Linked Life Data

11943193

Source:http://linkedlifedata.com/resource/pubmed/id/11943193

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2002-4-10
pubmed:abstractText
p204 overexpression in retinoblastoma (Rb)-/- mouse embryo fibroblasts or transfection of p204 mutated at both Rb-binding sites confer growth advantages, resulting in a significantly higher number of foci in a cell focus assay. To investigate the possibility that mutated p204 acquires malignant transformation capability, NIH3T3 cells were stably transfected with the expression vector pRcRSV204 double-mutant (p204dm) harboring both the C-terminal deletion up to amino acid 568 and the point mutation from glutamic acid to lysine at position 427, and analyzed for markers typical of cell immortalization and transformation. We detected a greater abundance of cell colonies in soft agar with p204dm-expressing cells than vector control cells. The p204dm-transfected cells also displayed two other characteristics associated with malignant transformation, i.e. growth under low-serum conditions and formation of tumors in athymic nude mice. Moreover, their telomerase activity was significantly higher than in the vector control cells. It would thus seem that p204, devoid of functional Rb-binding motifs, can become oncogenic.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
27
pubmed:volume
515
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
51-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
The interferon-inducible gene, Ifi204, acquires malignant transformation capability upon mutation at the Rb-binding sites.
pubmed:affiliation
Department of Public Health and Microbiology, Medical School, Via Santena 9, 10126, Turin, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't