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Qingshan Ma,Zhanqiao Yu,Bing Han,Qing Wang,Rijun Zhang 한국미생물학회 2012 The journal of microbiology Vol.50 No.2
Lacticin Q is a broad-spectrum class II bacteriocin with potential as an alternative to conventional antibiotics. The objective of this study was to produce recombinant lacticin Q using a small ubiquitin-related modifier (SUMO) fusion protein expression system. The 168-bp lacticin Q gene was cloned into the expression vector pET SUMO and transformed into Escherichia coli BL21(DE3). The soluble fusion protein was recovered with a Ni-NTA Sepharose column (95% purity); 130 mg protein was obtained per liter of fermentation culture. The SUMO tag was then proteolytically cleaved from the protein, which was re-applied to the column. Finally, about 32 mg lacticin Q (≥96% purity) was obtained. The recombinant protein exhibited antimicrobial properties similar to that of the native protein, demonstrating that lacticin Q had been successfully expressed by the SUMO fusion system.
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Genistein inhibit the proliferation induced by zearalenone in MCF-7 cells
Wang, Dingfa,Ma, Qingshan,Zhang, Niya,Qi, Desheng The Korean Society of Toxicogenomics and Toxicopro 2010 Molecular & cellular toxicology Vol.6 No.1
Zearalenone (ZEA) is a nonsteroidal estrogenic mycotoxin and exists widely in the moldy feeds and food. Genistein (GEN) is a natural isoflavone phytoestrogen. ZEA has adverse effects on animal's reproduction performance and immunologic function, also can induce the proliferation of MCF-7 cells. However, the interactive effect of ZEA and GEN on proliferation and cell cycle in MCF-7 cells is remain poorly understood. Here, the interactive effect of ZEA and GEN on proliferation and cell cycle in MCF-7 cells were determined through MTT assay and flow cytometry, respectively. Results demonstrated that ZEA(10 and 20 nM) could stimulate the proliferation of MCF-7 cells and significantly increase S phase distribution (P< 0.05). RT-PCR analysis revealed that ZEA could significantly increase estrogen receptor (ER) $\alpha$ mRNA expression (P < 0.05), while GEN (16 and $32\;{\mu}M$) could inhibit proliferation and lessen S phase distribution of MCF-7 cells (P < 0.05) which were induced by ZEA. In the co-administration treatments of GEN and ZEA, $ER\alpha$ mRNA expression decreased, bcl-2 decreased and bax increased at both mRNA and protein levels compared to those with ZEA alone. These results showed that the proliferative activity of ZEA could be repressed by GEN through regulating the expression of ER, bax and bcl-2 in MCF-7 cells.
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