Document Detail


Functional defect in neutrophil cytosols from two patients with autosomal recessive cytochrome-positive chronic granulomatous disease.
MedLine Citation:
PMID:  2539395     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The kinetics of activation of the respiratory burst oxidase in the cell-free oxidase-activating system have been explained by a three-stage mechanism in which the membrane-associated oxidase components M: (a) take up a cytosolic factor S to form a complex M.S that is (b) slowly converted in the second stage to a precatalytic species [M.S]*, which finally (c) takes up two more (possibly identical) cytosolic components, C alpha and C beta, to successively generate [M.S]*C alpha, a low-activity (i.e., high Km) oxidase, and finally [M.S]*C alpha C beta, the ordinary (i.e., low Km) oxidase (Babior, B.M., R. Kuver, and J.T. Curnutte. 1988. J. Biol. Chem. 263:1713-1718). Studies with the cell-free oxidase-activating system from normal neutrophils and from neutrophils obtained from two patients with type II (autosomal recessive cytochrome-positive) chronic granulomatous disease (CGD) have suggested that (a) the defective element in the cytosol from patient neutrophils is S; (b) in normal neutrophil cytosol, S is limiting with respect to M; and (c) C alpha and C beta interact cooperatively with the activated precursor complex [M.S]*. It was further speculated that S might be identical to the nonphosphorylated progenitor of the phosphorylated 48-kD proteins that are missing in certain forms of CGD, and that other forms of type II CGD besides the one described in this report remain to be discovered.
Authors:
J T Curnutte; P J Scott; B M Babior
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  83     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  1989 Apr 
Date Detail:
Created Date:  1989-05-15     Completed Date:  1989-05-15     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1236-40     Citation Subset:  AIM; IM    
Affiliation:
Department of Basic and Clinical Research, Scripps Clinic, La Jolla, California 92037.
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MeSH Terms
Descriptor/Qualifier:
Cell-Free System
Cytosol / enzymology,  physiology*
Enzyme Activation
Genes, Recessive
Granulomatous Disease, Chronic / enzymology*,  genetics,  pathology
Humans
Kinetics
NADH, NADPH Oxidoreductases / metabolism*,  physiology
NADPH Oxidase*
Neutrophils / enzymology,  physiology*
Superoxides / biosynthesis*
Grant Support
ID/Acronym/Agency:
AI-24227/AI/NIAID NIH HHS; AI-24838/AI/NIAID NIH HHS; RR-00833/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
11062-77-4/Superoxides; EC 1.6.-/NADH, NADPH Oxidoreductases; EC 1.6.3.1/NADPH Oxidase; EC 1.6.99.-/superoxide-forming enzyme
Comments/Corrections

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