PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31887333-0	2020	TCDD inhibited the osteogenic differentiation of human fetal palatal mesenchymal cells through AhR and BMP-2/TGF-beta/Smad signaling.	Polychlorinated Dibenzodioxins	0-4	aryl hydrocarbon receptor	Homo sapiens	95-98	
31887333-5	2020	Further investigation of the underlying molecular mechanisms revealed that exposure to TCDD activated aryl hydrocarbon receptor (AhR) signaling and inhibited BMP-2/TGF-beta1/Smad pathway molecules.	Polychlorinated Dibenzodioxins	87-91	aryl hydrocarbon receptor	Homo sapiens	102-127	
31887333-5	2020	Further investigation of the underlying molecular mechanisms revealed that exposure to TCDD activated aryl hydrocarbon receptor (AhR) signaling and inhibited BMP-2/TGF-beta1/Smad pathway molecules.	Polychlorinated Dibenzodioxins	87-91	aryl hydrocarbon receptor	Homo sapiens	129-132	
31887333-6	2020	The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation.	Polychlorinated Dibenzodioxins	149-153	aryl hydrocarbon receptor	Homo sapiens	20-23	
31887333-6	2020	The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation.	Polychlorinated Dibenzodioxins	149-153	aryl hydrocarbon receptor	Homo sapiens	61-64	
31887333-6	2020	The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation.	Polychlorinated Dibenzodioxins	149-153	aryl hydrocarbon receptor	Homo sapiens	61-64	
31887333-6	2020	The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation.	Polychlorinated Dibenzodioxins	207-211	aryl hydrocarbon receptor	Homo sapiens	20-23	
31887333-6	2020	The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation.	Polychlorinated Dibenzodioxins	207-211	aryl hydrocarbon receptor	Homo sapiens	61-64	
31887333-6	2020	The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation.	Polychlorinated Dibenzodioxins	207-211	aryl hydrocarbon receptor	Homo sapiens	61-64	
31887333-7	2020	The cotreatment with TGF-beta1 or BMP-2 and TCDD significantly relieved the activation of AhR and rescued the impairment of osteogenesis caused by TCDD.	Polychlorinated Dibenzodioxins	44-48	aryl hydrocarbon receptor	Homo sapiens	90-93	
31887333-8	2020	Taken together, our findings indicated that TCDD inhibited the osteogenic differentiation of hFPMCs via crosstalk between AhR and BMP-2/TGF-beta1/Smad signaling pathway.	Polychlorinated Dibenzodioxins	44-48	aryl hydrocarbon receptor	Homo sapiens	122-125