Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
The responsiveness of the Nrf2 pathway may act as a major determinant of susceptibility to tobacco smoke-induced emphysema by upregulating antioxidant defenses and decreasing lung inflammation and alveolar cell apoptosis.
|
15520857 |
2004 |
Central neuroblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results together suggest that NO signals the transcriptional up-regulation of NQO1 and other detoxifying enzyme and protective genes through Nrf2 via the ARE to counteract NO-induced apoptosis of neuroblastoma cells.
|
14985350 |
2004 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Keap1-dependent ubiquitination of Nrf2 is inhibited following exposure of cells to quinone-induced oxidative stress and sulforaphane, a cancer-preventive isothiocyanate.
|
15572695 |
2004 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
A strategy for cancer prevention: stimulation of the Nrf2-ARE signaling pathway.
|
15252150 |
2004 |
Pneumonitis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The responsiveness of the Nrf2 pathway may act as a major determinant of susceptibility to tobacco smoke-induced emphysema by upregulating antioxidant defenses and decreasing lung inflammation and alveolar cell apoptosis.
|
15520857 |
2004 |
Childhood Neuroblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results together suggest that NO signals the transcriptional up-regulation of NQO1 and other detoxifying enzyme and protective genes through Nrf2 via the ARE to counteract NO-induced apoptosis of neuroblastoma cells.
|
14985350 |
2004 |
Autoimmune Diseases
|
0.070 |
AlteredExpression
|
group |
BEFREE |
Activation of cytoprotective Nrf2/ARE-regulated genes can suppress inflammatory responses, whereas decreased expression of these genes results in autoimmune disease and enhanced inflammatory responses to oxidant insults.
|
15032691 |
2004 |
Carcinogenesis
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
Nrf2 also mediates protection against oxidative stress and influences inflammatory processes, both of which contribute to carcinogenesis.
|
16054659 |
2005 |
Amyotrophic Lateral Sclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Both Nrf2 and HO-1 levels were increased and co-localized with reactive astrocytes in the degenerating lumbar spinal cord of rats expressing the amyotrophic lateral sclerosis-linked SOD1 G93A mutation.
|
15870071 |
2005 |
Arteriosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
To gain further insight into the roles that Nrf2 plays in the development of atherosclerosis, we examined how Nrf2 regulates gene expression in response to anti-atherogenic laminar flow (L-flow) or pro-atherogenic oscillatory flow (O-flow).
|
15917255 |
2005 |
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
LHGDN |
To gain further insight into the roles that Nrf2 plays in the development of atherosclerosis, we examined how Nrf2 regulates gene expression in response to anti-atherogenic laminar flow (L-flow) or pro-atherogenic oscillatory flow (O-flow).
|
15917255 |
2005 |
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
To gain further insight into the roles that Nrf2 plays in the development of atherosclerosis, we examined how Nrf2 regulates gene expression in response to anti-atherogenic laminar flow (L-flow) or pro-atherogenic oscillatory flow (O-flow).
|
15917255 |
2005 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Nrf2 knockout mice are greatly predisposed to chemical-induced DNA damage and exhibit higher susceptibility towards cancer development in several models of chemical carcinogenesis.
|
16054659 |
2005 |
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Nrf2 knockout mice are greatly predisposed to chemical-induced DNA damage and exhibit higher susceptibility towards cancer development in several models of chemical carcinogenesis.
|
16054659 |
2005 |
Chemical Carcinogenesis
|
0.050 |
Biomarker
|
phenotype |
BEFREE |
Nrf2 knockout mice are greatly predisposed to chemical-induced DNA damage and exhibit higher susceptibility towards cancer development in several models of chemical carcinogenesis.
|
16054659 |
2005 |
Acute Promyelocytic Leukemia
|
0.040 |
Biomarker
|
disease |
BEFREE |
Interestingly, part of the translocated Nrf2 colocalized with the promyelocytic leukemia protein in the promyelocytic leukemia nuclear bodies.
|
15657364 |
2005 |
Promyelocytic leukemia
|
0.030 |
Biomarker
|
disease |
BEFREE |
Interestingly, part of the translocated Nrf2 colocalized with the promyelocytic leukemia protein in the promyelocytic leukemia nuclear bodies.
|
15657364 |
2005 |
Motor neuron atrophy
|
0.030 |
AlteredExpression
|
disease |
BEFREE |
Nrf2 leads to the expression of antioxidant and cytoprotective enzymes such as heme oxygenase-1 and a group of enzymes involved in glutathione metabolism that prevent motor neuron degeneration.
|
16909019 |
2005 |
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Dysfunctional KEAP1-NRF2 interaction in non-small-cell lung cancer.
|
17020408 |
2006 |
Liver carcinoma
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Low dose (7.5 J/m(2)) UVB exposure of mouse hepatoma, mouse keratinocyte, and human skin fibroblast cells led to the nuclear accumulation of Nrf2 and up-regulation of ARE-mediated gene expression.
|
16951152 |
2006 |
Carcinogenesis
|
0.400 |
AlteredExpression
|
phenotype |
BEFREE |
On the contrary, and intriguingly, high dose (20 J/m(2)) UVB exposure of cells led to the nuclear exclusion of Nrf2 and down-regulation of chemoprotective gene expression with possible implications in UVB carcinogenesis.
|
16951152 |
2006 |
Liver neoplasms
|
0.370 |
AlteredExpression
|
group |
BEFREE |
Low dose (7.5 J/m(2)) UVB exposure of mouse hepatoma, mouse keratinocyte, and human skin fibroblast cells led to the nuclear accumulation of Nrf2 and up-regulation of ARE-mediated gene expression.
|
16951152 |
2006 |
Arteriosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Based on our findings, we suggest that Nrf2-dependent HO-1 expression induced by HA inhibits MCP-1 secretion, VCAM-1 expression and NF-kappaB activation associated with vascular injury and inflammation in atherosclerosis.
|
16246346 |
2006 |
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Based on our findings, we suggest that Nrf2-dependent HO-1 expression induced by HA inhibits MCP-1 secretion, VCAM-1 expression and NF-kappaB activation associated with vascular injury and inflammation in atherosclerosis.
|
16246346 |
2006 |
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Loss of KEAP1 function leading to constitutive activation of NRF2-mediated gene expression in cancer suggests that tumor cells manipulate the NRF2 pathway for their survival against chemotherapeutic agents.
|
17020408 |
2006 |