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Regulated Expression and Function of the c-Myc Antagonist, Mad1, During a Molecular Switch from Proliferation to Differentiation

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C-Myc in B-Cell Neoplasia

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 224))

Abstract

Myc, Max, Mad, Mxi1 and mSin3 comprise a transcription factor superfamily in which the central protein is Max. All family members (except mSin3) must dimerize with Max through their respective helix loop helix (HLH) and leucine zipper (LZ) domains to cooperatively bind DNA in a sequence specific manner (reviewed in [15]). In contrast to the transactivating property of Myc/Max heterodimers [1, 18, 21], Max heterodimerization with Mad or Mxi1, followed by the tethering of mSin3, to target genes results in suppression of transcription [3, 33]. Although Mad/Max heterodimers have been shown to antagonize Myc function in transformation and the mechanism(s) involved require multiple protein-protein and protein-DNA interactions [4, 20, 23, 33], how Mad functions in differentiation is unknown.

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Authors and Affiliations

  1. NCI-Navy Medical Oncology Branch, National Cancer Institute, NIH, University of Health Sciences, Bethesda, MD, 20889-5105, USA

    C. M. Cultraro, T. Bino & S. Segal

  2. Uniformed Services, University of Health Sciences, Bethesda, MD, 20889-5105, USA

    S. Segal

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  1. C. M. Cultraro
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  2. T. Bino
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  3. S. Segal
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Editors and Affiliations

  1. Laboratory of Genetics, Building 37, Room 2B04, National Cancer Institute, National Institutes of Health, 37 Convert Drive MSC4255, Bethesda, MD, 20892-4255, USA

    Michael Potter M.D. (Chief) (Chief)

  2. Basel Institute for Immunology, Grenzacherstr. 487, CH-4055, Basel, Switzerland

    Fritz Melchers (Director) (Director)

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© 1997 Springer-Verlag Berlin Heidelberg

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Cultraro, C.M., Bino, T., Segal, S. (1997). Regulated Expression and Function of the c-Myc Antagonist, Mad1, During a Molecular Switch from Proliferation to Differentiation. In: Potter, M., Melchers, F. (eds) C-Myc in B-Cell Neoplasia. Current Topics in Microbiology and Immunology, vol 224. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60801-8_15

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  • DOI: https://doi.org/10.1007/978-3-642-60801-8_15

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-64560-0

  • Online ISBN: 978-3-642-60801-8

  • eBook Packages: Springer Book Archive

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