PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31535397-6	2020	The results of this study propose a mechanistic pathway by which the inhibition of TLR4 using TAK-242 could augment apoptotic cell death through the alteration of both nuclear factor-kB- and p53-related apoptosis genes in breast cancer cells, especially cells with overexpression of TLR4.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	94-101	tumor protein p53	Homo sapiens	191-194	
33476981-3	2021	Pharmacological inhibition of TLR4 signaling by TAK242 or its siRNA-mediated knockdown in p53 mutant or wild-type glioma cells resulted in either increased or decreased SOCS1 expression and promoter activity, respectively.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	48-54	tumor protein p53	Homo sapiens	90-93