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Regulation of phagocyte function by low molecular weight GTP-binding proteins
Abstract
Abstract: The mechanisms used by phagocytic leukocytes in the process of bacterial killing are regulated by GTP‐binding proteins of the Ras superfamily. In particular, the formation of toxic oxygen metabolites via the NADPH oxidase requires the action of both Rac and Rap1A proteins. Rac2 forms a third cytosolic component of the human neutrophil NADPH oxidase. Rac2 is active in its GTP‐bound form, and requires post‐translational processing (isoprenylation) in order to interact with regulatory proteins which stimulate the exchange of GTP for GDP. In the resting neutrophil, Rac is localized to the cytosol in the form of a complex with a GDP dissociation inhibitor (GDI) protein. Upon cell activation, this complex is disrupted to enable Rac to translocate to the active oxidase at the plasma membrane. The Rac‐GDI complex may be regulated by the release of specific lipids known to be generated during phagocyte activation.
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“its deficiency results in impairment of both neutrophil chemotaxis in response to Formylmethionyl-Leucyl-Phenylalanine (fMLP) and superoxide production”
From Hematopoietic-specific Rho GTPases Rac2 and RhoH and human blood disorders (2013) · cites this paper as [21]
In the citing paper
“and is therefore associated with phagocyte immunodeficiency in humans17,18,19,20,21,22,23.”
From Hematopoietic-specific Rho GTPases Rac2 and RhoH and human blood disorders (2013) · cites this paper as [21]
In the citing paper
“Rac2 has been identified as a component of the phagocytic oxidase complex in neutrophils (Figure 1A)”
From Hematopoietic-specific Rho GTPases Rac2 and RhoH and human blood disorders (2013) · cites this paper as [21]
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Research works printed but not linked: 14
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Cited by
Hematopoietic-specific Rho GTPases Rac2 and RhoH and human blood disorders
Troeger, A., & Williams, D. A. (2013) · Experimental Cell Research · doi:10.1016/j.yexcr.2013.07.002 · Cited by 73
Metadata
- Authors
- Bokoch, G. M.
- Venue
- European Journal of Haematology
- Publisher
- Wiley
- Published
- 1993-11
- Volume
- 51
- Issue
- 5
- Pages
- 313-317
- ISSN
- 0902-4441
- 1600-0609
- Cited by
- 15
- References
- 0
- Language
- en
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