 -damaged RGC-5 cells, imipramine activated TrkB pathways through extracellular signal-regulated protein kinase/TrkB phosphorylation.	Imipramine	61-71	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	82-86	
27127489-4	2016	Western blot assay showed that in H2O2 -damaged RGC-5 cells, imipramine activated TrkB pathways through extracellular signal-regulated protein kinase/TrkB phosphorylation.	Imipramine	61-71	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	150-154	
27127489-6	2016	Finally, TrkB-IgG intervention was able to reverse the protective effect of imipramine on H2O2 -induced RGC-5 apoptosis.	Imipramine	76-86	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	9-13	
27127489-7	2016	Imipramine therefore protects RGCs from oxidative stress-induced apoptosis through the TrkB signaling pathway.	Imipramine	0-10	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	87-91	
26481532-4	2015	OBJECTIVE AND METHODS: In the present study we investigated whether acute or chronic treatment with imipramine, escitalopram, reboxetine and bupropion would cause changes in CREB, BDNF, TrkB and GPR39-Zn(2+) receptor proteins (measured by Western Blot) in the frontal cortex of mice fed with a low-zinc diet.	Imipramine	100-110	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	186-190	
21666748-6	2011	However, the tricyclic AD imipramine readily induced the phosphorylation of TrkB receptors in conditional bdnf-/- knock-out mice (132.4+-8.5% of control; P = 0.01), indicating that BDNF is not required for the TrkB activation.	Imipramine	26-36	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	76-80	
21666748-6	2011	However, the tricyclic AD imipramine readily induced the phosphorylation of TrkB receptors in conditional bdnf-/- knock-out mice (132.4+-8.5% of control; P = 0.01), indicating that BDNF is not required for the TrkB activation.	Imipramine	26-36	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	210-214	
17314919-2	2007	We have previously shown that the antidepressants imipramine and fluoxetine produce a rapid autophosphorylation of TrkB in the rodent brain.	Imipramine	50-60	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	115-119