Source:http://linkedlifedata.com/resource/pubmed/id/10378698
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
19
|
pubmed:dateCreated |
1999-6-25
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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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:month |
May
|
pubmed:issn |
0950-9232
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
13
|
pubmed:volume |
18
|
pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3034-8
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading | |
pubmed:year |
1999
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pubmed:articleTitle |
Reassessing the role of C-MYB in tumorigenesis.
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pubmed:affiliation |
CRC Centre for Cell and Molecular Biology, Institute of Cancer Research, London, UK.
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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