Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-6-25
pubmed:abstractText
We have previously found that transforming growth factor-beta (TGF-beta) induces an increase in radical oxygen species (ROS) production that mediates its apoptotic effects in fetal hepatocytes. In this paper we show that TGF-beta activates p38 mitogen-activated protein kinase (p38MAPK) and ROS may be responsible for this activation. Activation of p38MAPK occurs late, coincident with the maximal production of ROS, it is inhibited by radical scavengers and it is accentuated by the presence of glutathione synthesis inhibitors. However, p38MAPK does not appear to be involved in any of the apoptotic events: loss of Bcl-x(L) levels, cytochrome c release, cleavage of caspase substrates and loss of cell viability.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
22
pubmed:volume
499
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
225-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Activation of p38MAPK by TGF-beta in fetal rat hepatocytes requires radical oxygen production, but is dispensable for cell death.
pubmed:affiliation
Departamento de Bioquímica y Biología Molecular (Centro Mixto CSIC/UCM), Facultad de Farmacia, Universidad Complutense de Madrid, Ciudad Universitaria, 28040, Madrid, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't