EZH1Enhancer of zeste homolog 1
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References in periodicals archive ?
The Inhibition of EZH1 Caused by TCP Facilitates M2 Macrophage Polarization.
In order to confirm the role of EZH1 during macrophage polarization, we silenced EZH1 in Thp1 cells with siRNA (Figures 3(c) and 3(d)).
However, after the silencing of EZH1, there was no significant difference between the siEZH1 group and the control group (Figure 4(b)).
In order to determine the role of the NF-[kappa]B pathway during EZH1 inhibition, an inhibitor for the NF-[kappa]B pathway (BMS-345541) was utilized.
Previously, our research group found that EZH1 could regulate NF-[kappa]B target genes through a nonclassical complex that was associated with SUZ12 and UTX.
Classic NF-[kappa]B consists of P50 and RelA (P65); the binding site of RelA 5,-AGAAATTCC-3; was found in the promoter region of EZH1 gene sequence, but to date, there is no proof regarding the regulation of NF-[kappa]B to EZH1 [34].
In the present study, it was found that TCP suppressed the activation of the NF-kappa B pathway and caused a decrease in EZH1 expression.
The authors hereby confirmed that the present work entitled "EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophages Polarization" has been submitted solely to Journal of Stem Cells International and that it is not concurrently under consideration for publication in another journal.
Nguyen et al., "EZH1 and EZH2 promote skeletal growth by repressing inhibitors of chondrocyte proliferation and hypertrophy," Nature Communications, vol.
Caption: Figure 3: Inhibition of EZH1 caused by TCP stimulation facilitates M2 macrophage polarization.