Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10113)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
TRIM21
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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Phospholipid hydroperoxide glutathione peroxidase (GPX4) [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 kidney failure | ICD-11: GB60 | |||
Responsed Drug | Fedratinib | Investigative | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
HK-2 cells | Normal | Homo sapiens | CVCL_0302 | |
In Vivo Model |
Mice were fasted for 12 h and anesthetized (1% pentobarbital sodium, i.p.) before surgery. Bilateral renal pedicles were clamped for 30 min, then remove the arterial clamps. The sham groups were treated in the same way, except for the clamping of the renal pedicle. Blood samples were collected 24 h after reperfusion, mice were killed, and kidney were collected for follow-up experiments. Fedratinib (5 mg/kg body weight) was injected (i.p.) into mice 24 h once in advance before surgery.
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Response regulation | A JAK2 inhibitor Fedratinib downregulated TRIM21 expression and reduced damage both in vivo and in vitro, which is correlated with the upregulation of GPX4. Our study showed that loss of TRIM21 could alleviate ferroptosis induced by I/R, revealed the mechanism of ubiquitination degradation of GPX4 by TRIM21 and suggested TRIM21 is a potential target for the treatment of acute kidney injury (AKI). | ||||
Acute kidney failure [ICD-11: GB60]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | E3 ubiquitin-protein ligase TRIM21 (TRIM21) | Protein coding | |||
Responsed Drug | Fedratinib | Investigative | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
HK-2 cells | Normal | Homo sapiens | CVCL_0302 | |
In Vivo Model |
Mice were fasted for 12 h and anesthetized (1% pentobarbital sodium, i.p.) before surgery. Bilateral renal pedicles were clamped for 30 min, then remove the arterial clamps. The sham groups were treated in the same way, except for the clamping of the renal pedicle. Blood samples were collected 24 h after reperfusion, mice were killed, and kidney were collected for follow-up experiments. Fedratinib (5 mg/kg body weight) was injected (i.p.) into mice 24 h once in advance before surgery.
Click to Show/Hide
|
||||
Response regulation | A JAK2 inhibitor Fedratinib downregulated TRIM21 expression and reduced damage both in vivo and in vitro, which is correlated with the upregulation of GPX4. Our study showed that loss of TRIM21 could alleviate ferroptosis induced by I/R, revealed the mechanism of ubiquitination degradation of GPX4 by TRIM21 and suggested TRIM21 is a potential target for the treatment of acute kidney injury (AKI). | ||||
Fedratinib
[Investigative]
In total 1 item(s) under this drug | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Response | [1] | ||||
Drug for Ferroptosis | Suppressor | ||||
Response Target | Phospholipid hydroperoxide glutathione peroxidase (GPX4) | Suppressor | |||
Responsed Disease | Acute kidney failure | ICD-11: GB60 | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
HK-2 cells | Normal | Homo sapiens | CVCL_0302 | |
In Vivo Model |
Mice were fasted for 12 h and anesthetized (1% pentobarbital sodium, i.p.) before surgery. Bilateral renal pedicles were clamped for 30 min, then remove the arterial clamps. The sham groups were treated in the same way, except for the clamping of the renal pedicle. Blood samples were collected 24 h after reperfusion, mice were killed, and kidney were collected for follow-up experiments. Fedratinib (5 mg/kg body weight) was injected (i.p.) into mice 24 h once in advance before surgery.
Click to Show/Hide
|
||||
Response regulation | A JAK2 inhibitor Fedratinib downregulated TRIM21 expression and reduced damage both in vivo and in vitro, which is correlated with the upregulation of GPX4. Our study showed that loss of TRIM21 could alleviate ferroptosis induced by I/R, revealed the mechanism of ubiquitination degradation of GPX4 by TRIM21 and suggested TRIM21 is a potential target for the treatment of acute kidney injury (AKI). | ||||