Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2006-4-19
pubmed:abstractText
The c-Myc oncogenic transcription factor plays a central role in many human cancers through the regulation of gene expression. Although the molecular mechanisms by which c-Myc and its obligate partner, Max, regulate gene expression are becoming better defined, genes or transcriptomes that c-Myc regulate are just emerging from a variety of different experimental approaches. Studies of individual c-Myc target genes and their functional implications are now complemented by large surveys of c-Myc target genes through the use of subtraction cloning, DNA microarray analysis, serial analysis of gene expression (SAGE), chromatin immunoprecipitation, and genome marking methods. To fully appreciate the differences between physiological c-Myc function in normal cells and deregulated c-Myc function in tumors, the challenge now is to determine how the authenticated transcriptomes effect the various phenotypes induced by c-Myc and to define how c-Myc transcriptomes are altered by the Mad family of proteins.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0070-217X
pubmed:author
pubmed:issnType
Print
pubmed:volume
302
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
145-67
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Myc target transcriptomes.
pubmed:affiliation
Department of Medicine, The Johns Hopkins University School of Medicine, Ross 1032, 720 Rutland Avenue, Baltimore, MD 21205, USA. llee12@jhmi.edu
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural