2016 Nobel Prize Winner Yoshinori Ohsumi's Discoveries Could Change How We Treat Disease
Japanese scientist Yoshinori Ohsumi, 71, won the 2016 Nobel Prize on Monday for his research on autophagy ― a metabolic recycling process in which cells eat parts of themselves to survive and stay healthy. His initial work, first started in 1992, focused on the genes behind the autophagy process in yeast cells. Autophagy, however, has implications for several human diseases, including cancer, neurodegenerative diseases, infectious diseases and diabetes. Now drugs that can target the process are being tested in early-stage clinical trials in human beings, which could fundamentally change everything from the way we treat dementia disorders to how we eradicate cancerous growths. Autophagy is a normal part of a cell’s lifespan. Individual cells can “eat” parts of themselves, especially old or damaged parts, and recycle the material to help keep themselves healthy. Think of it like recycling: By shedding damaged or dying parts inside the cell, the cell has a new resource from which to repair itself and keep itself running. Autophagy helps address normal damage and wear and tear to cells, but also plays a role in everything from fighting bacterial or viral infections to in-cell differentiation in embryo development. A dysfunctional autophagy process has also been linked to Type 2 diabetes and other genetic diseases, the Nobel Prize site notes. In particular, it may play an important role in two distinct disease types that are diff...
In this study, we use ChIP-Seq to identify Dppa4 binding genome-wide in three distinct cell types: mouse embryonic stem cells (mESC), embryonal carcinoma cells, and 3T3 fibroblasts ectopically expressing Dppa4. We find a core set of Dppa4 binding sites shared across cell types, and also a substantial number of sites unique to each cell type. Across cell types Dppa4 shows a preference for binding to regions with active chromatin signatures, and can influence chromatin modifications at target genes. In 3T3 fibroblasts with enforced Dppa4 expression, Dppa4 represses the cell cycle inhibitor Cdkn2c and activates Ets family tra...
Publication date: Available online 19 July 2018Source: Stem Cell ResearchAuthor(s): Stephanie N. Iwasa, Milos R. Popovic, Cindi M. MorsheadAbstractMany cell types respond to electric fields (EFs) through cell migration, a process termed galvanotaxis. The galvanotactic response is critical for development and wound healing. Here we investigated whether skin-derived precursor cells (SKPs), which have the potential to differentiate into mesodermal and peripheral neural cell types, undergo directed migration in the presence of an EF. We found that EF application promotes SKP migration towards the anode. The migratory response ...
Conclusions: LUCAT1 was upregulated in ccRCC tissues and renal cancer cell lines, and significantly correlated with malignant stage and poor prognosis in ccRCC. LUCAT1 promoted proliferation and invasion in ccRCC cells through the AKT/GSK-3 β signaling pathway. We also revealed that LUCAT1 overexpression was induced by chemokine CXCL2. These findings indicate that the CXCL2/LUCAT1/AKT/GSK-3β axis is a potential therapeutic target and molecular biomarker for ccRCC.Cell Physiol Biochem 2018;48:891 –904
Conclusion: Our results have revealed a novel mechanism by which ALKBH5 inhibits pancreatic cancer motility by demethylating lncRNA KCNK15-AS1, identifying a potential therapeutic target for pancreatic cancer.Cell Physiol Biochem 2018;48:838 –846
Conclusion: Lower expression of miR-374a is associated with poor prognosis and miR-374a improves tumor biological behavior in bladder cancer cells, suggesting that miR-374a might be a novel small-molecule therapeutic target.Cell Physiol Biochem 2018;48:815 –826
Conclusions: Our data revealbiological and functional interactions between immunotherapy and radiotherapy through the miR-195/-16 family regulatory cascade.Cell Physiol Biochem 2018;48:801 –814
Conclusions: Exposure to metformin in combination with FTY720 potently induces apoptosis in MM cells in a ROS-dependent manner, suggesting that a strategy combining these agents warrants further investigation in MM.Cell Physiol Biochem 2018;48:785 –800
In conclusion, we focus on the various newer molecular mechanisms that are associated with the basic understanding of neuroinflammation in neurodegeneration.
Publication date: November 2018Source: Clinica Chimica Acta, Volume 486Author(s): Jieli Li, Jing Ma, Elizabeth A. Wagar, Dong Liang, Qing H. MengAbstractBackgroundVoriconazole (VOR), an antifungal agent, is clinically monitored to guide therapeutic dosing and avoid toxicity. It is believed that measurement of serum unbound VOR provides more accurate information, especially in hypoalbuminemia patients. We developed and validated an accurate, simple and fast test with ultrafiltration and ultra-performance liquid chromatography (UPLC)-tandem mass spectrometry (MS/MS) to measure unbound VOR in human serum.MethodsThe Agilent UP...
ConclusionsLower serum UA concentrations may be associatedwith lower BMD values and higher prevalence of clinical fractures independent of potential confounders except for BMD values at each site. These findings need to be confirmed by further prospective studies.
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