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  1. Article ; Online: Inhibitor of DNA Binding 1 Is Induced during Kidney Ischemia-Reperfusion and Is Critical for the Induction of Hypoxia-Inducible Factor-1α

    Dan Wen / Yan-Fang Zou / Yao-Hui Gao / Qian Zhao / Yin-Yin Xie / Ping-Yan Shen / Yao-Wen Xu / Jing Xu / Yong-Xi Chen / Xiao-Bei Feng / Hao Shi / Wen Zhang

    BioMed Research International, Vol

    2016  Volume 2016

    Abstract: In this study, rat models of acute kidney injury (AKI) induced by renal ischemia-reperfusion (I/R) and HK-2 cell models of hypoxia-reoxygenation (H/R) were established to investigate the expression of inhibitor of DNA binding 1 (ID1) in AKI, and the ... ...

    Abstract In this study, rat models of acute kidney injury (AKI) induced by renal ischemia-reperfusion (I/R) and HK-2 cell models of hypoxia-reoxygenation (H/R) were established to investigate the expression of inhibitor of DNA binding 1 (ID1) in AKI, and the regulation relationship between ID1 and hypoxia-inducible factor 1 alpha (HIF-1α). Through western blot, quantitative real-time PCR, immunohistochemistry, and other experiment methods, the induction of ID1 after renal I/R in vivo was observed, which was expressed mainly in renal tubular epithelial cells (TECs). ID1 expression was upregulated in in vitro H/R models at both the protein and mRNA levels. Via RNAi, it was found that ID1 induction was inhibited with silencing of HIF-1α. Moreover, the suppression of ID1 mRNA expression could lead to decreased expression and transcription of HIF-1α during hypoxia and reoxygenation. In addition, it was demonstrated that both ID1 and HIF-1α can regulate the transcription of twist. This study demonstrated that ID1 is induced in renal TECs during I/R and can regulate the transcription and expression of HIF-1α.
    Keywords Medicine ; R
    Subject code 610
    Language English
    Publishing date 2016-01-01T00:00:00Z
    Publisher Hindawi Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article: Hypoxia inducible factor-1α suppresses Peroxiredoxin 3 expression to promote proliferation of CCRCC cells

    Xi, Hao / Yao-Hui Gao / Dong-Yan Han / Qian-Yu Li / Li-Jin Feng / Wei Zhang / Guo Ji / Jia-Cheng Xiao / Hui-Zhen Zhang / Qing Wei

    Federation of European Biochemical Societies FEBS letters. 2014 Sept. 17, v. 588, no. 18

    2014  

    Abstract: Peroxiredoxin 3 (Prx3) is a mitochondrial member of the antioxidant family of thioredoxin peroxidases that uses mitochondrial thioredoxin 2 as a source of reducing equivalents to scavenge hydrogen peroxide (H2O2). Here, we report that the protein levels ... ...

    Abstract Peroxiredoxin 3 (Prx3) is a mitochondrial member of the antioxidant family of thioredoxin peroxidases that uses mitochondrial thioredoxin 2 as a source of reducing equivalents to scavenge hydrogen peroxide (H2O2). Here, we report that the protein levels of Prx3 are significantly reduced in VHL-deficient clear cell renal cell carcinoma (CCRCC). Furthermore, stabilization of HIF-1α protein, caused either by VHL deficiency under normoxia, or by hypoxia, significantly reduced Prx3 expression. Luciferase-reporter and chromatin-immunoprecipitation assays indicated that HIF-1α binds to the hypoxia-responsive elements of PRDX3 promoter and represses its transcription. Finally, shRNA-based assays suggested that Prx3 downregulation is required for the HIF-1α-dependent proliferation of CCRCC cells. Taken together, our results shed new light onto the mechanism of HIF-1α-dependent proliferation in CCRCC cells.
    Keywords antioxidants ; hydrogen peroxide ; hypoxia ; hypoxia-inducible factor 1 ; mitochondria ; neoplasm cells ; normoxia ; peroxiredoxin
    Language English
    Dates of publication 2014-0917
    Size p. 3390-3394.
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2014.07.030
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: VHL deficiency augments anthracycline sensitivity of clear cell renal cell carcinomas by down-regulating ALDH2

    Yao-Hui Gao / Zhao-Xia Wu / Li-Qi Xie / Cai-Xia Li / Yu-Qin Mao / Yan-Tao Duan / Bing Han / San-Feng Han / Yun Yu / Hao-Jie Lu / Peng-Yuan Yang / Tian-Rui Xu / Jing-Lin Xia / Guo-Qiang Chen / Li-Shun Wang

    Nature Communications, Vol 8, Iss 1, Pp 1-

    2017  Volume 14

    Abstract: The VHL tumour suppressor gene is lost in approximately 70% of clear cell renal cell carcinoma (ccRCC). In this study, the authors demonstrate that VHL loss in these tumours augments anthracyclines chemotherapy by down-regulation of ALDH2. ...

    Abstract The VHL tumour suppressor gene is lost in approximately 70% of clear cell renal cell carcinoma (ccRCC). In this study, the authors demonstrate that VHL loss in these tumours augments anthracyclines chemotherapy by down-regulation of ALDH2.
    Keywords Science ; Q
    Language English
    Publishing date 2017-06-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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