NDLI: Drosophila Myc is oncogenic in mammalian cells and plays a role in the diminutive phenotype

Content Provider	PubMed Central
Author	Nicole, Schreiber-agus Stein, David Chen, Ken Goltz, Jason s. Stevens, Leslie Depinho, Ronald a.
Copyright Year	1997
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.
Starting Page	1235
File Format	PDF
ISSN	10916490
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	4
Volume Number	94
Language	English
Publisher	The National Academy of Sciences of the USA
Publisher Date	1997-02-18
Access Restriction	Open
Rights Holder	The National Academy of Sciences of the USA
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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