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  • CELL-LINES  (1)
  • Cortisol  (1)
  • 1
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; CELL ; Germany ; human ; PATHWAY ; SYSTEM ; GENE ; GENES ; PROTEIN ; LINES ; ACTIVATION ; MARKER ; T cell ; T cell activation ; T cells ; T-CELL ; T-CELLS ; BINDING ; CELL-LINES ; SIGNAL ; virus ; IDENTIFICATION ; NUMBER ; CELL-LINE ; LINE ; HUMAN-IMMUNODEFICIENCY-VIRUS ; representational difference analysis ; GENE-PRODUCT ; SUBSET ; PRODUCTS ; HIV ; IMMUNODEFICIENCY VIRUS ; NUCLEOCYTOPLASMIC TRANSPORT ; TAP ; 60S RIBOSOMAL-SUBUNITS ; CD83 ; CRM1 ; IMMUNODEFICIENCY-VIRUS REV ; LEPTOMYCIN B ; RAN ; RECEPTOR CRM1 ; RNA export
    Abstract: In metazoans, the nuclear export of bulk mRNAs is mediated by the export receptor TAP, together with its binding partner p15. A number of viral mRNAs, including the unspliced and partially spliced mRNA species of the human immunodeficiency virus (HIV), however, use an alternative export route via the importin beta-related export receptor CRM1. This raises the question of whether a subset of cellular mRNAs might be exported by CRM1 as well. To identify such mRNAs, we performed a systematic screen in different cell lines, using representational difference analyses of cDNA (cDNA-RDA). In HeLa and Cl-4 cells no cellular transcripts could be identified as exported via CRM1. In contrast, we found a number of CRM1-dependent mRNAs in Jurkat T cells, most of which are induced during a T cell response. One of the identified gene products, the dendritic cell marker CD83, was analyzed in detail. CD83 expression depends on a functional CRM1 pathway in activated Jurkat T cells as well as in a heterologous expression system, independent of activation. Our results point to an important role of the CRM1-dependent export pathway for the expression of CD83 and other genes under conditions of T cell activation. (c) 2006 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16580684
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  • 2
    ISSN: 1432-1076
    Keywords: Growth hormone ; Cortisol ; Glucocorticoid therapy ; Cushing's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cortisol and growth hormone (GH) secretion (spontaneous variations at night and the release induced by insulin hypoglycaemia) were investigated in 69 children and adolescents. Statistical analysis of approximately 600 pairs of cortisol and GH values in this study demonstrated that physiological fluctuations of cortisol do not alter GH secretion. A review of the literature shows that GH secretion is consistently depressed in Cushing's disease of central origin and in Cushing's syndrome due to adrenal carcinoma. When acutely administered, doses higher than 100 mg of cortisol (or equivalent amounts of other steroids) per adult are necessary to block GH secretion and the hormones have to be given several hours previously. In long-term steroid treatment, suppression of GH is observed in only 1 out of 3 patients. The effect apparently does not persist beyond elimination of the last dose, i.e. generally not longer than 12 to 24 h. These data can be taken as a rationale for intermittent or alternating dosage schedules, and for the use of short acting derivatives if long-term, high-dose steroid treatment is necessary in children. It remains to be established whether growth deficiency in exogenous hypercortisolism is due to suppression of GH secretion, decreased production of somatomedins, direct antagonism of the action of somatomedins on growing cartilage, or a combination of these mechanisms.
    Type of Medium: Electronic Resource
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