Cold-adapted alginate lyases have unique advantages for alginate oligosaccharide (AOS) preparation and brown seaweed processing. Robust and cold-adapted alginate lyases are urgently needed for industrial applications. In this study, a cold-adapted alginate lyase-producing strain Vibrio sp. W2 was screened. Then, the gene ALYW201 was cloned from Vibrio sp. W2 and expressed in a food-grade host, Yarrowia lipolytica. The secreted Alyw201 showed the activity of 64.2 U/mL, with a molecular weight of approximate 38.0 kDa, and a specific activity of 876.4 U/mg. Alyw201 performed the highest activity at 30 °C, and more than 80% activity at 25–40 °C. Furthermore, more than 70% of the activity was obtained in a broad pH range of 5.0–10.0. Alyw201 was also NaCl-independent and salt-tolerant. The degraded product was that of the oligosaccharides of DP (Degree of polymerization) 2–6. Due to its robustness and its unique pH-stable property, Alyw201 can be an efficient tool for industrial production.
Embryonic stem (ES) cells are derived from blastocysts. They can differentiate into the three embryonic germ layers and essentially any type of somatic cells. Therefore, they hold great potentials in tissue regeneration therapy. The ethical issues associated with the use of human embryonic stem cells are resolved by the technical break-through of generating induced pluripotent stem (iPS) cells from various types of somatic cells. However, how ES and iPS cells self-renew and maintain their pluripotency is still largely unknown in spite of the great progresses that have been made in the last two decades. Integrative genome-wide approaches, such as gene expression microarray, chromatin immunoprecipitation based microarray (ChIP-chip) and chromatin immunoprecipitation followed by massive parallel sequencing (ChIP-seq) offer unprecedented opportunities to elucidate the mechanism of the pluripotency, reprogramming and DNA damage response of ES and iPS cells. This review summarized the fundamental biological questions about ES and iPS cells and reviewed the recent advances in ES and iPS cell research using genome-wide technologies. In the end, we offered our perspectives on the future of genome-wide studies on stem cells.
Malignant melanoma represents a sort of neoplasm deriving from melanocytes or cells developing from melanocytes. The balance of energy and energy-associated body composition and body mass index could be altered by exercise, thereby directly affecting the microenvironment of neoplasm. However, few studies have examined the mechanism of genes induced by exercise and the pathways involved in melanoma. This study used three separate datasets to perform comprehensive bioinformatics analysis and then screened the probable genes and pathways in the process of exercise-promoted melanoma. In total, 1,627 differentially expressed genes (DEGs) induced by exercise were recognized. All selected genes were largely enriched in NF-kappa B, Chemokine signaling pathways, and the immune response after gene set enrichment analysis. The protein-protein interaction network was applied to excavate DEGs and identified the most relevant and pivotal genes. The top 6 hub genes (Itgb2, Wdfy4, Itgam, Cybb, Mmp2, and Parp14) were identified, and importantly, 5 hub genes (Itgb2, Wdfy4, Itgam, Cybb, and Parp14) were related to weak disease-free survival and overall survival (OS). In conclusion, our findings demonstrate the prognostic value of exercise-induced genes and uncovered the pathways of these genes in melanoma, implying that these genes might act as prognostic biomarkers for melanoma.
Background: Traumatic brain injury (TBI) is a major cause of disability worldwide, without definitive and effective intervention. Dexmedetomidine (DEX) has a neuroprotective effect against TBI; however, the detailed mechanism underlying this effect remains unclear.Methods: Ten male Sprague Dawley rats were used to establish a TBI model. The rats were randomly divided into two groups: the TBI group (TBI, control group) and the DEX treatment group (DEX). The next day, the neurological function of the rats were evaluated by the modified neurological severity score (mNSS). Then, the rats were sacrificed, and RNA sequencing was performed to identify differentially expressed messenger RNAs (mRNAs) and microRNAs (miRNAs) in brain tissue samples. Additionally, we performed a bioinformatics analysis to explore the candidate genes and pathways that might play important roles in DEX-induced neuroprotection. The most significantly differentially expressed miRNAs and possible hub genes were validated by quantitate reverse transcription-polymerase chain reaction (qRT-PCR) using more samples.Results: In the DEX group, 517 mRNAs (352 up-regulated and 165 down-regulated) and 35 miRNAs (18 up-regulated and 17 down-regulated) were differentially expressed compared to the TBI group. Gene Ontology analysis revealed the up-regulated mRNAs to be significantly enriched in microtubule-based movement or processes, microtubule and tubulin binding. Kyoto Encyclopedia of Genes and Genomes analysis showed that these up-regulated mRNAs were significantly enriched in the B-cell receptor signaling pathway as well as the cell cycle pathway. Also, Lyn and Cdk1 were found to be associated with the B-cell receptor signaling and cell cycle pathways, respectively. Furthermore, the down-regulated miRNAs were significantly enriched in cellular components, although no significant Gene Ontology terms or KEGG pathways were found for the down-regulated mRNAs or up-regulated miRNAs.Conclusions: Differentially expressed mRNAs and miRNAs were identified after the administration of DEX in a TBI rat model. The B-cell receptor signaling pathway and the cell cycle pathway might be involved in the neuroprotective effect of DEX against TBI, Lyn and Cdk1 might be hub genes.
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