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  1. Article: H2S: A Novel Gasotransmitter that Signals by Sulfhydration.

    Paul, Bindu D / Snyder, Solomon H

    Trends in biochemical sciences

    2015  Volume 40, Issue 11, Page(s) 687–700

    Abstract: Hydrogen sulfide (H2S) is a member of the growing family of gasotransmitters. Once regarded ... in the fashion of other chemical messengers. Thus, novel cellular mechanisms have evolved to mediate its effects ... This review focuses on sulfhydration (or persulfidation), which appears to be the principal ...

    Abstract Hydrogen sulfide (H2S) is a member of the growing family of gasotransmitters. Once regarded as a noxious molecule predominantly present in the atmosphere, H2S is now known to be synthesized endogenously in mammals. H2S participates in a myriad of physiological processes ranging from regulation of blood pressure to neuroprotection. Its chemical nature precludes H2S from being stored in vesicles and acting on receptor proteins in the fashion of other chemical messengers. Thus, novel cellular mechanisms have evolved to mediate its effects. This review focuses on sulfhydration (or persulfidation), which appears to be the principal post-translational modification elicited by H2S.
    MeSH term(s) Gasotransmitters/metabolism ; Hydrogen Sulfide/metabolism ; Signal Transduction
    Chemical Substances Gasotransmitters ; Hydrogen Sulfide (YY9FVM7NSN)
    Language English
    Publishing date 2015-10-01
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 194216-5
    ISSN 1362-4326 ; 0968-0004 ; 0376-5067
    ISSN (online) 1362-4326
    ISSN 0968-0004 ; 0376-5067
    DOI 10.1016/j.tibs.2015.08.007
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    In stock of ZB MED Cologne/Königswinter

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  2. Article: H2S: A Novel Gasotransmitter that Signals by Sulfhydration

    Paul, Bindu D / Solomon H. Snyder

    Trends in biochemical sciences. 2015 Nov., v. 40

    2015  

    Abstract: Hydrogen sulfide (H2S) is a member of the growing family of gasotransmitters. Once regarded ... in the fashion of other chemical messengers. Thus, novel cellular mechanisms have evolved to mediate its effects ... This review focuses on sulfhydration (or persulfidation), which appears to be the principal ...

    Abstract Hydrogen sulfide (H2S) is a member of the growing family of gasotransmitters. Once regarded as a noxious molecule predominantly present in the atmosphere, H2S is now known to be synthesized endogenously in mammals. H2S participates in a myriad of physiological processes ranging from regulation of blood pressure to neuroprotection. Its chemical nature precludes H2S from being stored in vesicles and acting on receptor proteins in the fashion of other chemical messengers. Thus, novel cellular mechanisms have evolved to mediate its effects. This review focuses on sulfhydration (or persulfidation), which appears to be the principal post-translational modification elicited by H2S.
    Keywords blood pressure ; hydrogen sulfide ; mammals ; neuroprotective effect ; post-translational modification ; proteins
    Language English
    Dates of publication 2015-11
    Size p. 687-700.
    Publishing place Elsevier Ltd
    Document type Article
    ZDB-ID 194220-7
    ISSN 0968-0004 ; 0376-5067
    ISSN 0968-0004 ; 0376-5067
    DOI 10.1016/j.tibs.2015.08.007
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    In stock of ZB MED Bonn / Germany

    Z 78/716: Show issues

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  3. Article: Efflux inhibition by H2S confers sensitivity to doxorubicin-induced cell death in liver cancer cells

    Stokes, Eric / Amadeo Parissenti / Baoqing Guo / Guangdong Yang / Lingyun Wu / Ming Fu / Rui Wang / Tian Shuang / Yanjie Zhang / Yanxi Pei

    Life sciences. 2018 Nov. 15, v. 213

    2018  

    Abstract: ... Our study provides a novel solution for reversing drug resistance in cancer cells by targeting H2S ... LXRα was S-sulfhydrated by H2S, and blockage of RXRβ S-sulfhydration abolished the inhibitory role ... Hydrogen sulfide (H2S), an important gasotransmitter, is involved in a variety of cellular ...

    Abstract Hydrogen sulfide (H2S), an important gasotransmitter, is involved in a variety of cellular functions and pathophysiologic processes. Drug resistance due to alterations in drug trafficking and metabolism severely limits the effectiveness of cancer therapy. This study examined the role of H2S in drug resistance in liver cancer cells.Human primary hepatocellular carcinoma cell line (HepG2) and doxorubicin (Dox)-resistant cells were used in this study. Cell survival was analyzed by MTT, Annexin V-FITC/propidium iodide staining and clonogenic assay. Western blotting was used for analysis of protein expression, and immunoprecipitation was used to determine interactions of LXR/RXR.The expression of H2S-generating enzyme cystathionine gamma-lyase (CSE) was inhibited by doxorubicin treatment in HepG2 cells, and H2S sensitized Dox-inhibited cell survival and colony formation. In addition, H2S promoted cellular retention of Dox by suppressing the expressions of ABCA1 and ABCG8. H2S significantly blocked Dox-induced heterodimer formation between LXRα and RXRβ and attenuated the binding of LXRα/RXRβ to the promoters of ABCA1 and ABCG8 genes. RXRβ but not LXRα was S-sulfhydrated by H2S, and blockage of RXRβ S-sulfhydration abolished the inhibitory role of H2S on LXRα/RXRβ heterodimer formation. CSE expression was reduced in Dox-resistant cells in comparison with their parental cells, while H2S could reverse drug resistance in Dox-resistant cells.Our study provides a novel solution for reversing drug resistance in cancer cells by targeting H2S signalling.
    Keywords cell death ; cell viability ; cystathionine gamma-lyase ; doxorubicin ; drug resistance ; genes ; hepatoma ; human cell lines ; hydrogen sulfide ; neoplasm cells ; pathophysiology ; precipitin tests ; protein synthesis ; staining ; therapeutics ; Western blotting
    Language English
    Dates of publication 2018-1115
    Size p. 116-125.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2018.10.031
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    In stock of ZB MED Bonn / Germany

    Z 73/732: Show issues

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