PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
27576776-0	2016	Toll-Like Receptor 4/MyD88-Mediated Signaling of Hepcidin Expression Causing Brain Iron Accumulation, Oxidative Injury, and Cognitive Impairment After Intracerebral Hemorrhage.	Iron	83-87	myeloid differentiation primary response gene 88	Mus musculus	21-26	
27576776-10	2016	TLR4-/- and MyD88-/- mice exhibited improvement in brain iron efflux at 7, 14, and 28 days after ICH, and the TLR4 antagonist (6R)-6-[N-(2-chloro-4-fluorophenyl) sulfamoyl] cyclohex-1-ene-1-carboxylate significantly decreased brain iron levels at days 14 and 28 after ICH and improved cognition impairment at day 28.	Iron	57-61	myeloid differentiation primary response gene 88	Mus musculus	12-17	
29556203-0	2018	MyD88 Adaptor Protein Is Required for Appropriate Hepcidin Induction in Response to Dietary Iron Overload in Mice.	Iron	92-96	myeloid differentiation primary response gene 88	Mus musculus	0-5	
29556203-4	2018	In this study, we analyzed the regulation of iron metabolism in MyD88-/- mice to further investigate MyD88 involvement in iron sensing and hepcidin induction.	Iron	122-126	myeloid differentiation primary response gene 88	Mus musculus	101-106	
29556203-5	2018	We show that mice lacking MyD88 accumulate significantly more iron in their livers than wild-type counterparts in response to dietary iron loading as they are unable to appropriately control hepcidin levels.	Iron	62-66	myeloid differentiation primary response gene 88	Mus musculus	26-31	
29556203-5	2018	We show that mice lacking MyD88 accumulate significantly more iron in their livers than wild-type counterparts in response to dietary iron loading as they are unable to appropriately control hepcidin levels.	Iron	134-138	myeloid differentiation primary response gene 88	Mus musculus	26-31	
29556203-7	2018	In conclusion, our results reveal a previously unknown link between MyD88 and iron homeostasis, and provide new insights into the regulation of hepcidin through the iron-sensing pathway.	Iron	78-82	myeloid differentiation primary response gene 88	Mus musculus	68-73	
22497726-4	2012	Using MyD88-deficient and TRIF-deficient mice, we show that MyD88 and TRIF signaling pathways are critical for up-regulation by lipopolysaccharide (LPS) of the iron regulator hepcidin.	Iron	160-164	myeloid differentiation primary response gene 88	Mus musculus	6-11	
22497726-5	2012	In addition, MyD88 signaling is required for the induction of lipocalin 2 secretion and iron sequestration in the spleen.	Iron	88-92	myeloid differentiation primary response gene 88	Mus musculus	13-18	
19454708-8	2009	With iron-restricted bacteria, the Lpp-related growth advantage was evident in infection of MyD88(-/-), but not of C57BL/6, mice.	Iron	5-9	myeloid differentiation primary response gene 88	Mus musculus	92-97	
19454708-9	2009	On the other hand, iron overload of the host restored the growth deficit of Deltalgt in MyD88(-/-), but not in immunocompetent C57BL/6 mice.	Iron	19-23	myeloid differentiation primary response gene 88	Mus musculus	88-93