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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Reviews on Cancer 1114 (1992), S. 129-146 
    ISSN: 0304-419X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 52 (1996), S. 1123-1129 
    ISSN: 1420-9071
    Keywords: c-myc ; max ; oncogene ; transcription ; cell cycle ; apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract c-myc was discovered as the cellular homologue of the transduced oncogene of several avian retroviruses. The gene encodes a transcription factor, which forms a heteromeric protein complex with a partner protein termed Max. In mammalian cells, Myc is a central regulator of cell proliferation and links external signals to the cell cycle machinery. Myc also induces cells to undergo apoptosis, unless specific signals provided either by cytokines or by oncogenes block the apoptotic pathway. Recent progress sheds light both on the factors regulating the function and expression of Myc and on the downstream targets in the cell cycle. Together, these findings suggest the existence of a novel signal transduction pathway regulating both apoptosis and proliferation.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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