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  • 1
    Electronic Resource
    Electronic Resource
    Ras-mediated cell proliferation and cell death: some clues from the interleukin-2 receptor system (1996)
    Springer
    Apoptosis 1 (1996), S. 175-182 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; cell proliferation ; IL-2 ; Ras
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Oncoproteins of the Ras family have been extensively studied because of their implication in human cancer. Their roles have been primarily assigned to the commandment of cell proliferation and suppression of apoptosis, which has also been demonstrated by the involvement of Ras activation in the signal transduction pathways triggered by most cytokine receptors. Nevertheless, the functions of Ras proteins have been extended in the last years by the findings showing that they can also act as promoters or enhancers of apoptosis in various systems and conditions. These considerations have raised the issue as to how the signals delivered by Ras are regulated and translated in terms of cellular responses, suggesting that signal complementation may direct the final fate of cells. As an example, the interleukin-2 receptor system may represent a useful model in which the meaning of Ras signals may be evaluated in terms of interactions with other simultaneous signalling events, since knowledge of the biochemical events triggered by the interaction of interleukin-2 with its cell surface receptor in lymphocytes has allowed the proposal of a complete signalling model arranged in three independent channels, one of which is mediated by Ras.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01321100
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  • 2
    Electronic Resource
    Electronic Resource
    Transgenic mice in apoptosis research (1998)
    Springer
    Apoptosis 3 (1998), S. 215-228 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; Bcl-2, CD95 ; superoxide ; dismutase ; glucocorticoid receptor ; Nur77 ; rhodopsin ; TNF ; transgenic mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Transgenic mice have proved to be a valuable tool in various aspects of apoptosis research. They are particularly useful for studying apoptosis-related gene products in primary cells which may lead to different effects from similar experiments using immortalized cell lines. They allow the impact of these gene products on multi-faceted physiological processes to be identified. Transgenic mice have been generated expressing molecules ranging from Bcl-2 and Bcl-2 family members to CD95, superoxide dismutase and rhodopsin. This review details some of the insights revealed from such studies in diverse areas ranging from lymphoid development to neurodegeneration and effects on intracellular signalling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009607121302
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  • 3
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    E2f1-3 switch from activators in progenitor cells to repressors in differentiating cells (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-12-18
    Description: In the established model of mammalian cell cycle control, the retinoblastoma protein (Rb) functions to restrict cells from entering S phase by binding and sequestering E2f activators (E2f1, E2f2 and E2f3), which are invariably portrayed as the ultimate effectors of a transcriptional program that commit cells to enter and progress through S phase. Using a panel of tissue-specific cre-transgenic mice and conditional E2f alleles we examined the effects of E2f1, E2f2 and E2f3 triple deficiency in murine embryonic stem cells, embryos and small intestines. We show that in normal dividing progenitor cells E2f1-3 function as transcriptional activators, but contrary to the current view, are dispensable for cell division and instead are necessary for cell survival. In differentiating cells E2f1-3 function in a complex with Rb as repressors to silence E2f targets and facilitate exit from the cell cycle. The inactivation of Rb in differentiating cells resulted in a switch of E2f1-3 from repressors to activators, leading to the superactivation of E2f responsive targets and ectopic cell divisions. Loss of E2f1-3 completely suppressed these phenotypes caused by Rb deficiency. This work contextualizes the activator versus repressor functions of E2f1-3 in vivo, revealing distinct roles in dividing versus differentiating cells and in normal versus cancer-like cell cycles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806193/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806193/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chong, Jean-Leon -- Wenzel, Pamela L -- Saenz-Robles, M Teresa -- Nair, Vivek -- Ferrey, Antoney -- Hagan, John P -- Gomez, Yorman M -- Sharma, Nidhi -- Chen, Hui-Zi -- Ouseph, Madhu -- Wang, Shu-Huei -- Trikha, Prashant -- Culp, Brian -- Mezache, Louise -- Winton, Douglas J -- Sansom, Owen J -- Chen, Danian -- Bremner, Rod -- Cantalupo, Paul G -- Robinson, Michael L -- Pipas, James M -- Leone, Gustavo -- 5 T32 CA106196-04/CA/NCI NIH HHS/ -- CA098956/CA/NCI NIH HHS/ -- P01CA097189/CA/NCI NIH HHS/ -- R01 CA098956/CA/NCI NIH HHS/ -- R01 CA098956-06A2/CA/NCI NIH HHS/ -- R01CA82259/CA/NCI NIH HHS/ -- R01CA85619/CA/NCI NIH HHS/ -- R01HD04470/HD/NICHD NIH HHS/ -- England -- Nature. 2009 Dec 17;462(7275):930-4. doi: 10.1038/nature08677.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Virology, Immunology and Medical Genetics, College of Medicine, The Ohio State University, Columbus, Ohio 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016602" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Apoptosis ; Cell Cycle/genetics/physiology ; *Cell Differentiation ; Cell Proliferation ; E2F Transcription Factors/deficiency/genetics/*metabolism ; E2F1 Transcription Factor/deficiency/genetics/metabolism ; E2F2 Transcription Factor/deficiency/genetics/metabolism ; E2F3 Transcription Factor/deficiency/genetics/metabolism ; Embryo, Mammalian/cytology/metabolism ; Embryonic Stem Cells/*cytology/*metabolism ; Female ; *Gene Expression Regulation ; Intestine, Small/cytology/metabolism ; Mice ; Mice, Transgenic ; Repressor Proteins/deficiency/genetics/*metabolism ; Retinoblastoma Protein/deficiency/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Protection of C. elegans from anoxia by HYL-2 ceramide synthase (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-18
    Description: Oxygen deprivation is rapidly deleterious for most organisms. However, Caenorhabditis elegans has developed the ability to survive anoxia for at least 48 hours. Mutations in the DAF-2/DAF-16 insulin-like signaling pathway promote such survival. We describe a pathway involving the HYL-2 ceramide synthase that acts independently of DAF-2. Loss of the ceramide synthase gene hyl-2 results in increased sensitivity of C. elegans to anoxia. C. elegans has two ceramide synthases, hyl-1 and hyl-2, that participate in ceramide biogenesis and affect its ability to survive anoxic conditions. In contrast to hyl-2(lf) mutants, hyl-1(lf) mutants are more resistant to anoxia than normal animals. HYL-1 and HYL-2 have complementary specificities for fatty acyl chains. These data indicate that specific ceramides produced by HYL-2 confer resistance to anoxia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Menuz, Vincent -- Howell, Kate S -- Gentina, Sebastien -- Epstein, Sharon -- Riezman, Isabelle -- Fornallaz-Mulhauser, Monique -- Hengartner, Michael O -- Gomez, Marie -- Riezman, Howard -- Martinou, Jean-Claude -- New York, N.Y. -- Science. 2009 Apr 17;324(5925):381-4. doi: 10.1126/science.1168532.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, University of Geneva, CH-1211 Geneva 4, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19372430" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Caenorhabditis elegans/cytology/genetics/*physiology ; Caenorhabditis elegans Proteins/*genetics/*metabolism ; *Cell Hypoxia ; Ceramides/biosynthesis/*physiology ; Gene Deletion ; Genes, Helminth ; Mutation ; Oxidoreductases/*genetics/*metabolism ; Oxygen/*physiology ; Receptor, Insulin/genetics/metabolism ; Saccharomyces cerevisiae/genetics/growth & development/physiology ; Sphingomyelins/biosynthesis/physiology ; Substrate Specificity ; Transformation, Genetic ; Transgenes
    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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