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  • 1
    Keywords: RECEPTOR ; APOPTOSIS ; CELLS ; EXPRESSION ; SURVIVAL ; tumor ; TUMOR-CELLS ; CELL ; human ; KINASE ; PATHWAY ; PATHWAYS ; TYROSINE KINASE ; COHORT ; DEATH ; LONG-TERM ; GENE ; DIFFERENTIATION ; TUMORS ; NEUROBLASTOMA-CELLS ; PATIENT ; ACTIVATION ; MECHANISM ; DOMAIN ; BINDING ; CELL-DEATH ; REGION ; LONG-TERM SURVIVAL ; specificity ; DOMAINS ; neuroblastoma ; signaling ; NEURONS ; medulloblastoma ; interaction ; LEVEL ; cell death ; TECHNOLOGY ; USA ; pediatric ; MEDIATOR ; TYROSINE ; 2-HIT MECHANISM ; CEREBRAL CAVERNOUS MALFORMATIONS ; P75 NEUROTROPHIN RECEPTOR
    Abstract: The TrkA receptor tyrosine kinase is crucial for differentiation and survival of nerve-growth-factor-dependent neurons. Paradoxically, TrkA also induces cell death in pediatric tumor cells of neural origin, via an unknown mechanism. Here, we show that CCM2, a gene product associated with cerebral cavernous malformations, interacts with the juxtamembrane region of TrkA via its phosphotyrosine binding (PTB) domain and mediates TrkA-induced death in diverse cell types. Both the PTB and Karet domains of CCM2 are required for TrkA-dependent cell death, such that the PTB domain determines the specificity of the interaction, and the Karet domain links to death pathways. Downregulation of CCM2 in medulloblastoma or neuroblastoma cells attenuates TrkA-dependent death. Combined high expression levels of CCM2 and TrkA are correlated with long-term survival in a large cohort of human neuroblastoma patients. Thus, CCM2 is a key mediator of TrkA-dependent cell death in pediatric neuroblastic tumors
    Type of Publication: Journal article published
    PubMed ID: 19755102
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  • 2
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary Background  Previous studies have indicated that solar and artificial ultraviolet (UV) radiation have a positive influence on psychological variables such as mood and emotional state. Circulating opioid peptides have been suggested as being important in this effect. Objectives  To investigate in a controlled trial the influence of UVA radiation on opioid peptide levels. Methods  We determined plasma levels of β-endorphin immunoreactive material (IRM) and met-enkephalin in UV-exposed ( n  = 35) and non-exposed ( n  = 9) healthy volunteers. On the first day of the study, blood samples were taken from the volunteers (time A). UVA irradiation was subsequently administered with an air-conditioned tanning device. During the UV exposures the volunteers wore opaque goggles. Twenty minutes after UV exposure, blood samples were collected again (time B). Within the following 3 weeks the volunteers had a series of five UV exposures. On the last day of the study (24 h after the sixth UV exposure) blood samples were collected (time C). The cumulative UVA doses were 96 J cm −2 for skin type II and 126 J cm −2 for skin type III. The controls had no UV exposures. Plasma β-endorphin IRM and met-enkephalin levels were determined using radioimmunoassays. Results  At all times of blood collection (A, B, C), there were no significant differences in plasma levels of β-endorphin IRM and met-enkephalin between UV-exposed and non-exposed volunteers ( P  〉 0·05). Conclusions  UVA irradiation does not significantly elevate plasma levels of β-endorphin IRM and met-enkephalin. Therefore we suggest that psychological benefits claimed to occur after UV exposure are unlikely to be mediated by the types of circulating opioid peptides measured in this study.
    Type of Medium: Electronic Resource
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