|
Arteriosclerosis
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Our data support an important role for NOXA1-dependent NADPH oxidase activity in VSMC plasticity during restenosis and atherosclerosis, augmenting VSMC proliferation and migration and KLF4-mediated transition to macrophage-like cells, plaque inflammation, and expansion.
|
30576919 |
2019 |
|
Atherosclerosis
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Our data support an important role for NOXA1-dependent NADPH oxidase activity in VSMC plasticity during restenosis and atherosclerosis, augmenting VSMC proliferation and migration and KLF4-mediated transition to macrophage-like cells, plaque inflammation, and expansion.
|
30576919 |
2019 |
|
Neointimal hyperplasia
|
0.020 |
Biomarker
|
disease |
BEFREE |
Neointimal hyperplasia following endovascular injury was lower in Noxa1-deficient mice versus the wild-type following endovascular injury.
|
30576919 |
2019 |
|
Arteriosclerosis
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
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.
|
20083677 |
2010 |
|
Atherosclerosis
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
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.
|
20083677 |
2010 |
|
Neointimal hyperplasia
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Adenovirus-mediated overexpression of NoxA1 in guidewire-injured mouse carotid arteries significantly increased superoxide production in medial VSMCs and enhanced neointimal hyperplasia.
|
20083677 |
2010 |
|
Atherosclerotic lesion
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
SMC-specific deletion of Noxa1 in Apoe<sup>-/-</sup> mice (Noxa1<sup>SMC-/-</sup>/Apoe<sup>-/-</sup>) similarly decreased vascular ROS levels and atherosclerotic lesion size.
|
30576919 |
2019 |
|
Vascular Diseases
|
0.010 |
AlteredExpression
|
group |
BEFREE |
These findings support the potential for modulation of NoxA1 expression as a viable approach for the treatment of vascular diseases.
|
20083677 |
2010 |
|
Malignant Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
To investigate whether NOX and NOX accessory gene expression might be a factor common to specific human tumour types, this study measured the expression levels of NOX genes 1-5, dual oxidase 1 and 2, as well as those of NOX accessory genes NoxO1, NoxA1, p47(phox), p67(phox) and p22(phox) in human cancer cell lines and in tumour and adjacent normal tissue pairs by quantitative, real-time RT-PCR.
|
19431059 |
2009 |
|
Primary malignant neoplasm
|
0.010 |
Biomarker
|
group |
BEFREE |
To investigate whether NOX and NOX accessory gene expression might be a factor common to specific human tumour types, this study measured the expression levels of NOX genes 1-5, dual oxidase 1 and 2, as well as those of NOX accessory genes NoxO1, NoxA1, p47(phox), p67(phox) and p22(phox) in human cancer cell lines and in tumour and adjacent normal tissue pairs by quantitative, real-time RT-PCR.
|
19431059 |
2009 |
|
Adenocarcinoma
|
0.010 |
Biomarker
|
group |
BEFREE |
Confocal microscopy revealed that Nox1, NOXO1, Nox activator 1, and p22(phox) were predominantly associated with Golgi apparatus in these cancer cells, while diffuse-type adenocarcinomas also contained cancer cells having Nox1 and its partner proteins in their nuclei.
|
18037128 |
2007 |