PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
22262768-5	2012	Heme-induced cell death required TNFR1 and TLR4/MyD88-dependent TNF production.	Heme	0-4	myeloid differentiation primary response gene 88	Mus musculus	48-53	
22262768-6	2012	Addition of TNF to Tlr4(-/-) or to Myd88(-/-) macrophages restored heme-induced cell death.	Heme	67-71	myeloid differentiation primary response gene 88	Mus musculus	35-40	
22262768-10	2012	Taken together, these results revealed that heme induces macrophage necrosis through 2 synergistic mechanisms: TLR4/Myd88-dependent expression of TNF and TLR4-independent generation of ROS.	Heme	44-48	myeloid differentiation primary response gene 88	Mus musculus	116-121	
22394415-0	2012	Heme activates TLR4-mediated inflammatory injury via MyD88/TRIF signaling pathway in intracerebral hemorrhage.	Heme	0-4	myeloid differentiation primary response gene 88	Mus musculus	53-58	
22394415-12	2012	CONCLUSIONS: Our findings suggest that heme potentiates microglial activation via TLR4, in turn inducing NF-kappaB activation via the MyD88/TRIF signaling pathway, and ultimately increasing cytokine expression and inflammatory injury in ICH.	Heme	39-43	myeloid differentiation primary response gene 88	Mus musculus	134-139	
33037139-2	2020	In these cells, heme can act as a prototypical damage-associated molecular pattern, inducing TLR4-dependent cytokine production through the MyD88 pathway, independently of TRIF.	Heme	16-20	myeloid differentiation primary response gene 88	Mus musculus	140-145	
32272082-4	2020	Here, we have demonstrated that interleukin (IL)-33 associated with erythrocytes and co-cooperated with heme to promote the generation of mature RPMs through activation of the MyD88 adaptor protein and ERK1/2 kinases downstream of the IL-33 receptor, IL1RL1.	Heme	104-108	myeloid differentiation primary response gene 88	Mus musculus	176-181