Linked Life Data

8055631

Source:http://linkedlifedata.com/resource/pubmed/id/8055631

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1994-9-15
pubmed:abstractText
The gap junctional communication capacity of six human carcinoma-derived tumorigenic cell lines (pancreatic, pharyngeal and cervical), two murine carcinoma-derived tumorigenic cell lines (bladder-derived and Ehrlich ascites) and one monkey non-tumorigenic cell line (kidney epithelium) have been compared by the dye-transfer technique. All the tumorigenic cell lines were communication defective, while the non-tumorigenic cell line was not. Moreover, six of the eight tumorigenic cell lines expressed a gap junction transcript coding for the connexin 43 (alpha 1). Finally, gap junction plaques were not detected between tumorigenic cells by immunofluorescence staining. Consequently, these data suggest that communication defects in tumorigenic cells may result from either abnormally low levels of translation of junction mRNA or alterations in the assembly of junction protein into cell surface plaques, and not from failure to produce junction transcripts. Furthermore, since induction of alpha 1 expression has been associated with dedifferentiation processes, the presence of alpha 1 mRNA might be a characteristic property of certain tumorigenic cells that originate from cells that do not normally express alpha 1 mRNA.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0143-3334
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1541-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Non-communicating human and murine carcinoma cells produce alpha 1 gap junction mRNA.
pubmed:affiliation
Department of Molecular Biology, Scripps Research Institute, La Jolla, CA 92037.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.