Sentence examples for mediating adipocyte differentiation from inspiring English sources

Previous reports of the action of BPA in mediating adipocyte differentiation have shown effects only when BPA is added in combination with the potent GR agonist DEX or other synthetic glucocorticoids.21 One study also showed a BPA-induced increase in 11β-hydroxysteroid dehydrogenase type 1 in human omental fat cells14 leading to activation of GR.

PPARγ as a member of PPARs is mainly rich in adipose tissue, mediating adipocyte differentiation and maturation (Mayoral et al. 2015), and the overexpression of PPARγ significantly attenuated lipid accumulation (Yu et al. 2015).

A comprehensive understanding of the regulatory mechanisms mediating adipocyte differentiation has great fundamental and medical value.

Similarly, suppression of LXR negatively regulates adipogenesis in C57BL/6 mouse cells [ 38] suggesting that LXRα can be an important transcription factor mediating adipocyte differentiation as well as adipogenic gene expression.

ATF-2 and CRE-BPa are required for BMP-2 and p38-dependent induction of peroxisome proliferator-activated receptor γ2 (PPaRγ2), a key transcription factor involved in mediating adipocyte differentiation.

Kanda, Y., Hinata, T., Kang, S. W. & Watanabe, Y. Reactive oxygen species mediate adipocyte differentiation in mesenchymal stem cells.

As a result of the finding that DLK depletion was inhibitory for accumulation of lipids in 3T3-L1 cells, we next sought to investigate whether the absence of DLK could disrupt the transcription factor cascade that mediates adipocyte differentiation.

Therefore, we conclude that TFZ mediates adipocyte differentiation on both stem cells and preadipocytes by activating PPARγ.

HIV protease inhibitors change the expression and localization of transcription factors, such as PPARγ or SREBP, which mediate adipocyte differentiation (Caron et al, 2001).

Our in vitro mechanistic experiments revealed that TBMEHP activates both PPARα- and PPARγ-mediated gene transcription and is capable of stimulating PPARγ-mediated adipocyte differentiation.

Consistent with such repressive role of Dok-1 on macrophage PPARγ activity, it was recently reported that Dok-1 is essential to mediate adipocyte response to insulin, by antagonizing activation of the Ras/Erk1/2 pathway that would otherwise maintain basal phosphorylation of PPARγ Ser-112 and limit its ability to promote terminal differentiation of adipocytes [52].