PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32824595-7	2020	Corroborating in vitro data, Myd88-/- knockout mice downregulated TNF, CXCL1; and phospho-p65 and phospho-IRF3 nuclear localization, upon poly I:C treatment in a mouse model of skin infection.	Poly I-C	138-146	myeloid differentiation primary response gene 88	Mus musculus	29-34	
18306459-9	2008	When cells were stimulated by poly (I:C), 3-phenyl-propenal significantly decreased TLR3 and MyD88 expression.	Poly I-C	30-40	myeloid differentiation primary response gene 88	Mus musculus	93-98	
30550930-9	2019	To validate the effects of poly(I:C) were mediated through MyD88, we tested female mice lacking Myd88.	Poly I-C	27-36	myeloid differentiation primary response gene 88	Mus musculus	59-64	
30550931-11	2019	MyD88 null mutants showed poly(I:C)-induced increases in alcohol intake.	Poly I-C	26-35	myeloid differentiation primary response gene 88	Mus musculus	0-5	
20006962-6	2010	Additional experiments utilizing CpG and Poly I:C stimulation to selectively activate the MyD88-dependent and -independent pathways via TLR9 and TLR3 substantiated the finding that malyngamide F acetate selectively inhibits the MyD88-dependent pathway.	Poly I-C	41-49	myeloid differentiation primary response gene 88	Mus musculus	90-95	
16585964-6	2006	Nrf2-deficient mouse embryonic fibroblasts showed greater activation of NF-kappaB and interferon regulatory factor 3 in response to LPS and polyinosinic-polycytidylic acid [poly(I:C)] stimulus, corroborating the effect of Nrf2 on MyD88-dependent and -independent signaling.	Poly I-C	140-171	myeloid differentiation primary response gene 88	Mus musculus	230-235