Linked Life Data

2827775

Source:http://linkedlifedata.com/resource/pubmed/id/2827775

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1988-3-14
pubmed:abstractText
Transplasmalemma electron transport by HeLa and pineal cells to reduce external ferricyanide is associated with proton release from the cells. Diferric transferrin also acts as an electron acceptor for the transmembrane oxidoreductase. We now show that reduction of external diferric transferrin by RPNA-209-1 SV40 transformed pineal cells is accompanied by proton release from the cells. The stoichiometry of proton release to electron transfer is much greater than would be expected from aniostropic electron flow across the membrane through protonated carriers. The proton release is not stimulated by apotransferrin and the diferric transferrin-stimulated activity is inhibited by apotransferrin. Apotransferrin also inhibits reduction of diferric transferrin by these cells. The proton release is dependent on external sodium ions and is inhibited by amiloride, which indicates that the proton release is mediated by the Na+/H+ antiport and that this antiport is activated by electron transport through the transmembrane dehydrogenase. Growth stimulation by diferric transferrin or other external oxidants can be based in part on activation of the Na+/H+ antiport.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
938
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
17-23
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Reduction of diferric transferrin by SV40 transformed pineal cells stimulates Na+/H+ antiport activity.
pubmed:affiliation
Department of Biological Sciences, Purdue University, West Lafayette, IN 47907.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't