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Citation
Schreiber-Agus, N., Stein, D., Chen, K., Goltz, J.S., Stevens, L., DePinho, R.A. (1997). Drosophila Myc is oncogenic in mammalian cells and plays a role in the diminutive phenotype.  Proc. Natl. Acad. Sci. U.S.A. 94(4): 1235--1240.
FlyBase ID
FBrf0092678
Publication Type
Research paper
Abstract

Biochemical and biological activities of Myc oncoproteins are highly dependent upon their association with another basic region helix-loop-helix/leucine zipper (bHLH/LZ) protein, Max. Our previous observation that the DNA-binding/dimerization region of Max is absolutely conserved throughout vertebrate evolution provided the basis for a yeast two-hybrid interaction screen that led to the isolation of the Drosophila Myc (dMyc1) protein. Structural conservation in regions of known functional significance is consistent with the ability of dMyc1 to interact with vertebrate Max, to transactivate gene expression in yeast cells, and to cooperate with activated H-RAS to effect the malignant transformation of primary mammalian cells. The ability of P-element-mediated ectopic expression of dmyc1 to reverse a subset of the phenotypic alterations associated with the diminutive mutation suggests that diminutive may correspond to dmyc1. This finding, along with the localization of dmyc1 expression to zones of high proliferative activity in the embryo, implicates dMyc1 as an integral regulator of Drosophila growth and development.

PubMed ID
PubMed Central ID
PMC19774 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Proc. Natl. Acad. Sci. U.S.A.
    Title
    Proceedings of the National Academy of Sciences of the United States of America
    Publication Year
    1915-
    ISBN/ISSN
    0027-8424
    Data From Reference
    Alleles (5)
    Genes (4)
    Insertions (1)
    Experimental Tools (1)
    Transgenic Constructs (2)