Linked Life Data

8576580

Source:http://linkedlifedata.com/resource/pubmed/id/8576580

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-3-13
pubmed:abstractText
The influence of human hepatocyte growth factor (HGF) on the transforming growth factor beta (TGF-beta) bioassay CCL-64 was examined. HGF induced proliferation of the CCL-64 cells and potently counteracted TGF-beta-induced growth inhibition. HGF was not inactivated by transient acidification to pH 2, a commonly used procedure to activate latent TGF-beta. HGF was a stronger mitogen for the mink lung cells than epidermal growth factor (EGF), a known stimulator of CCL-64 cell growth. Costimulation of the cells by these two cytokines resulted in an additive effect on proliferation. In complex biological fluids containing large amounts of HGF, the TGF-beta concentration can be underestimated when determined by the CCL-64 assay. When a fixed amount of TGF-beta is added, the CCL-64 cells can be used as a reliable bioassay for HGF with a sensitivity of about 1 ng/ml.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1759
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
189
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
59-64
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Hepatocyte growth factor reverses the TGF-beta-induced growth inhibition of CCL-64 cells. A novel bioassay for HGF and implications for the TGF-beta bioassay.
pubmed:affiliation
Institute of Cancer Research and Molecular Biology, University of Trondheim, Norway. magneb@mtsrv.mtfs.unit.no
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't