Recombinant T2 RNase glycoprotein, which showed a certain degree of homology to Omega-1 from Schistosoma mansoni eggs, was expressed in adult worms of Schistosoma japonicum, but not in eggs of S. japonicum. The direct biological role of the recombinant T2 RNase protein in activation of hepatic stellate cells (HSCs) remains unknown. In the present study, the immortalized human HSC line (LX-2 cells) was treated with the recombinant T2 RNase protein at indicated concentrations for various time points in vitro. The expression levels of α-smooth muscle actin (α-SMA) and Smad4 were detected by Western blot. The results showed that the recombinant T2 RNase protein significantly diminished the expression levels of α-SMA and Smad4 in LX-2 cells. The upregulated expression levels of α-SMA and Smad4 by TGF-β1 in LX-2 cells were both suppressed by the recombinant T2 RNase protein. These data suggest that the recombinant T2 RNase protein may be a potential target of therapeutic strategy for the treatment of hepatic fibrosis.
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http://dx.doi.org/10.1007/s00436-016-5178-z | DOI Listing |
Int J Biol Macromol
December 2024
State Key Laboratory of Cellular Stress Biology, Innovation Centre for Cell Signalling Network, Engineering Research Centre of Molecular Diagnostics of the Ministry of Education, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China; National Institute for Data Science in Health and Medicine Engineering, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, Fujian 361102, China. Electronic address:
Despite its limitations, restriction enzyme (RE)-mediated cleavage remains the prevalent method for generating sticky ends in DNA assembly. Here, we present RNase HII Fusion (RH2Fusion), a robust system for user-defined sticky ends, enabling scarless assembly of multiple DNA fragments alongside simultaneous site-directed mutagenesis (SDM) at multiple sites. In bacterial cells, DNA fragments with ribonucleotide modifications are expected to form complementary 3' overhangs after RNase HII treatment, followed by annealing and recombination via the bacterial self-repair system.
View Article and Find Full Text PDFCell Tissue Bank
December 2024
NHS Blood and Transplant, Tissue Services R&D, 14 Estuary Banks, Speke, Liverpool, L24 8RB, UK.
Methods Mol Biol
December 2024
Section of Vaccine Design and Poxvirus Vectors, Division of Viral Diseases, Directorate of Science Reference and Surveillance, The Public Health Agency of Canada, Winnipeg, MB, Canada.
Vaccinia virus (VACV) demonstrates a wide host range, which is determined by its host range genes including the E3L and K3L. The E3L and K3L deletion mutant VACV (VACVΔE3ΔK3) is only able to replicate in cells defective in PKR and RNase L activity. Interestingly, by expressing a K3 ortholog from another poxvirus, the host range of the VACVΔE3ΔK3 can be fine-tuned to specific host species.
View Article and Find Full Text PDFParasit Vectors
November 2024
Department of Reproductive Medicine, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, China.
Background: Malaria remains a serious public health problem worldwide, particularly in Africa. Resistance to antimalarial drugs is an essential issue for malaria control and elimination. Currently, polymerase chain reaction (PCR) combined with Sanger sequencing is regarded as the gold standard for mutation detection.
View Article and Find Full Text PDFEur J Neurosci
December 2024
Institute of Pharmacology and Toxicology, University of Zurich, Zurich, Switzerland.
The suprachiasmatic nucleus (SCN) is the master clock that directly dictates behavioural rhythms to anticipate the earth's light/dark cycles. Although post-transcriptional regulators called microRNAs have been implicated in physiological SCN function, how the absence of the entire mature miRNome impacts SCN output has not yet been explored. To study the behavioural consequences of miRNA depletion in the SCN, we first generated a mouse model in which Dicer is inactivated in the SCN by crossing Syt10 mice with Dicer mice to study behavioural consequences of miRNA depletion in the SCN.
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