The small molecule compound G36 is the first selective Nox1 downregulator to reduce expression and function of Nox1, which is under constitutive control of G protein-coupled estrogen receptor (GPER).

The NADPH oxidase (Nox) proteins catalyze the regulated formation of reactive oxygen species (ROS) which play key roles as signaling molecules in several physiological and pathophysiological processes. ROS generation by the Nox1 member of the Nox ...

We employed our NOX1 antibody to characterize NOX1 expression in a panel of 30 human colorectal cancer cell lines, and correlated protein expression with NOX1 mRNA expression and superoxide production in a subset of these cells.

May 18, 2022 · NOX2 and NOX2-like isoforms (NOX1, NOX3, and NOX4) are coupled to the membrane subunit p22 phox. Cytosolic subunits activate NOX1, NOX2, and NOX3 whereas NOX4 activation involves p22 phox and...

Jan 18, 2010 · Given the potential therapeutic importance of cell-specific inhibition of NADPH oxidase, we investigated the role of Nox activator 1 (NoxA1), a homolog of p67phox, in VSMC NADPH oxidase function and atherosclerosis.

Feb 13, 2019 · PDIA1 is known to support vascular Nox1 NADPH oxidase expression/activation. Since deregulated reactive oxygen species (ROS) production underlies tumor growth, we proposed that PDIA1 is an...

Given the potential therapeutic importance of cell-specific inhibition of NADPH oxidase, we investigated the role of Nox activator 1 (NoxA1), a homolog of p67phox, in VSMC NADPH oxidase function and atherosclerosis.

NoxA1ds is a potent and highly selective NADPH oxidase 1 (NOX1) inhibitor (IC50=20 nM). NoxA1ds inhibits NOX1-derived O2- production in HT-29 human colon cancer cells. NoxA1ds attenuates VEGF-induced human pulmonary artery endothelial cell migration under hypoxic conditions in vitro.

Here, the use of Nox1 -/- and Nox1 +/+ mice as experimental models of human responses demonstrated a critical role of NOX1 in collagen-dependent platelet activation and pathological arterial thrombosis, as tested in vivo by carotid occlusion assays.

We propose that NOX1-dependent mTORC1 activation via S100A9 oxidation in VPS41-/VPS39-positive lysosomes is crucial for colon CSC proliferation and colon cancer progression.