Linked Life Data

12391220

Source:http://linkedlifedata.com/resource/pubmed/id/12391220

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2002-10-22
pubmed:abstractText
The hemopoietic-specific Rho family GTPase Rac2 shares 92% amino acid identity with ubiquitously expressed Rac1. Neutrophils from rac2(-/-) mice have multiple defects, including chemoattractant-stimulated NADPH oxidase activity and chemotaxis, which may result from an overall reduction in cellular Rac or mechanisms that discriminate Rac1 and Rac2. We show that murine neutrophils have similar amounts of Rac1 and Rac2, unlike human neutrophils, which express predominantly Rac2. An affinity precipitation assay for Rac-GTP showed that although FMLP-induced activation of both isoforms in wild-type neutrophils, approximately 4-fold more Rac2-GTP was detected than Rac1-GTP. Wild-type and Rac2-deficient neutrophils have similar levels of total Rac1. FMLP-induced Rac1-GTP in rac2(-/-) neutrophils was approximately 3-fold greater than in wild-type cells, which have similar levels of total Rac1, yet FMLP-stimulated F-actin, chemotaxis, and superoxide production are markedly impaired in rac2(-/-) neutrophils. Heterozygous rac2(+/-) neutrophils, which had intermediate levels of total and FMLP-induced activated Rac2, exhibited intermediate functional responses to FMLP, suggesting that Rac2 was rate limiting for these functions. Thus, phenotypic defects in FMLP-stimulated Rac2-deficient neutrophils appear to reflect distinct activation and signaling profiles of Rac1 and Rac2, rather than a reduction in the total cellular level of Rac.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
169
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5043-51
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:12391220-Actins, pubmed-meshheading:12391220-Animals, pubmed-meshheading:12391220-Chemotaxis, Leukocyte, pubmed-meshheading:12391220-Enzyme Inhibitors, pubmed-meshheading:12391220-Female, pubmed-meshheading:12391220-Gene Dosage, pubmed-meshheading:12391220-Heterozygote Detection, pubmed-meshheading:12391220-Humans, pubmed-meshheading:12391220-Male, pubmed-meshheading:12391220-Mice, pubmed-meshheading:12391220-Mice, Inbred C57BL, pubmed-meshheading:12391220-Mice, Knockout, pubmed-meshheading:12391220-N-Formylmethionine Leucyl-Phenylalanine, pubmed-meshheading:12391220-NADPH Oxidase, pubmed-meshheading:12391220-Neutrophil Activation, pubmed-meshheading:12391220-Neutrophils, pubmed-meshheading:12391220-Phosphatidylinositol 3-Kinases, pubmed-meshheading:12391220-Protein Isoforms, pubmed-meshheading:12391220-rac GTP-Binding Proteins, pubmed-meshheading:12391220-rac1 GTP-Binding Protein, pubmed-meshheading:12391220-src-Family Kinases
pubmed:year
2002
pubmed:articleTitle
Chemoattractant-stimulated Rac activation in wild-type and Rac2-deficient murine neutrophils: preferential activation of Rac2 and Rac2 gene dosage effect on neutrophil functions.
pubmed:affiliation
Herman B Wells Center for Pediatric Research and Department of Pediatrics (Hematology/Oncology), Indiana University Medical School, Indianapolis 46202, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't