Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10293)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
USP7
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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Transferrin receptor protein 1 (TFRC) [Driver; 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/Driver | ||||
Responsed Disease | Ischemia/reperfusion injury | ICD-11: DB98 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Ubiquitin mediated proteolysis | hsa04120 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
CHO-S/H9C2 cells | Normal | Cricetulus griseus | CVCL_A0TS | |
In Vivo Model |
Male Sprague-Dawley (SD) rats (250-300 g) were purchased from the Laboratory Animal Center, Xiangya School of Medicine, Central South University, China. Briefly, a left thoracotomy was carried out in the fourth intercostal space and the heart was exposed via opening the pericardium. The left coronary artery was around via a 4-0 silk suture and a snare was formed by passing both ends of the suture via a short polyethylene tubing. Blockage of the coronary artery was conducted via clamping the snare against the heart surface. Reperfusion was performed by release of the snare. The sham group conducted the same procedure but without ischemia (the snare was not tightened). To establish the I/R injury model, the rat hearts were subjected to 1 h-ischemia plus 3 h-reperfusion.
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Response regulation | A novel pathway of USP7/p53/TfR1 has been identified in the ischemia/reperfusion (I/R)-treated rat hearts, where up-regulation of USP7 promotes ferrptosis via activation of the p53/TfR1 pathway. | ||||
Heme oxygenase 1 (HMOX1) [Driver; Suppressor]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [2] | ||||
Target for Ferroptosis | Driver/Suppressor | ||||
Responsed Disease | Spinal cord injury | ICD-11: ND51 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Ubiquitin mediated proteolysis | hsa04120 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
rSCs (Rat spinal cords) | ||||
In Vivo Model |
Forty-eight adult female Sprague-Dawley rats weighing 200-220 g were purchased from Hunan SJA Laboratory Animal Co., Ltd. (Hunan, China) and divided into the following eight groups: sham (n = 6), SCI (n = 6), SCI + lentivirus (LV)-negative control 1 (NC1) (n = 6), SCI + LV-HMOX-1 (n = 6), SCI + LV-NC2 (n = 6), SCI + LV-USP7 (n = 6), SCI + LV-USP7 + sh-NC (n = 6), and SCI + LV-USP7 + sh-HMOX-1 (n = 6) groups. One week after animal adaptation and 30 min before operation, a subcutaneous injection of buprenorphine (0.05 mg/kg) was administered to the rats, along with inhalation of 5% isoflurane and an intraperitoneal injection of ketamine (75 mg/kg) and thiazide (10 mg/kg).
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Response regulation | In spinal cord injury (SCI) rats, USP7 directly bound to HMOX-1 and its overexpression promoted HMOX-1 expression via deubiquitination. To sum up, USP7 overexpression facilitated the expression of HMOX-1 through deubiquitination, thereby reducing ferroptosis and alleviating SCI. | ||||
Ischemia/reperfusion injury [ICD-11: DB98]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Ubiquitin carboxyl-terminal hydrolase 7 (USP7) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Ubiquitin mediated proteolysis | hsa04120 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
CHO-S/H9C2 cells | Normal | Cricetulus griseus | CVCL_A0TS | |
In Vivo Model |
Male Sprague-Dawley (SD) rats (250-300 g) were purchased from the Laboratory Animal Center, Xiangya School of Medicine, Central South University, China. Briefly, a left thoracotomy was carried out in the fourth intercostal space and the heart was exposed via opening the pericardium. The left coronary artery was around via a 4-0 silk suture and a snare was formed by passing both ends of the suture via a short polyethylene tubing. Blockage of the coronary artery was conducted via clamping the snare against the heart surface. Reperfusion was performed by release of the snare. The sham group conducted the same procedure but without ischemia (the snare was not tightened). To establish the I/R injury model, the rat hearts were subjected to 1 h-ischemia plus 3 h-reperfusion.
Click to Show/Hide
|
||||
Response regulation | A novel pathway of USP7/p53/TfR1 has been identified in the ischemia/reperfusion (I/R)-treated rat hearts, where up-regulation of USP7 promotes ferrptosis via activation of the p53/TfR1 pathway. | ||||
Spinal cord injury [ICD-11: ND51]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [2] | ||||
Target Regulator | Ubiquitin carboxyl-terminal hydrolase 7 (USP7) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Ubiquitin mediated proteolysis | hsa04120 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
rSCs (Rat spinal cords) | ||||
In Vivo Model |
Forty-eight adult female Sprague-Dawley rats weighing 200-220 g were purchased from Hunan SJA Laboratory Animal Co., Ltd. (Hunan, China) and divided into the following eight groups: sham (n = 6), SCI (n = 6), SCI + lentivirus (LV)-negative control 1 (NC1) (n = 6), SCI + LV-HMOX-1 (n = 6), SCI + LV-NC2 (n = 6), SCI + LV-USP7 (n = 6), SCI + LV-USP7 + sh-NC (n = 6), and SCI + LV-USP7 + sh-HMOX-1 (n = 6) groups. One week after animal adaptation and 30 min before operation, a subcutaneous injection of buprenorphine (0.05 mg/kg) was administered to the rats, along with inhalation of 5% isoflurane and an intraperitoneal injection of ketamine (75 mg/kg) and thiazide (10 mg/kg).
Click to Show/Hide
|
||||
Response regulation | In spinal cord injury (SCI) rats, USP7 directly bound to HMOX-1 and its overexpression promoted HMOX-1 expression via deubiquitination. To sum up, USP7 overexpression facilitated the expression of HMOX-1 through deubiquitination, thereby reducing ferroptosis and alleviating SCI. | ||||
References