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  • 1
    Electronic Resource
    Electronic Resource
    Cloning of a gene that encodes a new member of the human cytotoxic cell protease family (1990)
    s.l. : American Chemical Society
    Biochemistry 29 (1990), S. 4042-4049 
    Details
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/bi00469a003
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    DNA fragmentation is an early event in cytokine-induced islet beta-cell destruction (1994)
    Springer
    Diabetologia 37 (1994), S. 733-738 
    Details
    ISSN: 1432-0428
    Keywords: Islet beta cells ; cytokines ; interleukin 1 ; tumour necrosis factor ; interferon gamma ; DNA damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The cytokines, interleukin 1, tumour necrosis factor, and interferon gamma are cytotoxic to islet beta cells, however, their mechanisms of beta-cell killing are not fully characterized. Since DNA damage is a mechanism of cytokine-induced cell death in some cell types, we sought evidence for cytotoxic effects of cytokines at a nuclear level in islet beta cells by measuring DNA fragmentation in rat islets and islet beta-cell lines. The individual cytokines, interleukin 1 (10 U/ml), tumour recrosis factor (103 U/ml) and interferon gamma (103 U/ml) inhibited insulin release from rat islets, but did not cause DNA fragmentation or destroy islet cells; by contrast, combination of the three cytokines induced DNA fragmentation and islet-cell death. Cytokine-induced DNA fragmentation preceded cell lysis in islet beta-cell lines (RINm5F, rat insulinoma cells; and NIT-1, NOD/Lt mouse transgenic beta cells), whereas in non-islet cell lines (GH-3, rat pituitary; and PC-12, rat adrenal) the cytokines induced cell lysis and no or late DNA fragmentation. Nicotinamide prevented both DNA fragmentation and destruction of RINm5F islet cells by the cytokines. These findings identify DNA as an early target of cytokine action in islet beta cells, and implicate DNA fragmentation as a mechanism of cytokine-induced beta-cell destruction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404328
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Analysis of cytokine mRNA expression in syngeneic islet grafts of NOD mice: interleukin 2 and interferon gamma mRNA expression correlate with graft rejection and interleukin 10 with graft survival (1994)
    Springer
    Diabetologia 37 (1994), S. 833-837 
    Details
    ISSN: 1432-0428
    Keywords: Key words Nonobese diabetic mouse, islet transplantation, cytokines.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The injection of complete Freund's adjuvant into diabetic nonobese diabetic (NOD) mice at the time of syngeneic islet transplantation prevents monocytic/lymphocytic cell infiltration into the islet graft, Beta-cell destruction, and autoimmune diabetes recurrence. We have used semiquantitative reverse transcriptase-polymerase chain reaction analysis to examine and compare cytokine mRNA expression profiles in islet grafts from complete Freund's adjuvant-injected and control NOD mice. Interleukin 10 mRNA expression was significantly increased whereas interleukin 2 and interferon gamma mRNA levels were significantly decreased in islet grafts from complete Freund's adjuvant-injected mice compared to control mice. Levels of mRNA for interleukin 1 beta, interleukin 4, and tumour necrosis factor alpha were not significantly different in islet grafts from complete Freund's adjuvant-injected and control mice. These findings suggest that a Th1 subset of lymphocytes and their cytokine products, interleukin 2 and interferon gamma, may be involved in the rejection of syngeneic islet grafts and diabetes recurrence in NOD mice, and that the protective effect of complete Freund's adjuvant may result from the induction of interleukin 10 production and consequent down-regulation of Th1 cells and cytokines in the islet graft. [Diabetologia (1994) 37: 833–837]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404341
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Analysis of cytokine mRNA expression in syngeneic islet grafts of NOD mice: interleukin 2 and interferon gamma mRNA expression correlate with graft rejection and interleukin 10 with graft survival (1994)
    Springer
    Diabetologia 37 (1994), S. 833-837 
    Details
    ISSN: 1432-0428
    Keywords: Nonobese diabetic mouse ; islet transplantation ; cytokines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The injection of complete Freund's adjuvant into diabetic nonobese diabetic (NOD) mice at the time of syngeneic islet transplantation prevents monocytic/lymphocytic cell infiltration into the islet graft, Beta-cell destruction, and autoimmune diabetes recurrence. We have used semiquantitative reverse transcriptase-polymerase chain reaction analysis to examine and compare cytokine mRNA expression profiles in islet grafts from complete Freund's adjuvant-injected and control NOD mice. Interleukin 10 mRNA expression was significantly increased whereas interleukin 2 and interferon gamma mRNA levels were significantly decreased in islet grafts from complete Freund's adjuvant-injected mice compared to control mice. Levels of mRNA for interleukin 1 beta, interleukin 4, and tumour necrosis factor alpha were not significantly different in islet grafts from complete Freund's adjuvant-injected and control mice. These findings suggest that a Th1 subset of lymphocytes and their cytokine products, interleukin 2 and interferon gamma, may be involved in the rejection of syngeneic islet grafts and diabetes recurrence in NOD mice, and that the protective effect of complete Freund's adjuvant may result from the induction of interleukin 10 production and consequent down-regulation of Th1 cells and cytokines in the islet graft.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404341
    Location Call Number Limitation Availability
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    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    DNA fragmentation is an early event in cytokine-induced islet beta-cell destruction (1994)
    Springer
    Diabetologia 37 (1994), S. 733-738 
    Details
    ISSN: 1432-0428
    Keywords: Key words Islet beta cells, cytokines, interleukin 1, tumour necrosis factor, interferon gamma, DNA damage.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The cytokines, interleukin 1, tumour necrosis factor, and interferon gamma are cytotoxic to islet beta cells, however, their mechanisms of beta-cell killing are not fully characterized. Since DNA damage is a mechanism of cytokine-induced cell death in some cell types, we sought evidence for cytotoxic effects of cytokines at a nuclear level in islet beta cells by measuring DNA fragmentation in rat islets and islet beta-cell lines. The individual cytokines, interleukin 1 (10 U/ml), tumour recrosis factor (103 U/ml) and interferon gamma (103 U/ml) inhibited insulin release from rat islets, but did not cause DNA fragmentation or destroy islet cells; by contrast, combination of the three cytokines induced DNA fragmentation and islet-cell death. Cytokine-induced DNA fragmentation preceded cell lysis in islet beta-cell lines (RINm5F, rat insulinoma cells; and NIT-1, NOD/Lt mouse transgenic beta cells), whereas in non-islet cell lines (GH-3, rat pituitary; and PC-12, rat adrenal) the cytokines induced cell lysis and no or late DNA fragmentation. Nicotinamide prevented both DNA fragmentation and destruction of RINm5F islet cells by the cytokines. These findings identify DNA as an early target of cytokine action in islet beta cells, and implicate DNA fragmentation as a mechanism of cytokine-induced beta-cell destruction. [Diabetologia (1994) 37: 733–738]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050172
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    Paper (German National Licenses)
    Fulltext
  • 6
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    Unknown
    Overexpression of the Insulin-Like Growth Factor II Receptor Increases {beta}-Amyloid Production and Affects Cell Viability [Articles] (2015)
    The American Society for Microbiology (ASM)
    Details
    Publication Date: 2015-06-20
    Description: Amyloid β (Aβ) peptides originating from amyloid precursor protein (APP) in the endosomal-lysosomal compartments play a critical role in the development of Alzheimer's disease (AD), the most common type of senile dementia affecting the elderly. Since insulin-like growth factor II (IGF-II) receptors facilitate the delivery of nascent lysosomal enzymes from the trans -Golgi network to endosomes, we evaluated their role in APP metabolism and cell viability using mouse fibroblast MS cells deficient in the murine IGF-II receptor and corresponding MS9II cells overexpressing the human IGF-II receptors. Our results show that IGF-II receptor overexpression increases the protein levels of APP. This is accompanied by an increase of β-site APP-cleaving enzyme 1 levels and an increase of β- and -secretase enzyme activities, leading to enhanced Aβ production. At the cellular level, IGF-II receptor overexpression causes localization of APP in perinuclear tubular structures, an increase of lipid raft components, and increased lipid raft partitioning of APP. Finally, MS9II cells are more susceptible to staurosporine-induced cytotoxicity, which can be attenuated by β-secretase inhibitor. Together, these results highlight the potential contribution of IGF-II receptor to AD pathology not only by regulating expression/processing of APP but also by its role in cellular vulnerability.
    Print ISSN: 0270-7306
    Electronic ISSN: 1098-5549
    Topics: Biology , Medicine
    Published by The American Society for Microbiology (ASM)
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  • 7
    facet.materialart.
    Unknown
    Autophagy degrades NK-derived granzyme B [Immunology] (2013)
    National Academy of Sciences
    Details
    Publication Date: 2013-10-23
    Description: Recent studies demonstrated that autophagy is an important regulator of innate immune response. However, the mechanism by which autophagy regulates natural killer (NK) cell-mediated antitumor immune responses remains elusive. Here, we demonstrate that hypoxia impairs breast cancer cell susceptibility to NK-mediated lysis in vitro via the activation of autophagy. This...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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