Biotechnology and applied biochemistry最新文献

Inflammation and oxidative stress (OS) are the major pathogenic characteristics of acute kidney injury (AKI). Studies have shown that Schisandrin (Sch) could regulate inflammatory disease. However, the function and mechanism of Sch in AKI progression are still unknown. Here, we investigated Sch's potential effects and mechanism on mice's renal damage and macrophages induced by lipopolysaccharide (LPS). Sch decreased LPS-induced inflammatory factor production while increasing the activity of related antioxidant enzymes in macrophages and mouse kidney tissues. Hematoxylin and eosin staining revealed that Sch may have the ability to profoundly inhibit inflammatory cell invasion and tissue damage caused by LPS in renal tissue. Furthermore, Western blot and immunohistochemical studies showed that Sch exerted its effects mainly through up-regulation of nuclear factor erythroid 2-related factor 2/heme oxygenase-1 and inhibition of Toll-like receptor 4‒mitogen-activated protein kinases/nuclear factor-kappa B pathways. Collectively, this study illustrates that Sch suppresses LPS-stimulated AKI by descending inflammation and OS, illuminating prospective AKI treatment options.

Nephropathia epidemica (NE), caused by Puumala (PUUV) orthohantavirus, is endemic in the Republic of Tatarstan (RT). There are limited options for NE prevention in RT. Currently, available vaccines are made using Haantan (HNTV) orthohantavirus antigens. In this study, the efficacy of microvesicles (MVs) loaded with PUUV antigens to induce the humoral immune response in small mammals was analyzed. Additionally, the cross-reactivity of serum from immunized small mammals and NE patients with HNTV, Dobrava, and Andes orthohantaviruses was investigated using nucleocapsid (N) protein peptide libraries. Finally, the selected peptides were analyzed for allergenicity, their ability to induce an autoimmune response, and their interaction with Class II HLA. Several N protein peptides were found to be cross-reactive with serum from MVs immunized small mammals. These cross-reactive epitopes were located in oligomerization perinuclear targeting and Daxx-interacting domains. Most cross-reactive peptides lack allergenic and autoimmune reactivity. Molecular docking revealed two cross-reacting peptides, N6 and N19, to have good binding with three Class II HLA alleles. These peptides could be candidates for developing vaccines and therapeutics for NE.

Retraction Statement: Inhibition of protein phosphatase 5 (PP5) suppresses survival and growth of colorectal cancer cells

Wang, J., Zhu, J., Dong, M., Yu, H., Dai, X. and Li, K. (2015), Inhibition of protein phosphatase 5 (PP5) suppresses survival and growth of colorectal cancer cells. Biotechnology and Applied Biochemistry, 62: 621−627. https://doi.org/10.1002/bab.1308

We apologize for errors in the retraction text wording which should have read as follows:

Streptavidin is a tetrameric protein with high specificity and affinity for biotin. The interaction between avidin and biotin has become a valuable tool in nanotechnology. In recent years, the site-specific biotin modification of proteins using biotin ligases, such as BirA, has attracted attention. This study established an in vivo method for achieving the complete biotinylation of target proteins using a single plasmid co-expressing BirA and its target proteins. Specifically, a biotin-modified protein was produced in Escherichia coli strain BL21(DE3) using a single plasmid containing genes encoding both BirA and a protein fused to BirA's substrate sequence, Avitag. This approach simplifies the production of biotinylated proteins in E. coli and allows the creation of various biotinylated protein types through gene replacement. Furthermore, the biotin modification rate of the obtained target protein could be evaluated using Native-PAGE without performing complicated isolation operations of biotinylated proteins. In Native-PAGE, biotin-modified proteins and unmodified proteins were confirmed as clearly different bands, and it was possible to easily derive the modification rate from the respective band intensities.

Retraction Statement: Lentivirus-mediated knockdown of Mphase phosphoprotein 8 inhibits proliferation of colon cancer cells

Liang, X., Liu, T., Zhang, W., Zhang, K., Guo, S. and Liang, J. (2017), Lentivirus-mediated knockdown of M-phase phosphoprotein 8 inhibits proliferation of colon cancer cells. Biotechnology and Applied Biochemistry, 64: 911−917. https://doi.org/10.1002/bab.1504

We apologize for errors in the retraction text wording which should have read as follows:

Retraction Statement: Long noncoding RNA linc-ITGB1 promotes cell migration and invasion in human breast cancer

Yan, M., Zhang, L., Li, G., Xiao, S., Dai, J. and Cen, X. (2017), Long noncoding RNA linc-ITGB1 promotes cell migration and invasion in human breast cancer. Biotechnology and Applied Biochemistry, 64: 5−13. https://doi.org/10.1002/bab.1461

We apologize for errors in the retraction text wording which should have read as follows:

Retraction Statement: Knockdown of GPR137 by RNAi inhibits pancreatic cancer cell growth and induces apoptosis

Cui, X., Liu, Y., Wang, B., Xian, G., Liu, X., Tian, X. and Qin, C. (2015), Knockdown of GPR137 by RNAi inhibits pancreatic cancer cell growth and induces apoptosis. Biotechnology and Applied Biochemistry, 62: 861−867. https://doi.org/10.1002/bab.1326

We apologize for errors in the retraction text wording which should have read as follows:

Retraction Statement: KLF8 is required for bladder cancer cell proliferation and migration

Liang, K., Liu, T., Chu, N., Kang, J., Zhang, R., Yu, Y., Li, D. and Lu, D. (2015), KLF8 is required for bladder cancer cell proliferation and migration. Biotechnology and Applied Biochemistry, 62: 628−633. https://doi.org/10.1002/bab.1310

We apologize for errors in the retraction text wording which should have read as follows:

Retraction Statement: Inhibition of GPR137 suppresses proliferation of medulloblastoma cells in vitro

Wang, C., Liang, Q., Chen, G., Jing, J. and Wang, S. (2015), Inhibition of GPR137 suppresses proliferation of medulloblastoma cells in vitro. Biotechnology and Applied Biochemistry, 62: 868−873. https://doi.org/10.1002/bab.1331

We apologize for errors in the retraction text wording which should have read as follows: