Linked Life Data

8621150

Source:http://linkedlifedata.com/resource/pubmed/id/8621150

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1996-6-19
pubmed:abstractText
Increased intracellular cyclic adenosine monophosphate (cAMP) levels have been shown in some reports to inhibit and in other studies to stimulate growth factor-mediated activation of the mitogen-activated protein kinase (MAP kinase) pathway, depending on the cell type examined. The relationship between cAMP and MAP kinase in hepatocytes has not been examined. In the current study, stimulation of primary cultures of rat hepatocytes with hepatocyte growth factor (HGF) or epidermal growth factor (EGF) increased Ras, Raf, and MAP kinase activity. Incubation of hepatocytes with cAMP-increasing agents blocked activation of Raf by both HGF and EGF, whereas activation of Ras was unaffected. MAP kinase activation by HGF was completely inhibited, whereas EGF-stimulated MAP kinase activity was only slightly reduced. Incubation of hepatocytes with pertussis toxin slightly blunted MAP kinase activation by EGF but not HGF. Increasing cAMP in hepatocytes preincubated with pertussis toxin completely inhibited the activation of MAP kinase by EGF. In conclusion, HGF activates MAP kinase in hepatocytes exclusively through an Raf-dependent pathway and this activation may be completely blocked by increasing cAMP. In contrast, EGF activates MAP kinase in hepatocytes through both Raf-dependent and Raf-independent pathways: the latter pathway probably involves a pertussis toxin-sensitive G protein.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0270-9139
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1167-73
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:8621150-Analysis of Variance, pubmed-meshheading:8621150-Animals, pubmed-meshheading:8621150-Calcium-Calmodulin-Dependent Protein Kinases, pubmed-meshheading:8621150-Cells, Cultured, pubmed-meshheading:8621150-Cyclic AMP, pubmed-meshheading:8621150-Enzyme Activation, pubmed-meshheading:8621150-Epidermal Growth Factor, pubmed-meshheading:8621150-Hepatocyte Growth Factor, pubmed-meshheading:8621150-Liver, pubmed-meshheading:8621150-Male, pubmed-meshheading:8621150-Pertussis Toxin, pubmed-meshheading:8621150-Protein-Serine-Threonine Kinases, pubmed-meshheading:8621150-Proto-Oncogene Proteins, pubmed-meshheading:8621150-Proto-Oncogene Proteins c-raf, pubmed-meshheading:8621150-Rats, pubmed-meshheading:8621150-Rats, Sprague-Dawley, pubmed-meshheading:8621150-Virulence Factors, Bordetella, pubmed-meshheading:8621150-ras Proteins
pubmed:year
1996
pubmed:articleTitle
Inhibitory actions of cyclic adenosine monophosphate and pertussis toxin define two distinct epidermal growth factor-regulated pathways leading to activation of mitogen-activated protein kinase in rat hepatocytes.
pubmed:affiliation
Division of Renal Diseases and Hypertension, University of Colorado Health Sciences Center, Denver 80262, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't