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排序方式: 共有319条查询结果,搜索用时 0 毫秒
311.
Neal G. Ravindra Mia Madel Alfajaro Victor Gasque Nicholas C. Huston Han Wan Klara Szigeti-Buck Yuki Yasumoto Allison M. Greaney Victoria Habet Ryan D. Chow Jennifer S. Chen Jin Wei Renata B. Filler Bao Wang Guilin Wang Laura E. Niklason Ruth R. Montgomery Stephanie C. Eisenbarth Sidi Chen Adam Williams Akiko Iwasaki Tamas L. Horvath Ellen F. Foxman Richard W. Pierce Anna Marie Pyle David van Dijk Craig B. Wilen 《PLoS biology》2021,19(3)
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Katerina Tomankova Hana Kolarova Klara Pizova Svatopluk Binder Petr Konecny Eva Kriegova Lukas Malina Jana Horakova Jakub Malohlava Kristina Kejlova Dagmar Jirova 《Food biophysics》2014,9(3):267-276
Many studies have been carried out on bioactivities of individual herbs/fruits using in cosmetics or as a diet products, however, no collective study on their comparative antioxidant activities against oxidative damage or on cytotoxicity effect has been reported. The aim of this work was study the cytotoxicity and antioxidative activity of eight extracts with hypothetical antioxidative influence in vitro. To further elucidate of a possible role of herbals/fruits extracts on cell protection was used on the healthy and UV-A damaged mouse fibroblast cells. The cell viability was detect using MTT assay. Kinetic production of reactive oxygen species, identification of cell death, cell cycle and gene expression C-FOS were measured. Intracellular and mitochondrial transmembrane potential was evaluate with JC-1 fluorescence probe. Comet assay was employed to detect the UV-A induced DNA damage. The results indicated that using the extracts decreased ROS production. It can lead to greatly enhance and promote the viability of cells. As the most effective antioxidant in quenching of the ROS, in cell viability and DNA presentation was determined Prunella Vulgaris. However, one of them (Wheat Germ Oil) caused increased production of ROS and low cell viability. 相似文献
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Mohammad Tezval Hossein Tezval Klaus Dresing Ewa Klara Stuermer Martina Blaschke Klaus Michael Stuermer Heide Siggelkow 《Journal of molecular histology》2009,40(5-6):331-341
Urocortin-1 (UCN) a corticotropin releasing-factor (CRF) related peptide, has been found to be expressed in many different tissues like the central nervous system, the cardiovascular system, adipose tissue, and skeletal muscle. The effects of UCN are mediated via stimulation of CRF-receptors 1 and 2 (CRFR1 and 2, CRFR’s) with a high affinity for CRFR2. It has been shown that the CRF-related peptides and CRFR’s are involved in the regulation of stress-related endocrine, autonomic and behavioural responses. Using immunocytochemistry, immunohistochemistry and RT–PCR, we now can show the differentiation dependent expression of UCN mRNA and peptide in human mesenchymal progenitor cells (MSCs) directed to the osteoblastic phenotype for the first time. UCN expression was down regulated by TGF-beta and BMP-2 in the early proliferation phase of osteoblast development, whereas dexamethasone (dex) minimally induced UCN gene expression during matrix maturation after 24 h stimulation. Stimulation of MSCs for 28 days with ascorbate/beta-glycerophosphate (asc/bGp) induced UCN gene expression at day 14. This effect was prevented when using 1,25-vitamin D3 or dex in addition. There was no obvious correlation to osteocalcin (OCN) gene expression in these experiments. In MSCs from patients with metabolic bone disease (n = 9) UCN gene expression was significantly higher compared to MSCs from normal controls (n = 6). Human MSCs did not express any of the CRFR’s during differentiation to osteoblasts. Our results indicate that UCN is produced during the development of MSCs to osteoblasts and differentially regulated during culture as well as by differentiation factors. The expression is maximal between proliferation and matrix maturation phase. However, UCN does not seem to act on the osteoblast itself as shown by the missing CRFR’s. Our results suggest new perspectives on the role of urocortin in human skeletal tissue in health and disease. 相似文献
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Annika Pfeiffer Nico P Dantuma Annika Pfeiffer Martijn S Luijsterburg Klara Acs Wouter W Wiegant Angela Helfricht Laura K Herzog Melania Minoia Claudia Böttcher Florian A Salomons Haico van Attikum Nico P Dantuma 《The EMBO journal》2017,36(8):1066-1083
The SUMO-targeted ubiquitin ligase RNF4 functions at the crossroads of the SUMO and ubiquitin systems. Here, we report that the deubiquitylation enzyme (DUB) ataxin-3 counteracts RNF4 activity during the DNA double-strand break (DSB) response. We find that ataxin-3 negatively regulates ubiquitylation of the checkpoint mediator MDC1, a known RNF4 substrate. Loss of ataxin-3 markedly decreases the chromatin dwell time of MDC1 at DSBs, which can be fully reversed by co-depletion of RNF4. Ataxin-3 is recruited to DSBs in a SUMOylation-dependent fashion, and in vitro it directly interacts with and is stimulated by recombinant SUMO, defining a SUMO-dependent mechanism for DUB activity toward MDC1. Loss of ataxin-3 results in reduced DNA damage-induced ubiquitylation due to impaired MDC1-dependent recruitment of the ubiquitin ligases RNF8 and RNF168, and reduced recruitment of 53BP1 and BRCA1. Finally, ataxin-3 is required for efficient MDC1-dependent DSB repair by non-homologous end-joining and homologous recombination. Consequently, loss of ataxin-3 sensitizes cells to ionizing radiation and poly(ADP-ribose) polymerase inhibitor. We propose that the opposing activities of RNF4 and ataxin-3 consolidate robust MDC1-dependent signaling and repair of DSBs. 相似文献
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