siRNA

AMFR gene silencing inhibits the differentiation of porcine preadipocytes

C. Z. Chen, Zhu, Y. N., Chai, M. L., Dai, L. S., Gao, Y., Jiang, H., Zhang, L. J., Ding, Y., Liu, S. Y., Li, Q. Y., Lu, W. F., Zhang, J. B., Chen, C. Z., Zhu, Y. N., Chai, M. L., Dai, L. S., Gao, Y., Jiang, H., Zhang, L. J., Ding, Y., Liu, S. Y., Li, Q. Y., Lu, W. F., Zhang, J. B., Chen, C. Z., Zhu, Y. N., Chai, M. L., Dai, L. S., Gao, Y., Jiang, H., Zhang, L. J., Ding, Y., Liu, S. Y., Li, Q. Y., Lu, W. F., and Zhang, J. B., AMFR gene silencing inhibits the differentiation of porcine preadipocytes, vol. 15, p. -, 2016.

Our study clarifies the role of the autocrine motility factor receptor (AMFR) gene in porcine preadipocyte differentiation. AMFR-siRNA was transfected into porcine preadipocytes and the preadipocytes were induced to differentiation. Subsequently, qRT-PCR was conducted to examine changes in mRNA expression of a series of genes in porcine preadipocytes, including AMFR, sterol-regulatory element-binding protein-1a (SREBP1a), SREBP2, insulin-induced gene 1 (Insig1), and Insig2.

Inhibition of gap junctions relieves the hepatotoxicity of TNF-α

Z. Y. Chen, Wang, R., Huang, F., Yuan, D. D., and Li, S. R., Inhibition of gap junctions relieves the hepatotoxicity of TNF-α, vol. 14, pp. 11896-11904, 2015.

The aim of this study was to observe the influence of gap junction (GJ) functional changes on the hepatotoxicity of TNF-α. Three different methods were employed to study functional effects of the GJ inhibition: 1) pretreatment with a GJ inhibitor; 2) inoculation of cells at high and low densities; and 3) inhibition of the expression of connexin 32 (Cx32) by small inhibitory RNA transfection. We then observed the influence of these treatments on hepatotoxicity following treatment with different concentrations of TNF-α for various duration.

Effects of kinase insert domain receptor (KDR) gene silencing on the sensitivity of A549 cells to erlotinib

W. L. Zhu and Liu, Y. H., Effects of kinase insert domain receptor (KDR) gene silencing on the sensitivity of A549 cells to erlotinib, vol. 14, pp. 15073-15080, 2015.

We investigated the effects of kinase insert domain receptor (KDR) gene silencing on the proliferation of A549 cells and their sensitivity to erlotinib. A KDR small interfering RNA (siRNA) sequence was designed and synthesized; then, it was transfected into A549 cells using LipofectamineTM 2000. KDR mRNA and protein expression after KDR gene silencing was detected by reverse transcription polymerase chain reaction and western blotting; the A549 cell cycle was detected by flow cytometry.

Subscribe to siRNA