Linked Life Data

7731715

Source:http://linkedlifedata.com/resource/pubmed/id/7731715

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1995-5-30
pubmed:abstractText
To determine the role of c-abl during cell growth, we constructed a retrovirus vector alpha A, capable of expressing an antisense RNA directed against the abl mRNA. Based on v-abl-mediated 3T3 transformation assay, we showed that the number of transformed foci was reduced 50-94% when alpha A-infected 3T3 cells were superinfected with A-MuLV. Up to a 100% of inhibition could be observed when the time of infection was lengthened. Introduction of the antisense sequence into NIH3T3 cells resulted in reduction of growth rate. These cells entered into S phase from G1 phase of the cell cycle earlier in time than untransduced cells. Thus c-abl serves as a checkpoint during G1/S transition in the cell cycle, and its reduction resulted in deregulation of cell growth.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
10
pubmed:geneSymbol
c-abl
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1607-14
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Deregulation of c-abl mediated cell growth after retroviral transfer and expression of antisense sequences.
pubmed:affiliation
Fels Institute for Cancer Research and Molecular Biology, Department of Biochemistry, Temple University, Philadelphia, Pennsylvania 19140, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't