Linked Life Data

11395181

Source:http://linkedlifedata.com/resource/pubmed/id/11395181

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-6-7
pubmed:abstractText
Apoptosis, a type of programmed cell death, is a decisive mechanism in cell processes such as homeostasis, development, and many diseases including cancer. In mammals, the mechanisms that trigger and control the process of apoptosis are complex, because it has been observed that many molecules might be involved, acting in distinct ways and depending on the cellular type. The process of apoptosis is characterized by specific biochemical and morphologic changes. However, important specific messengers such as Ca(2)+ act in active proliferation as well as in apoptosis. At present, there is convincing evidence that a sustained increase in intracellular Ca(2)+ can activate cytotoxic mechanisms in various cells and tissues. Several ionic channels located in the cytoplasmic membrane might participate in the entry of calcium into the cytosol during apoptosis. Among these ionic channels, the purinoreceptors P2X and the channels of capacitative entry of calcium have been described. Pro- and anti-apoptotic molecules such as bax and bcl-2, respectively, have also been shown to participate in the process. We have recently found the activation of a Ca(2)+-permeable, nonselective cation channel of 23 pS conductance in prostatic cancer (LNCaP) exclusively in cells previously induced to apoptosis. Our findings are discussed taking into account the different ion channels that might participate in programmed cell death in prostate cancer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0188-4409
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
175-85
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Apoptosis and cell death channels in prostate cancer.
pubmed:affiliation
Instituto de Fisiología Celular, Universidad Nacional Autónoma de México (UNAM), Mexico City, Mexico.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't