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    TLR Interacts with CREBH to Modulate HDL [Molecular Bases of Disease] (2016)
    The American Society for Biochemistry and Molecular Biology (ASBMB)
    Details
    Publikationsdatum: 2016-10-29
    Beschreibung: Bacterial endotoxin can induce inflammatory and metabolic changes in the host. In this study, we revealed a molecular mechanism by which a stress-inducible, liver-enriched transcription factor, cAMP-responsive element-binding protein hepatic-specific (CREBH), modulates lipid profiles to protect the liver from injuries upon the bacterial endotoxin lipopolysaccharide (LPS). LPS challenge can activate CREBH in mouse liver tissues in a toll-like receptor (TLR)/MyD88-dependent manner. Upon LPS challenge, CREBH interacts with TNF receptor-associated factor 6 (TRAF6), an E3 ubiquitin ligase that functions as a key mediator of TLR signaling, and this interaction relies on MyD88. Further analysis demonstrated that TRAF6 mediates K63-linked ubiquitination of CREBH to facilitate CREBH cleavage and activation. CREBH directly activates expression of the gene encoding Apolipoprotein A4 (ApoA4) under LPS challenge, leading to modulation of high-density lipoprotein (HDL) in animals. CREBH deficiency led to reduced production of circulating HDL and increased liver damage upon high-dose LPS challenge. Therefore, TLR/MyD88-dependent, TRAF6-facilitated CREBH activation represents a mammalian hepatic defense response to bacterial endotoxin by modulating HDL.
    Print ISSN: 0021-9258
    Digitale ISSN: 1083-351X
    Thema: Biologie , Chemie und Pharmazie
    Publiziert von The American Society for Biochemistry and Molecular Biology (ASBMB)
    Standort Signatur Einschränkungen Verfügbarkeit
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    Study on detection method of distorted voltage sag in distribution network under the background of incorporating new energy (2017)
    Institute of Physics (IOP)
    Details
    Publikationsdatum: 2017-11-10
    Beschreibung: An advanced voltage sag detection method and compensation technique can improve the power quality of the distribution network to a entirely new level. A high performance voltage sag detection method demands fast response and good accuracy, even detecting distorted grid voltage sag caused by new energy accessing to distribution network. The voltage sag detection method, based on sliding window iterative discrete fourier transfer (DFT) algorithm, has excellent filtering ability but long detection time. On the other hand, the voltage sag detection method, based on nonrecursive DFT algorithm, has short detection time but poor filtering ability. Aiming to meet the requirements of fast response and good accuracy, this paper proposed a voltage sag detection method based on improved nonrecursive DFT algorithm. By means of disturbance filter, which is combined with several notch filters and a low-pass filter, the filter characteristic of nonrecursive DFT algorithm has been improved, and ...
    Print ISSN: 1755-1307
    Digitale ISSN: 1755-1315
    Thema: Geographie , Geologie und Paläontologie , Physik
    Publiziert von Institute of Physics (IOP)
    Standort Signatur Einschränkungen Verfügbarkeit
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    Host miR155 Promotes Tumor Growth (2015)
    The American Association for Cancer Research (AACR)
    Details
    Publikationsdatum: 2015-02-03
    Beschreibung: miR155 is a regulator of immune cell development and function that is generally thought to be immunostimulatory. However, we report here that genetic ablation of miR155 renders mice resistant to chemical carcinogenesis and the growth of several transplanted tumors, suggesting that miR155 functions in immunosuppression and tumor promotion. Host miR155 deficiency promoted overall antitumor immunity despite the finding of defective responses of miR155-deficient dendritic cells and antitumor T cells. Further analysis of immune cell compartments revealed that miR155 regulated the accumulation of functional myeloid-derived suppressive cells (MDSC) in the tumor microenvironment. Specifically, miR155 mediated MDSC suppressor activity through at least two mechanisms, including SOCS1 repression and a reduced ability to license the generation of CD4+Foxp3+ regulatory T cells. Importantly, we demonstrated that miR155 expression was required for MDSC to facilitate tumor growth. Thus, our results revealed a contextual function for miR155 in antitumor immunity, with a role in MDSC support that appears to dominate in tumor-bearing hosts. Overall, the balance of these cellular effects appears to be a root determinant of whether miR155 promotes or inhibits tumor growth. Cancer Res; 75(3); 519–31. ©2014 AACR.
    Print ISSN: 0008-5472
    Digitale ISSN: 1538-7445
    Thema: Medizin
    Publiziert von The American Association for Cancer Research (AACR)
    Standort Signatur Einschränkungen Verfügbarkeit
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