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  • 1
    Online Resource
    Online Resource
    Mouse models of medulloblastoma
    Editorial Office of Chinese Journal of Cancer ; 2011
    In:  Chinese Journal of Cancer
    Details
    In: Chinese Journal of Cancer, Editorial Office of Chinese Journal of Cancer
    Type of Medium: Online Resource
    ISSN: 1000-467X , 1944-446X
    URL: Article
    DOI: 10.5732/cjc.011.10040
    Language: Unknown
    Publisher: Editorial Office of Chinese Journal of Cancer
    Publication Date: 2011
    detail.hit.zdb_id: 2439836-6
    detail.hit.zdb_id: 2922913-3
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  • 2
    Online Resource
    Online Resource
    Genomics of medulloblastoma: from Giemsa-banding to next-generation sequencing in 20 years
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2010
    In:  Neurosurgical Focus Vol. 28, No. 1 ( 2010-01), p. E6-
    Details
    In: Neurosurgical Focus, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 28, No. 1 ( 2010-01), p. E6-
    Abstract: Advances in the field of genomics have recently enabled the unprecedented characterization of the cancer genome, providing novel insight into the molecular mechanisms underlying malignancies in humans. The application of high-resolution microarray platforms to the study of medulloblastoma has revealed new oncogenes and tumor suppressors and has implicated changes in DNA copy number, gene expression, and methylation state in its etiology. Additionally, the integration of medulloblastoma genomics with patient clinical data has confirmed molecular markers of prognostic significance and highlighted the potential utility of molecular disease stratification. The advent of next-generation sequencing technologies promises to greatly transform our understanding of medulloblastoma pathogenesis in the next few years, permitting comprehensive analyses of all aspects of the genome and increasing the likelihood that genomic medicine will become part of the routine diagnosis and treatment of medulloblastoma.
    Type of Medium: Online Resource
    ISSN: 1092-0684
    URL: Article
    DOI: 10.3171/2009.10.FOCUS09218
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2010
    detail.hit.zdb_id: 2026589-X
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  • 3
    Online Resource
    Online Resource
    Type 1 interferon suppresses expression and glucocorticoid induction of glucocorticoid-induced leucine zipper (GILZ)
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 13 ( 2022-11-23)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 13 ( 2022-11-23)
    Abstract: SLE is a systemic multi-organ autoimmune condition associated with reduced life expectancy and quality of life. Glucocorticoids (GC) are heavily relied on for SLE treatment but are associated with detrimental metabolic effects. Type 1 interferons (IFN) are central to SLE pathogenesis and may confer GC insensitivity. Glucocorticoid-induced leucine zipper (GILZ) mediates many effects of GC relevant to SLE pathogenesis, but the effect of IFN on GC regulation of GILZ is unknown. We performed in vitro experiments using human PBMC to examine the effect of IFN on GILZ expression. JAK inhibitors tofacitinib and tosylate salt were used in vivo and in vitro respectively to investigate JAK-STAT pathway dependence of our observations. ChiP was performed to examine glucocorticoid receptor (GR) binding at the GILZ locus. Several public data sets were mined for correlating clinical data. High IFN was associated with suppressed GILZ and reduced GILZ relevant to GC exposure in a large SLE population. IFN directly reduced GILZ expression and suppressed the induction of GILZ by GC in vitro in human leukocytes. IFN actions on GILZ expression were dependent on the JAK1/Tyk2 pathway, as evidenced by loss of the inhibitory effect of IFN on GILZ in the presence of JAK inhibitors. Activation of this pathway led to reduced GR binding in key regulatory regions of the GILZ locus. IFN directly suppresses GILZ expression and GILZ upregulation by GC, indicating a potential mechanism for IFN-induced GC resistance. This work has important implications for the ongoing development of targeted GC-sparing therapeutics in SLE.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    DOI: 10.3389/fimmu.2022.1034880
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2606827-8
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