PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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