PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26519956-4	2016	Results revealed that PCB118 promoted the generation of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecule-1 (ICAM-1) in a time- and dose-related manner and decreased sodium/iodide symporter (NIS) protein expression.	2,3',4,4',5-pentachlorobiphenyl	22-28	interleukin 6	Rattus norvegicus	56-69	
26519956-4	2016	Results revealed that PCB118 promoted the generation of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecule-1 (ICAM-1) in a time- and dose-related manner and decreased sodium/iodide symporter (NIS) protein expression.	2,3',4,4',5-pentachlorobiphenyl	22-28	interleukin 6	Rattus norvegicus	71-75	
26519956-5	2016	Moreover, stimulation with PCB118 resulted in the upregulation of the aryl hydrocarbon receptor (AhR)-responsive gene cytochrome P450 1A1 in FRTL-5 cells; whereas pretreatment with the AhR inhibitor alpha-naphthoflavone or AhR small interfering RNA (siRNA) suppressed AhR, CYP1A1, IL-6, and ICAM-1 and restored NIS expression.	2,3',4,4',5-pentachlorobiphenyl	27-33	interleukin 6	Rattus norvegicus	281-285	
26519956-6	2016	In vivo and in vitro studies also suggested that the c-Jun N-terminal kinase (JNK) pathway was activated on PCB118 exposure, and the experiments using siRNA for JNK partially blocked PCB118-induced upregulation of IL-6 and ICAM-1 and downregulation of NIS.	2,3',4,4',5-pentachlorobiphenyl	108-114	interleukin 6	Rattus norvegicus	214-218	
26519956-6	2016	In vivo and in vitro studies also suggested that the c-Jun N-terminal kinase (JNK) pathway was activated on PCB118 exposure, and the experiments using siRNA for JNK partially blocked PCB118-induced upregulation of IL-6 and ICAM-1 and downregulation of NIS.	2,3',4,4',5-pentachlorobiphenyl	183-189	interleukin 6	Rattus norvegicus	214-218	
26519956-7	2016	Altogether, PCB118 stimulates production of IL-6, TNF-alpha, and ICAM-1 in the thyroid through AhR and JNK activations and subsequently interferes with NIS expression, resulting in the disruption of thyroid structure and function.	2,3',4,4',5-pentachlorobiphenyl	12-18	interleukin 6	Rattus norvegicus	44-48