Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
19
pubmed:dateCreated
1999-6-25
pubmed:abstractText
Hematopoietic tumors in both humans and mice frequently up-regulate expression of the c-myb gene, but it is unclear whether this is a cause or a consequence of the leukemic state. Recent results placing super-activation of the c-Myb protein at the bottom of a kinase-activated signal transduction pathway indicate that it may be a downstream effector of transformation induced by other oncogenes. The relationship between c-Myb and the serine-threonine kinase pim-1, its immediate activator, is discussed, together with the possibility that c-Myb, like pim-1, may be able to synergize with c-Myc to induce tumors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3034-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Reassessing the role of C-MYB in tumorigenesis.
pubmed:affiliation
CRC Centre for Cell and Molecular Biology, Institute of Cancer Research, London, UK.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't