Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10019)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
BACH1
can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
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Solute carrier family 40 member 1 (SLC40A1) [Suppressor; Marker]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Marker/Suppressor | ||||
Responsed Disease | Acute myocardial infarction | ICD-11: BA41 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell metastasis | |||||
In Vitro Model |
mEFs (Mouse embryonic fibroblasts) | ||||
In Vivo Model |
The generation of Bach1-/-mice on the C57BL/6J background was described previously. Mice 13 weeks of age were analyzed for models of AMI. The mice were subjected to ligation of the proximal LAD to induce AMI. They were randomly assigned to sham or AMI, DMSO, or DFX groups.
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Response regulation | BACH1 accelerates ferroptosis by suppressing labile iron metabolism. And ferritin genes (Fth1 and Ftl1) and the ferroportin gene (Slc40a1) were dramatically up-regulated in Bach1-/- MEFs. BACH1 controls the threshold of ferroptosis induction and may represent a therapeutic target for alleviating ferroptosis-related diseases, including myocardial infarction. | ||||
Ferritin light chain (FTL) [Suppressor]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Acute myocardial infarction | ICD-11: BA41 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell metastasis | |||||
In Vitro Model |
mEFs (Mouse embryonic fibroblasts) | ||||
In Vivo Model |
The generation of Bach1-/-mice on the C57BL/6J background was described previously. Mice 13 weeks of age were analyzed for models of AMI. The mice were subjected to ligation of the proximal LAD to induce AMI. They were randomly assigned to sham or AMI, DMSO, or DFX groups.
Click to Show/Hide
|
||||
Response regulation | BACH1 accelerates ferroptosis by suppressing labile iron metabolism. And ferritin genes (Fth1 and Ftl1) and the ferroportin gene (Slc40a1) were dramatically up-regulated in Bach1-/- MEFs. BACH1 controls the threshold of ferroptosis induction and may represent a therapeutic target for alleviating ferroptosis-related diseases, including myocardial infarction. | ||||
Ferritin heavy chain (FTH1) [Suppressor; Marker]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Marker/Suppressor | ||||
Responsed Disease | Acute myocardial infarction | ICD-11: BA41 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell metastasis | |||||
In Vitro Model |
mEFs (Mouse embryonic fibroblasts) | ||||
In Vivo Model |
The generation of Bach1-/-mice on the C57BL/6J background was described previously. Mice 13 weeks of age were analyzed for models of AMI. The mice were subjected to ligation of the proximal LAD to induce AMI. They were randomly assigned to sham or AMI, DMSO, or DFX groups.
Click to Show/Hide
|
||||
Response regulation | BACH1 accelerates ferroptosis by suppressing labile iron metabolism. And ferritin genes (Fth1 and Ftl1) and the ferroportin gene (Slc40a1) were dramatically up-regulated in Bach1-/- MEFs. BACH1 controls the threshold of ferroptosis induction and may represent a therapeutic target for alleviating ferroptosis-related diseases, including myocardial infarction. | ||||
Acute myocardial infarction [ICD-11: BA41]
In total 3 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Transcription regulator protein BACH1 (BACH1) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell metastasis | |||||
In Vitro Model |
mEFs (Mouse embryonic fibroblasts) | ||||
In Vivo Model |
The generation of Bach1-/-mice on the C57BL/6J background was described previously. Mice 13 weeks of age were analyzed for models of AMI. The mice were subjected to ligation of the proximal LAD to induce AMI. They were randomly assigned to sham or AMI, DMSO, or DFX groups.
Click to Show/Hide
|
||||
Response regulation | BACH1 accelerates ferroptosis by suppressing labile iron metabolism. And ferritin genes (Fth1 and Ftl1) and the ferroportin gene (Slc40a1) were dramatically up-regulated in Bach1-/- MEFs. BACH1 controls the threshold of ferroptosis induction and may represent a therapeutic target for alleviating ferroptosis-related diseases, including myocardial infarction. | ||||
Experiment 2 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Transcription regulator protein BACH1 (BACH1) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell metastasis | |||||
In Vitro Model |
mEFs (Mouse embryonic fibroblasts) | ||||
In Vivo Model |
The generation of Bach1-/-mice on the C57BL/6J background was described previously. Mice 13 weeks of age were analyzed for models of AMI. The mice were subjected to ligation of the proximal LAD to induce AMI. They were randomly assigned to sham or AMI, DMSO, or DFX groups.
Click to Show/Hide
|
||||
Response regulation | BACH1 accelerates ferroptosis by suppressing labile iron metabolism. And ferritin genes (Fth1 and Ftl1) and the ferroportin gene (Slc40a1) were dramatically up-regulated in Bach1-/- MEFs. BACH1 controls the threshold of ferroptosis induction and may represent a therapeutic target for alleviating ferroptosis-related diseases, including myocardial infarction. | ||||
Experiment 3 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Transcription regulator protein BACH1 (BACH1) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell metastasis | |||||
In Vitro Model |
mEFs (Mouse embryonic fibroblasts) | ||||
In Vivo Model |
The generation of Bach1-/-mice on the C57BL/6J background was described previously. Mice 13 weeks of age were analyzed for models of AMI. The mice were subjected to ligation of the proximal LAD to induce AMI. They were randomly assigned to sham or AMI, DMSO, or DFX groups.
Click to Show/Hide
|
||||
Response regulation | BACH1 accelerates ferroptosis by suppressing labile iron metabolism. And ferritin genes (Fth1 and Ftl1) and the ferroportin gene (Slc40a1) were dramatically up-regulated in Bach1-/- MEFs. BACH1 controls the threshold of ferroptosis induction and may represent a therapeutic target for alleviating ferroptosis-related diseases, including myocardial infarction. | ||||