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BRG1 Promotes chromatin remodeling around DNA damage sites
Wenjing Qi,Hongyu Chen,Chengwen Lu,Qingpan Bu,Xiaoguang Wang,Liping Han 한국통합생물학회 2018 Animal cells and systems Vol.22 No.6
Chromatin remodeling complexes play important roles in various DNA metabolism processes, including DNA damage repair. BRG1 is the core subunit of the SWI/SNF complex, which plays critical roles in cell cycle regulation, cell development, cell differentiation, and tumorigenesis. In the present study, we report that BRG1 depletion increased the percentage of apoptotic cells in etoposide-treated cells. Moreover, western blotting and immunofluorescence data showed that BRG1 depletion decreased H2AX phosphorylation and caused defective phosphorylated histone H2AX (γH2AX) clearance. Furthermore, we found that in both SW13 and U2OS cells, BRG1 expression could increase the sensitivity of genomic DNA to micrococcal nuclease (MNase) and facilitate chromatin relaxation around DNA damage sites. Thus, the results provide evidence that BRG1 plays an important role in early DNA damage repair by remodeling the chromatin structure near DNA damage sites.
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Utility-based User Association In Heterogeneous Wireless Networks
Yanjia Qi,Hongyu Wang 한국정보통신학회 2015 2016 INTERNATIONAL CONFERENCE Vol.7 No.1
With many types of small cells and heterogeneous wireless networks emerging, how to allocate correct base station to a mobile user becomes a critical and challenging problem. Previous research proposed several methods such as RSRP-based, RE, RE with ABS and Bias-based cell selection. However, these methods do not consider mobile users" satisfaction degree. This paper considers a general utility maximization problem for joint optimization of mobile user associations and bandwidth allocations in cellular networks. The problem can incorporate a large class of network topologies and constraints. We first get optimal bandwidth allocation in multi-path connection scenario which can be applied in carrier aggregation scenarios where users can connect multiple base stations. Then we use truncation method to help user find specific optimal serving base station. Because the problem is non-convex, we show that the optimization admits a separable dual decomposition. This property enables fast computation of global optimal solution on the utility in an efficient, distributed implementation manner via augmented Lagrangian techniques. Simulations show in heterogeneous networks with macrocells and picocells, the proposed method achieves much better cell-edge users and median users performances than conventional cell selection method.
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Xiujuan Tian,Wenjing Qi,Hongyu Chen,Xianlu Zeng,Liping Han,Donghui Mi 한국통합생물학회 2016 Animal cells and systems Vol.20 No.5
In pre-initiation complexes, RNA helicase A interacts with β-actin and acts as a bridging factor linking nuclear actin with RNA polymerase II (Pol II). In addition, β-actin participates in Pol IIdependent transcription elongation by interacting with the positive transcription elongation factor Cdk9. However, many relationships between β-actin and Pol II remain to be identified. In an interleukin 6 (IL-6)-induced p21 expression model, we demonstrated that β-actin knockdown reduced p21 expression. Immunofluorescence analysis showed that the colocalization of β-actin and Pol II increased significantly in cells treated with IL-6. It is known that the Rpb5, Rpb6 and Rpb7 subunits are located at the surface of the enzyme. We next constructed recombinant pcDNA-HA-Rpb5, pcDNA-HA-Rpb6 and pcDNA-HA-Rpb7 plasmids and expressed the three polymerase II subunits in HepG2 cells. We found that β-actin could be immunoprecipitated with HA-Rpb5 and HA-Rpb7. A Glutathione-S-transferase pull-down assay revealed that β-actin was associated with Rpb5 and Rpb7 in vitro. Furthermore, overexpression of Rpb5 and Rpb7 in cells reduced p21 expression significantly, suggesting that Rpb5 and Rpb7 competitively interact with β-actin. This study shows that β-actin associates with Pol II subunits through direct proteinprotein interactions and provides fundamental insight into Pol II transcriptional regulation.
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Preparation and Effect Analysis of {10–12} Extension Twins at the Edge of AZ31 Magnesium Alloy Plate
Zhiquan Huang,Chuanlu Qi,Yanchun Zhu,Guowei Yang,Hongyu Lai,Jinchao Zou 대한금속·재료학회 2021 METALS AND MATERIALS International Vol.27 No.11
The edge samples of AZ31 magnesium alloy plate after hot rolling and annealing were compressed along the rolling direction(RD) under different deformation conditions. Then, the optimal conditions for the generation of {10–12} extension twinsand the microtexture evolution of edge samples were studied by using EBSD. The results show that the texture strength ofthe hot-rolled AZ31 magnesium alloy plate was significantly greater than that of the middle part. When the compressivestrain along the RD was small at the edge of the rolled piece at room temperature, a large number of extension twin layerswere generated. Grain matrix and twins coexisted. As the strain increased to 8.19%, the grains completely transformed intoextension twins. Along with the generation of extension twins, hard-oriented grains were consumed in large quantities andthe weakening effect of the basal texture was proportional to the volume fraction of the extension twins, while at high temperature(250 °C), the slip dominated the plastic deformation process.
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Qingxia Huang,Jing Li,Jinjin Chen,Zepeng Zhang,Peng Xu,Hongyu Qi,Zhaoqiang Chen,Jiaqi Liu,Jing Lu,Mengqi Shi,Yibin Zhang,Ying Ma,Daqing Zhao,Xiangyan Li The Korean Society of Ginseng 2023 Journal of Ginseng Research Vol.47 No.3
Background: Ginsenoside compound K (CK), the main active metabolite in Panax ginseng, has shown good safety and bioavailability in clinical trials and exerts neuroprotective effects in cerebral ischemic stroke. However, its potential role in the prevention of cerebral ischemia/reperfusion (I/R) injury remains unclear. Our study aimed to investigate the molecular mechanism of ginsenoside CK against cerebral I/R injury. Methods: We used a combination of in vitro and in vivo models, including oxygen and glucose deprivation/reperfusion induced PC12 cell model and middle cerebral artery occlusion/reperfusion induced rat model, to mimic I/R injury. Intracellular oxygen consumption and extracellular acidification rate were analyzed by Seahorse multifunctional energy metabolism system; ATP production was detected by luciferase method. The number and size of mitochondria were analyzed by transmission electron microscopy and MitoTracker probe combined with confocal laser microscopy. The potential mechanisms of ginsenoside CK on mitochondrial dynamics and bioenergy were evaluated by RNA interference, pharmacological antagonism combined with co-immunoprecipitation analysis and phenotypic analysis. Results: Ginsenoside CK pretreatment could attenuate mitochondrial translocation of DRP1, mitophagy, mitochondrial apoptosis, and neuronal bioenergy imbalance against cerebral I/R injury in both in vitro and in vivo models. Our data also confirmed that ginsenoside CK administration could reduce the binding affinity of Mul1 and Mfn2 to inhibit the ubiquitination and degradation of Mfn2, thereby elevating the protein level of Mfn2 in cerebral I/R injury. Conclusion: These data provide evidence that ginsenoside CK may be a promising therapeutic agent against cerebral I/R injury via Mul1/Mfn2 mediated mitochondrial dynamics and bioenergy.
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