Linked Life Data

19559621

Source:http://linkedlifedata.com/resource/pubmed/id/19559621

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2009-7-14
pubmed:abstractText
When mitochondrial function is compromised and the mitochondrial membrane potential (Deltapsi(m)) falls below a threshold, the F(1)F(o)-ATP synthase can reverse, hydrolysing ATP to pump protons out of the mitochondrial matrix. Although this activity can deplete ATP and precipitate cell death, it is limited by the mitochondrial protein IF(1), an endogenous F(1)F(o)-ATPase inhibitor. IF(1), therefore, preserves ATP at the expense of Deltapsi(m). Despite a wealth of detailed knowledge on the biochemistry of the interaction of IF(1) and the F(1)F(o)-ATPase, little is known about its physiological activity. Emerging research suggests that IF(1) has a wider ranging impact on mitochondrial structure and function than previously thought.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0968-0004
pubmed:author
pubmed:issnType
Print
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
343-50
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
IF(1): setting the pace of the F(1)F(o)-ATP synthase.
pubmed:affiliation
Department of Cell and Developmental Biology, University College London, UK.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't