Two cytosolic components of the human neutrophil respiratory burst oxidase translocate to the plasma membrane during cell activation - PubMed (original) (raw)
Two cytosolic components of the human neutrophil respiratory burst oxidase translocate to the plasma membrane during cell activation
R A Clark et al. J Clin Invest. 1990 Mar.
Abstract
The superoxide-forming respiratory burst oxidase of human neutrophils is composed of membrane-associated catalytic components and cytosolic constituents required for oxidase activation. This study concerns the hypothesis that cytosolic oxidase components translocate to a membrane fraction when neutrophils are stimulated and the oxidase is activated. A polyclonal antiserum that recognizes two discrete cytosolic oxidase components of 47 and 67 kD was used to probe transfer blots of electrophoresed membrane and cytosol fractions of resting and stimulated neutrophils. In contrast to their strictly cytosolic localization in unstimulated cells, both proteins were detected in membrane fractions of neutrophils activated by phorbol esters and other stimuli. This translocation event was a function of stimulus concentration as well as time and temperature of exposure to the stimulus. It was inhibited by concentrations of N-ethylmaleimide that blocked superoxide formation but was unaffected by 2-deoxyglucose. There was a correlation between translocation of the cytosolic proteins and activation of the oxidase as determined by superoxide formation. Quantitative analyses suggested that approximately 10% of total cellular p47 and p67 became membrane-associated during phorbol ester activation of the oxidase. Analysis of Percoll density gradient fractions indicated that the target membrane for translocation of both proteins was the plasma membrane rather than membranes of either specific or azurophilic granules. In the cell-free oxidase system arachidonate-dependent but membrane-independent precipitation of the cytosolic oxidase proteins was demonstrated. The data show that activation of the respiratory burst oxidase in stimulated human neutrophils is closely associated with translocation of the 47- and 67-kD cytosolic oxidase components to the plasma membrane. We suggest that this translocation event is important in oxidase activation.
Similar articles
- Translocation of Rac correlates with NADPH oxidase activation. Evidence for equimolar translocation of oxidase components.
Quinn MT, Evans T, Loetterle LR, Jesaitis AJ, Bokoch GM. Quinn MT, et al. J Biol Chem. 1993 Oct 5;268(28):20983-7. J Biol Chem. 1993. PMID: 8407934 - Inhibition of NADPH-oxidase activity in human polymorphonuclear neutrophils by lipophilic ascorbic acid derivatives.
Schmid E, Figala V, Ullrich V. Schmid E, et al. Mol Pharmacol. 1994 May;45(5):815-25. Mol Pharmacol. 1994. PMID: 8190099 - Activation factors of neutrophil NADPH oxidase complex.
Umeki S. Umeki S. Life Sci. 1994;55(1):1-13. doi: 10.1016/0024-3205(94)90076-0. Life Sci. 1994. PMID: 8015344 Review. - Subcellular localization and dynamics of components of the respiratory burst oxidase.
Borregaard N. Borregaard N. J Bioenerg Biomembr. 1988 Dec;20(6):637-51. doi: 10.1007/BF00762546. J Bioenerg Biomembr. 1988. PMID: 2854126 Review.
Cited by
- Neutrophil Activated by the Famous and Potent PMA (Phorbol Myristate Acetate).
Damascena HL, Silveira WAA, Castro MS, Fontes W. Damascena HL, et al. Cells. 2022 Sep 16;11(18):2889. doi: 10.3390/cells11182889. Cells. 2022. PMID: 36139464 Free PMC article. Review. - Involvement of GTP in cell-free activation of neutrophil NADPH oxidase. Studies with GTP analogues.
Klinger E, Aviram I. Klinger E, et al. Biochem J. 1992 Jul 15;285 ( Pt 2)(Pt 2):635-9. doi: 10.1042/bj2850635. Biochem J. 1992. PMID: 1637353 Free PMC article. - Superoxide generation of phagocytes and nonphagocytic cells.
Meier B. Meier B. Protoplasma. 2001;217(1-3):117-24. doi: 10.1007/BF01289420. Protoplasma. 2001. PMID: 11732328 Review. - Regulation of NADPH oxidase activity by Rac GTPase activating protein(s).
Heyworth PG, Knaus UG, Settleman J, Curnutte JT, Bokoch GM. Heyworth PG, et al. Mol Biol Cell. 1993 Nov;4(11):1217-23. doi: 10.1091/mbc.4.11.1217. Mol Biol Cell. 1993. PMID: 8305740 Free PMC article. - Low NADPH oxidase activity in Epstein-Barr-virus-immortalized B-lymphocytes is due to a post-transcriptional block in expression of cytochrome b558.
Chetty M, Thrasher AJ, Abo A, Casimir CM. Chetty M, et al. Biochem J. 1995 Feb 15;306 ( Pt 1)(Pt 1):141-5. doi: 10.1042/bj3060141. Biochem J. 1995. PMID: 7864801 Free PMC article.
References
- Proc Natl Acad Sci U S A. 1988 May;85(10):3319-23 - PubMed
- Proc Natl Acad Sci U S A. 1989 Sep;86(18):7195-9 - PubMed
- Biochem Biophys Res Commun. 1988 May 16;152(3):993-1001 - PubMed
- Ann Intern Med. 1988 Jul 15;109(2):127-42 - PubMed
- Blood. 1988 Jul;72(1):322-7 - PubMed
Publication types
MeSH terms
Substances
Grants and funding
- I01 BX000513/BX/BLRD VA/United States
- R37 AI020866/AI/NIAID NIH HHS/United States
- AI-20866/AI/NIAID NIH HHS/United States
- AI-28412/AI/NIAID NIH HHS/United States
- HL-34327/HL/NHLBI NIH HHS/United States
- R01 AI020866/AI/NIAID NIH HHS/United States
LinkOut - more resources
Full Text Sources