Linked Life Data

8503904

Source:http://linkedlifedata.com/resource/pubmed/id/8503904

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1993-7-1
pubmed:abstractText
Epidermal growth factor (EGF) can stimulate proliferation and 92 kDa gelatinase/matrix metalloproteinase (MMP-9) expression. The induction of MMP-9 is not only pathologically significant for invasion and metastasis, but also serves as a semiquantitative measure of EGF signal transduction. In order to examine the role of mutated ras p21 in EGF signal transduction, an activated Ha-ras-transformed human keratinocyte cell line was developed and characterized. Overexpression of the mutated Ha-ras p21 in these cells was demonstrated. Our results showed that EGF induced 92 kDa MMP-9 secretion was doubled in the ras-transformed keratinocytes in comparison to the parent cells. The karyotype, the expression of EGF receptor (EGFR) and transforming growth factor (TGF) alpha at the mRNA level remained unchanged. These results suggest that the presence of high levels of mutated ras p21 may be responsible for the aberrant EGF signal transduction and contributes to transformation. In addition, a reduction of TGF beta expression at mRNA level by 70% was found in the activated Ha-ras-transformed keratinocytes when compared to the parent cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
193
pubmed:geneSymbol
Ha-ras
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
167-74
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Altered epidermal growth factor signal transduction in activated Ha-ras-transformed human keratinocytes.
pubmed:affiliation
Department of Medicine, University of Connecticut Health Center, Farmington 06032.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't