Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-8-13
pubmed:abstractText
Vertebrate myb genes encode DNA-binding proteins that regulate transcription and have been implicated in regulation of cell proliferation, differentiation, and apoptosis. We have demonstrated that the single myb gene in Drosophila melanogaster, Dm myb, is required for the G(2)/M transition of the cell cycle and for suppression of endoreduplication. Recently, it has become apparent that the family of proteins containing Myb-related DNA-binding domains is much larger than originally believed and that the biochemical properties and functions of these proteins are diverse. We undertook studies to characterize the biochemical properties of the Drosophila Myb protein (DMyb). We now provide evidence that in addition to having homology with the vertebrate Myb proteins, the Drosophila Myb protein (DMyb) shares its biochemical properties. DMyb binds to a similar consensus sequence and activates transcription from a reporter construct regulated by vertebrate Myb proteins. We also show that DMyb proteins carrying mutations corresponding to previously isolated mutant alleles of Dm myb are less active as transcriptional activators than wild-type DMyb, indicating that a decrease in transcriptional activation ability is likely to cause the mutant phenotypes.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1079-9796
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
446-55
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:articleTitle
The role of transcriptional activation in the function of the Drosophila myb gene.
pubmed:affiliation
The G. W. Hooper Foundation, University of Illinois at Chicago, College of Medicine, Chicago, Illinois 60607-7170, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't