Institution
Xuzhou Medical College
Education•Xuzhou, China•
About: Xuzhou Medical College is a education organization based out in Xuzhou, China. It is known for research contribution in the topics: Cancer & Cell growth. The organization has 12721 authors who have published 7802 publications receiving 102970 citations.
Topics: Cancer, Cell growth, Apoptosis, Medicine, Protein kinase B
Papers published on a yearly basis
Papers
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TL;DR: In vivo data offer novel insights into the chaperone function of IbpB, or sHSPs in general, and suggest that the preferential protection on the protein synthesis machine and metabolic enzymes may dominantly contribute to the well known protective effect of sH SPs on cell survival against stresses.
53 citations
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TL;DR: It is demonstrated that luteolin prevents ischemia-reperfusion injury by reducing necrosis and apoptosis in rat cardiomyocytes by improving heart rate and limiting the decline of left ventricular systolic pressure and elevation ofleft ventricular end-diastolic pressure to some extent.
53 citations
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TL;DR: Overexpression of the SIRT6 gene could inhibit apoptosis and induce autophagy, which might be involved in repairing kidney damage caused by LPS.
Abstract: Sirtuin 6 (SIRT6) has the function of regulating autophagy. The aim of this study was to investigate the mechanism through which SIRT6 relieved acute kidney injury (AKI) caused by sepsis. The AKI model was established with lipopolysaccharides (LPS) using mice. Hematoxylin-eosin (HE) staining and streptavidin-perosidase (SP) staining was used to observe kidney tissue and test SIRT6 and LC3B proteins in kidney. Enzyme-linked immunosorbent assay (ELISA) was performed to detected the tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) concentrations. Cell counting kit-8 (CCK-8) assay and flow cytometry were carried out to test the cell viability and apoptosis rate respectively. Protein and mRNA were determined by Western blot and quantitative real-time polymerase chain reaction (qRT-PCR). AKI induced by LPS had self-repairing ability. At 12 h after modeling, the expression levels of TNF-α, IL-6, SIRT6 and LC3B-II/LC3B-I were first significantly increased and were then significantly decreased at 48 h after modeling. LPS inhibited the growth of HK-2 cells and promoted the expressions of TNF-α, IL-6, SIRT6 and LC3B. Overexpression of SIRT6 down-regulated the secretion of TNF-α and IL-6 induced by LPS. SIRT6 overexpression inhibited apoptosis induced by LPS and promoted autophagy in HK-2 cells. Silencing of the SIRT6 gene not only promoted the secretion of TNF-α and IL-6 by HK-2 cells, but also promoted apoptosis and reduced autophagy. LPS up-regulated the expression of SIRT6 gene in HK-2 cells. Overexpression of the SIRT6 gene could inhibit apoptosis and induce autophagy, which might be involved in repairing kidney damage caused by LPS.
53 citations
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TL;DR: This study provides a new crosstalk mechanism between Hippo/YAP and Wnt/β-catenin pathways, which suggests a new strategy for human glioma treatment.
Abstract: Hippo/YAP pathway is known to be important for development, growth and organogenesis, and dysregulation of this pathway leads to tumor progression.We and others find that YAP is up-regulated in human gliomas and associated with worse prognosis of patients. However, the role and mechanism of YAP in glioma progression is largely unknown. The expression of YAP in glioma tissues was detected by quantitative polymerase chain reaction (qPCR) and immunoblotting. The effect of YAP on glioma progression was examined using cell growth assays and intracranial glioma model. The effect of YAP on β-catenin protein level, subcellular location and transcription activity was examined by immunoblotting, immunofluorescence and RT-PCR. Firstly, knockdown of YAP inhibited glioma cell proliferation in vitro and tumor growth in vivo. In addition, YAP modulated the protein level, subcellular location and transcription activity of β-catenin via regulating the activity of GSK3β. Lastly, β-catenin partially mediated the effect of YAP on glioma cell proliferation. Our findings identify that YAP promotes human glioma growth through enhancing Wnt/β-catenin signaling. In addition, this study provides a new crosstalk mechanism between Hippo/YAP and Wnt/β-catenin pathways, which suggests a new strategy for human glioma treatment.
53 citations
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TL;DR: Findings indicate that ephrinB–EphB receptor activation and redistribution in DRG and DH neurons after nerve injury could contribute to neuropathic pain and may also provide a new mechanism underlying DR‐induced analgesia in clinic.
53 citations
Authors
Showing all 12775 results
Name | H-index | Papers | Citations |
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Liang Wang | 98 | 1718 | 45600 |
Chang Liu | 97 | 1099 | 39573 |
Wei Wang | 95 | 3544 | 59660 |
Yu Liu | 66 | 1262 | 20577 |
Deling Kong | 65 | 388 | 16515 |
Zhimou Yang | 61 | 222 | 12522 |
Xu-Feng Huang | 61 | 332 | 13074 |
Guangming Lu | 60 | 476 | 13218 |
Dan Ding | 59 | 212 | 12494 |
Jian Cao | 58 | 486 | 11074 |
Yuanjin Zhao | 57 | 328 | 12076 |
Jie Yang | 56 | 488 | 11382 |
Lei Wang | 54 | 1076 | 15189 |
Xiaodong Shi | 52 | 323 | 8910 |
Wei Pan | 50 | 408 | 9037 |