| + |
hydrogen peroxide | up-regulates activity 
chemical modification
|
KEAP1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279845 |
CYS226 |
EFFNLSHcQLVTLIS |
Homo sapiens |
|
| pmid |
sentence |
| 32284348 |
In response to oxidative stress, the direct binding of stressors to reactive cysteine residues results in a conformation change in KEAP1, which inhibits the ubiquitination of NRF2. the sensor for H2O2 consists of four residues within KEAP1: Cys226, Cys613, Cys622, and Cys624.KEAP1 uses multiple sensing mechanisms to coordinate the NRF2-dependent oxidative stress response. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279846 |
CYS613 |
VAVTMEPcRKQIDQQ |
Homo sapiens |
|
| pmid |
sentence |
| 32284348 |
In response to oxidative stress, the direct binding of stressors to reactive cysteine residues results in a conformation change in KEAP1, which inhibits the ubiquitination of NRF2. the sensor for H2O2 consists of four residues within KEAP1: Cys226, Cys613, Cys622, and Cys624.KEAP1 uses multiple sensing mechanisms to coordinate the NRF2-dependent oxidative stress response. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279847 |
CYS622 |
KQIDQQNcTC |
Homo sapiens |
|
| pmid |
sentence |
| 32284348 |
In response to oxidative stress, the direct binding of stressors to reactive cysteine residues results in a conformation change in KEAP1, which inhibits the ubiquitination of NRF2. the sensor for H2O2 consists of four residues within KEAP1: Cys226, Cys613, Cys622, and Cys624.KEAP1 uses multiple sensing mechanisms to coordinate the NRF2-dependent oxidative stress response. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-279848 |
CYS624 |
IDQQNCTc |
Homo sapiens |
|
| pmid |
sentence |
| 32284348 |
In response to oxidative stress, the direct binding of stressors to reactive cysteine residues results in a conformation change in KEAP1, which inhibits the ubiquitination of NRF2. the sensor for H2O2 consists of four residues within KEAP1: Cys226, Cys613, Cys622, and Cys624.KEAP1 uses multiple sensing mechanisms to coordinate the NRF2-dependent oxidative stress response. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| + |
hydrogen peroxide | up-regulates
chemical activation
|
TXN |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-131049 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15556622 |
We show that 10 and 50 microm h2o2 and short-term exposure to shear stress significantly increased trx-1 mrna and protein levels in endothelial cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
hydrogen peroxide | up-regulates 
|
MAPK7 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-113758 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11782488 |
These findings suggest that c-src mediated bmk1 activation by h(2)o(2) may counteract ischemic cellular damage probably through the activation of mef2c transcription factor. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Brain |
| + |
SOD2 | up-regulates quantity
chemical modification
|
hydrogen peroxide |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272283 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29301787 |
Oxidative stress contributes to diabetes mellitus (DM)–induced endothelial dysfunction, which is one of the most common causes of cardiovascular morbidity and mortality.1,2 The major cellular defense against superoxide (O2•−) is SODs (superoxide dismutases), which consists of the SOD1 (cytoplasmic copper zinc SOD [Cu/ZnSOD]), the SOD2 (mitochondrial MnSOD), and the SOD3 (extracellular Cu/ZnSOD). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SOD1 | up-regulates quantity
chemical modification
|
hydrogen peroxide |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272287 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29301787 |
Oxidative stress contributes to diabetes mellitus (DM)–induced endothelial dysfunction, which is one of the most common causes of cardiovascular morbidity and mortality.1,2 The major cellular defense against superoxide (O2•−) is SODs (superoxide dismutases), which consists of the SOD1 (cytoplasmic copper zinc SOD [Cu/ZnSOD]), the SOD2 (mitochondrial MnSOD), and the SOD3 (extracellular Cu/ZnSOD). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
hydrogen peroxide | up-regulates
|
ROS |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272278 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 35681445 |
The ROS, including superoxide anion, hydrogen peroxide, and nitric oxide, play both beneficial and detrimental roles depending upon their levels and cellular microenvironment. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SOD3 | up-regulates quantity
chemical modification
|
hydrogen peroxide |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272273 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29301787 |
Oxidative stress contributes to diabetes mellitus (DM)–induced endothelial dysfunction, which is one of the most common causes of cardiovascular morbidity and mortality.1,2 The major cellular defense against superoxide (O2•−) is SODs (superoxide dismutases), which consists of the SOD1 (cytoplasmic copper zinc SOD [Cu/ZnSOD]), the SOD2 (mitochondrial MnSOD), and the SOD3 (extracellular Cu/ZnSOD). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
4.0
hydrogen peroxide