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Mol. Cells 2003; 16(3): 271-277

Published online January 1, 1970

© The Korean Society for Molecular and Cellular Biology

Molecular Mechanism for Activation of Superoxide-producing NADPH Oxidases

Ryu Takeya, Hideki Sumimoto

Abstract

The membrane-integrated protein gp91phox, existing as a heterodimer with p22phox, functions as the catalytic core of the phagocyte NADPH oxidase, which plays a crucial role in host defence. The oxidase, dormant in resting cells, becomes activated to produce superoxide, a precursor of microbicidal oxidants, by interacting with the adaptor proteins p47phox and p67phox as well as the small GTPase Rac. In the past few years, several proteins homologous to gp91phox were discovered as superoxide-producing NAD(P)H oxidases (Nox

Keywords gp91phox; NADPH Oxidase; Nox1; Noxa1; Noxo1; ROS; Superoxide.

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Minireview

Mol. Cells 2003; 16(3): 271-277

Published online December 31, 2003

Copyright © The Korean Society for Molecular and Cellular Biology.

Molecular Mechanism for Activation of Superoxide-producing NADPH Oxidases

Ryu Takeya, Hideki Sumimoto

Abstract

The membrane-integrated protein gp91phox, existing as a heterodimer with p22phox, functions as the catalytic core of the phagocyte NADPH oxidase, which plays a crucial role in host defence. The oxidase, dormant in resting cells, becomes activated to produce superoxide, a precursor of microbicidal oxidants, by interacting with the adaptor proteins p47phox and p67phox as well as the small GTPase Rac. In the past few years, several proteins homologous to gp91phox were discovered as superoxide-producing NAD(P)H oxidases (Nox

Keywords: gp91phox, NADPH Oxidase, Nox1, Noxa1, Noxo1, ROS, Superoxide.

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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