Linked Life Data

15889622

Source:http://linkedlifedata.com/resource/pubmed/id/15889622

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-5-13
pubmed:abstractText
Proteins of the Bcl-2 family are key regulators of apoptosis. Bax can be regarded as pro-apoptotic, whereas Bcl-2 is perceived as anti-apoptotic. It has been proposed that an increased ratio of pro-apoptotic Bax to anti-apoptotic Bcl-2 can be associated with apoptosis. Since prostaglandin A2 (PGA2) and 2-methoxyestradiol (2-ME) play an active role in the induction of apoptosis, the influence of 20 microg/ml PGA2 and 1 microM 2-ME was investigated on Bax and Bcl-2 expression levels in cervical carcinoma cells. Both PGA2 and 2-ME exposure led to statistically significant increases in Bax expression levels. Cells were shown to be more susceptible to the effects of 2-ME than to the effects caused by PGA2. In contrast, no statistically significant effects were observed on Bcl-2 expression levels after exposure to PGA2 and 2-ME. The Bax/Bcl-2 ratios for PGA2- and 2-ME-exposed cells were 2.06 and 1.87 respectively, normalised against Bcl-2 levels. Further investigation of the function and regulation of the Bcl-2 family will allow researchers to consider potential pathways of apoptosis signaling mechanisms for diseases where apoptosis can potentially be controlled.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0388-6107
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
87-90
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Influence of prostaglandin A2 and 2-methoxyestradiol on Bax and Bcl-2 expression levels in cervical carcinoma cells.
pubmed:affiliation
Department of Physiology, University of Pretoria, Pretoria, South Africa. annie.joubert@up.ac.za
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't