Pub. Date : 2020 Feb 15
PMID : 31887333
11 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
1 | TCDD inhibited the osteogenic differentiation of human fetal palatal mesenchymal cells through AhR and BMP-2/TGF-beta/Smad signaling. | Polychlorinated Dibenzodioxins | aryl hydrocarbon receptor | Homo sapiens |
2 | 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 | aryl hydrocarbon receptor | Homo sapiens |
3 | 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 | aryl hydrocarbon receptor | Homo sapiens |
4 | 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 | aryl hydrocarbon receptor | Homo sapiens |
5 | 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 | aryl hydrocarbon receptor | Homo sapiens |
6 | 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 | aryl hydrocarbon receptor | Homo sapiens |
7 | 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 | aryl hydrocarbon receptor | Homo sapiens |
8 | 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 | aryl hydrocarbon receptor | Homo sapiens |
9 | 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 | aryl hydrocarbon receptor | Homo sapiens |
10 | 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 | aryl hydrocarbon receptor | Homo sapiens |
11 | 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 | aryl hydrocarbon receptor | Homo sapiens |