Linked Life Data

11224519

Source:http://linkedlifedata.com/resource/pubmed/id/11224519

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-3-26
pubmed:abstractText
A Rac GTPase-regulated multiprotein NADPH oxidase is critical for the formation of reactive oxygen species (ROS) in phagocytic leukocytes and other nonphagocytic cells. NADPH oxidase reduces molecular oxygen to form superoxide anion in a two-step process. Electrons are initially transferred from NADPH to cytochrome b-associated FAD, then to cytochrome b heme and finally to molecular oxygen. We show here that Rac is required for both electron-transfer reactions. Mutational and biophysical analysis shows that Rac and p67phox independently regulate cytochrome b to catalyze the transfer of electrons from NADPH to FAD. However, they must interact with each other to induce the subsequent transfer of electrons from FAD to cytochrome b heme and molecular oxygen. This two-step model of regulation by Rac GTPase may provide a means of more effectively controlling the inflammatory responses of phagocytic leukocytes.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1529-2908
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
211-5
pubmed:dateRevised
2009-11-3
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Molecular basis for Rac2 regulation of phagocyte NADPH oxidase.
pubmed:affiliation
Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't