Linked Life Data

11894116

Source:http://linkedlifedata.com/resource/pubmed/id/11894116

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-3-14
pubmed:abstractText
It has been reported that expression of Bax by Tet-On system induces apoptosis in Jurkat cells. The parental Jurkat cells have mutation of Bax gene and do not express Bax protein. Wild-type Bax-bearing cells express endogenous Bax protein and it is still unclear whether overexpression of Bax alone can sufficiently induce apoptosis in these cells in the absence of any cytotoxic stimulus. To investigate this, wild-type Bax-bearing K562 cells were transfected with Tet-On Bax-inducible system (pTet-On and pTRE-Bax plasmids), and Bax-inducible stable cell lines were established. Overexpression of Bax in wild-type Bax-bearing K562 cells without any cyctotoxic signal resulted in increase of apoptotic cells, caspase-3 activation, mitochondrial release of cytochrome c, and mitochondrial membrane potential change. Western blotting and confocal microscopy revealed that overexpression of Bax was detected in mitochondria. A pancaspase inhibitor, zVAD-fmk, which has no effect on mitochondrial cytochrome c release and mitochondrial membrane potential change inhibited the apoptotic events in the presence of overexpressed Bax in mitochondria. These findings suggest that Bax protein, when present above a threshold level, is sufficient to trigger an apoptosis cascade, and its initiation requires simultaneous caspase activation probably not mediated by mitochondrial cytochrome c release and mitochondrial membrane potential change in K562 cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1019-6439
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
723-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Bax-induction alone is sufficient to activate apoptosis cascade in wild-type Bax-bearing K562 cells, and the initiation of apoptosis requires simultaneous caspase activation.
pubmed:affiliation
The Second Department of Internal Medicine, Mie University School of Medicine, Tsu 514-8507, Japan. tohruk@clin.medic.mie-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't