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The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Chemoattractant-Stimulated Rac Activation in Wild-Type and Rac2-Deficient Murine Neutrophils: Preferential Activation of Rac2 and Rac2 Gene Dosage Effect on Neutrophil Functions

Li, Shijun, Yamauchi, Akira, Marchal, Christophe C, Molitoris, Jason K, Quilliam, Lawrence A, Dinauer, Mary C·2002·The Journal of Immunology
DOI 10.4049/jimmunol.169.9.5043
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Abstract

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, ≈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 ≈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 Rac 1 and Rac2, rather than a reduction in the total cellular level of Rac.

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Cited by

Metadata

Authors
Li, S., Yamauchi, A., Marchal, C. C., Molitoris, J. K., Quilliam, L. A., & Dinauer, M. C.
Affiliations
  • Herman B Wells Center for Pediatric Research and Departments of Pediatrics (Hematology/Oncology), Microbiology/Immunology, and Medical and Molecular Genetics, Biochemistry and Molecular Biology , Indianapolis, IN 46202
  • Walther Oncology Center and Walther Cancer Institute , Indianapolis, IN 46202
  • James Whitcomb Riley Hospital for Children, Indiana University Medical School , Indianapolis, IN 46202
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2002-11-01
Volume
169
Issue
9
Pages
5043-5051
ISSN
  • 0022-1767
  • 1550-6606
DOI
10.4049/jimmunol.169.9.5043
Cited by
109
References
5
Language
en
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)

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