PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
15081597-6	2004	In a separate study, subcutaneous injections of FK506 (2 or 10 mg/kg) for 2 weeks markedly increased heat shock protein-70 (Hsp-70) immunostaining in sensory neurons, motor neurons, Purkinje cells, and other regions of the brain (in particular, the amygdala) from nonintoxicated and AC-intoxicated rats compared to controls.	Tacrolimus	48-53	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	101-122	
18577426-0	2008	Analysis of FK506-mediated protection in an organotypic model of spinal cord damage: heat shock protein 70 levels are modulated in microglial cells.	Tacrolimus	12-17	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	85-106	
18577426-7	2008	Hsp70 induction was restricted to microglial cells in spinal cord slices treated with either glutamate or FK506.	Tacrolimus	106-111	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	0-5	
18577426-10	2008	These observations suggest that FK506 might protect spinal cord tissue by targeting on microglial cells and that transient downregulation of Hsp70 on these cells after excitotoxicity is a relevant mechanism of action of FK506.	Tacrolimus	220-225	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	141-146	
17359722-0	2006	[Effect of tacrolimus on apoptosis and expression of heat shock protein 70 after acute spinal cord injury in rats].	Tacrolimus	11-21	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	53-74	
17359722-1	2006	OBJECTIVE: To investigate the effect of tacrolimus on expression of heat shock protein 70 (HSP 70) after spinal cord injuries (SCI) in rats and the relationship between expression of HSP 70 and apoptosis of neural cells.	Tacrolimus	40-50	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	68-89	
17359722-1	2006	OBJECTIVE: To investigate the effect of tacrolimus on expression of heat shock protein 70 (HSP 70) after spinal cord injuries (SCI) in rats and the relationship between expression of HSP 70 and apoptosis of neural cells.	Tacrolimus	40-50	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	91-97	
17359722-7	2006	RESULTS: Compared with the injury group, the expression of HSP 70 was significantly higher in the tacrolimus group, and the peak expression of HSP 70 mRNA and protein was respectively observed at 6, 24 h after SCI.	Tacrolimus	98-108	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	59-65	
17359722-10	2006	CONCLUSIONS: Tacrolimus may inhibit activity of Caspase-3, attenuate apoptosis of neural cells and ameliorate neurological function recovery after SCI by inducing high expression of HSP 70.	Tacrolimus	13-23	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	182-188	
15081597-8	2004	Thus, the ability of FK506 to increase Hsp-70 expression may underlie its neuroprotective action.	Tacrolimus	21-26	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	39-45	
20465949-7	2010	In the cerebrum and sciatic nerve pellet, the level of HSP70 in the FK506 groups increased by 11.6%, 33.3% and 56.3%, 58.5% (P < 0.01), but no significant changes existed in spinal cord.	Tacrolimus	68-73	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	55-60	
20465949-12	2010	CONCLUSION: The administration of FK506 has dramatically neuroprotective effects against the development of ACR neuropathy, which may be related to up-regulating the expression of HSP70 and Bcl-2 with down-regulating the expression of Bax.	Tacrolimus	34-39	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	180-185	
15081597-6	2004	In a separate study, subcutaneous injections of FK506 (2 or 10 mg/kg) for 2 weeks markedly increased heat shock protein-70 (Hsp-70) immunostaining in sensory neurons, motor neurons, Purkinje cells, and other regions of the brain (in particular, the amygdala) from nonintoxicated and AC-intoxicated rats compared to controls.	Tacrolimus	48-53	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	124-130	
12642403-8	2003	(3) FK506 and V-10,367 rapidly induced the expression of Hsp70 and Hsp27, but not Hsp90.	Tacrolimus	4-9	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	57-62	
11411802-11	2001	FK506 enhanced the induction of Hsp70, but CsA again had no effect on Hsp70 induction.	Tacrolimus	0-5	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	32-37	
11740384-5	2001	were used to induce ischemic tolerance in Sprague-Dawley rats, and the induction of heat shock protein (hsp) 70 by CsA or FK506 was evaluated overtime.	Tacrolimus	122-127	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	84-111	
11740384-6	2001	Rats were pretreated with CsA or FK506 6 hr before I/R injury when hsp70 was maximally expressed, and were killed 24 hr later.	Tacrolimus	33-38	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	67-72	
11740384-11	2001	CONCLUSIONS: Pretreatment with low-dose CsA or FK506 prevents subsequent I/R injury, and this effect may be related to the induction of hsp70.	Tacrolimus	47-52	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	136-141