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  • 1
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    NF-kappaB-induced loss of MyoD messenger RNA: possible role in muscle decay and cachexia (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-29
    Description: MyoD regulates skeletal muscle differentiation (SMD) and is essential for repair of damaged tissue. The transcription factor nuclear factor kappa B (NF-kappaB) is activated by the cytokine tumor necrosis factor (TNF), a mediator of skeletal muscle wasting in cachexia. Here, the role of NF-kappaB in cytokine-induced muscle degeneration was explored. In differentiating C2C12 myocytes, TNF-induced activation of NF-kappaB inhibited SMD by suppressing MyoD mRNA at the posttranscriptional level. In contrast, in differentiated myotubes, TNF plus interferon-gamma (IFN-gamma) signaling was required for NF-kappaB-dependent down-regulation of MyoD and dysfunction of skeletal myofibers. MyoD mRNA was also down-regulated by TNF and IFN-gamma expression in mouse muscle in vivo. These data elucidate a possible mechanism that may underlie the skeletal muscle decay in cachexia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guttridge, D C -- Mayo, M W -- Madrid, L V -- Wang, C Y -- Baldwin, A S Jr -- AI35098/AI/NIAID NIH HHS/ -- CA72771/CA/NCI NIH HHS/ -- K01 CA78595/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 29;289(5488):2363-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lineberger Comprehensive Cancer Center, Curriculum in Genetics and Molecular Biology, Department of Biology, University of North Carolina, Chapel Hill, Mason Farm Road, Campus Box 7295, Chapel Hill, NC, 27599-7295, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11009425" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; Cachexia/*etiology/metabolism/pathology ; Cell Differentiation ; Cell Line ; Cricetinae ; DNA-Binding Proteins/genetics/metabolism ; Down-Regulation ; *I-kappa B Proteins ; Interferon-gamma/pharmacology ; Interleukins/pharmacology ; Mice ; Mice, Inbred Strains ; Mice, Nude ; Muscle, Skeletal/*cytology/*metabolism/pathology ; MyoD Protein/*genetics/metabolism ; NF-kappa B/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Transcription Factor RelA ; Transcription, Genetic ; Transfection ; Tumor Necrosis Factor-alpha/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    NF-kappaB antiapoptosis: induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to suppress caspase-8 activation (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: Tumor necrosis factor alpha (TNF-alpha) binding to the TNF receptor (TNFR) potentially initiates apoptosis and activates the transcription factor nuclear factor kappa B (NF-kappaB), which suppresses apoptosis by an unknown mechanism. The activation of NF-kappaB was found to block the activation of caspase-8. TRAF1 (TNFR-associated factor 1), TRAF2, and the inhibitor-of-apoptosis (IAP) proteins c-IAP1 and c-IAP2 were identified as gene targets of NF-kappaB transcriptional activity. In cells in which NF-kappaB was inactive, all of these proteins were required to fully suppress TNF-induced apoptosis, whereas c-IAP1 and c-IAP2 were sufficient to suppress etoposide-induced apoptosis. Thus, NF-kappaB activates a group of gene products that function cooperatively at the earliest checkpoint to suppress TNF-alpha-mediated apoptosis and that function more distally to suppress genotoxic agent-mediated apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, C Y -- Mayo, M W -- Korneluk, R G -- Goeddel, D V -- Baldwin, A S Jr -- AI35098/AI/NIAID NIH HHS/ -- CA 75080/CA/NCI NIH HHS/ -- CA73756/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1680-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Endodontics, School of Dentistry, Lineberger Comprehensive Cancer Center, and Curriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, NC 27599-7295, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733516" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 3 ; Caspase 8 ; Caspase 9 ; *Caspases ; Cysteine Endopeptidases/*metabolism ; Cytochrome c Group/metabolism ; Enzyme Activation ; Etoposide/pharmacology ; Gene Expression Regulation ; Humans ; Inhibitor of Apoptosis Proteins ; Mitochondria/metabolism ; NF-kappa B/*metabolism ; Proteins/*genetics/physiology ; Signal Transduction ; TNF Receptor-Associated Factor 1 ; TNF Receptor-Associated Factor 2 ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/pharmacology ; Ubiquitin-Protein Ligases
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Requirement of NF-kappaB activation to suppress p53-independent apoptosis induced by oncogenic Ras (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997
    Description: The ras proto-oncogene is frequently mutated in human tumors and functions to chronically stimulate signal transduction cascades resulting in the synthesis or activation of specific transcription factors, including Ets, c-Myc, c-Jun, and nuclear factor kappa B (NF-kappaB). These Ras-responsive transcription factors are required for transformation, but the mechanisms by which these proteins facilitate oncogenesis have not been fully established. Oncogenic Ras was shown to initiate a p53-independent apoptotic response that was suppressed through the activation of NF-kappaB. These results provide an explanation for the requirement of NF-kappaB for Ras-mediated oncogenesis and provide evidence that Ras-transformed cells are susceptible to apoptosis even if they do not express the p53 tumor-suppressor gene product.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mayo, M W -- Wang, C Y -- Cogswell, P C -- Rogers-Graham, K S -- Lowe, S W -- Der, C J -- Baldwin, A S Jr -- CA13106/CA/NCI NIH HHS/ -- CA52072/CA/NCI NIH HHS/ -- CA72771/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Dec 5;278(5344):1812-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9388187" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adenovirus E1A Proteins/genetics/metabolism ; Animals ; *Apoptosis ; Cell Line, Transformed ; Cell Survival ; *Cell Transformation, Neoplastic ; *Gene Expression Regulation, Neoplastic ; *Genes, p53 ; *Genes, ras ; Mice ; NF-kappa B/*metabolism ; Rats ; Transfection ; Tumor Suppressor Protein p53/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Role of transcriptional activation of I kappa B alpha in mediation of immunosuppression by glucocorticoids (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-10-13
    Description: Glucocorticoids are potent immunosuppressive drugs, but their mechanism is poorly understood. Nuclear factor kappa B (NF-kappa B), a regulator of immune system and inflammation genes, may be a target for glucocorticoid-mediated immunosuppression. The activation of NF-kappa B involves the targeted degradation of its cytoplasmic inhibitor, I kappa B alpha, and the translocation of NF-kappa B to the nucleus. Here it is shown that the synthetic glucocorticoid dexamethasone induces the transcription of the I kappa B alpha gene, which results in an increased rate of I kappa B alpha protein synthesis. Stimulation by tumor necrosis factor causes the release of NF-kappa B from I kappa B alpha. However, in the presence of dexamethasone this newly released NF-kappa B quickly reassociates with newly synthesized I kappa B alpha, thus markedly reducing the amount of NF-kappa B that translocates to the nucleus. This decrease in nuclear NF-kappa B is predicted to markedly decrease cytokine secretion and thus effectively block the activation of the immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheinman, R I -- Cogswell, P C -- Lofquist, A K -- Baldwin, A S Jr -- AI35098/AI/NIAID NIH HHS/ -- CA52515/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Oct 13;270(5234):283-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7569975" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Nucleus/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Dexamethasone/*pharmacology ; HeLa Cells ; Humans ; *I-kappa B Proteins ; *Immunosuppression ; Immunosuppressive Agents/*pharmacology ; Lipopolysaccharides/pharmacology ; NF-kappa B/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Signal Transduction/drug effects ; Transcription Factor RelA ; Transcription, Genetic/drug effects ; Tumor Necrosis Factor-alpha/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    TNF- and cancer therapy-induced apoptosis: potentiation by inhibition of NF-kappaB (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-01
    Description: Many cells are resistant to stimuli that can induce apoptosis, but the mechanisms involved are not fully understood. The activation of the transcription factor nuclear factor-kappa B (NF-kappaB) by tumor necrosis factor (TNF), ionizing radiation, or daunorubicin (a cancer chemotherapeutic compound), was found to protect from cell killing. Inhibition of NF-kappaB nuclear translocation enhanced apoptotic killing by these reagents but not by apoptotic stimuli that do not activate NF-kappaB. These results provide a mechanism of cellular resistance to killing by some apoptotic reagents, offer insight into a new role for NF-kappaB, and have potential for improvement of the efficacy of cancer therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, C Y -- Mayo, M W -- Baldwin, A S Jr -- 1F32-CA69790-01/CA/NCI NIH HHS/ -- AI35098/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 1;274(5288):784-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Curriculum in Genetics and Molecular Biology and Department of Endodontics, School of Dentistry, University of North Carolina, Chapel Hill, NC 27599-7295, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8864119" target="_blank"〉PubMed〈/a〉
    Keywords: Antibiotics, Antineoplastic/*pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; *Apoptosis/drug effects/radiation effects ; Cell Nucleus/metabolism ; Cycloheximide/pharmacology ; DNA-Binding Proteins/metabolism ; Daunorubicin/*pharmacology ; Humans ; *I-kappa B Proteins ; Interleukin-1/pharmacology ; Leupeptins/pharmacology ; NF-kappa B/*antagonists & inhibitors/metabolism/*physiology ; Neoplasms/drug therapy/radiotherapy ; Protein Synthesis Inhibitors/pharmacology ; *Radiation, Ionizing ; Staurosporine/pharmacology ; Transcription Factor RelA ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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