Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10452)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
SRSF1
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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Nuclear factor erythroid 2-related factor 2 (NFE2L2) [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 | Glioblastoma | ICD-11: 2A00 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
LN-229 cells | Glioblastoma | Homo sapiens | CVCL_0393 | |
| U-251MG cells | Astrocytoma | Homo sapiens | CVCL_0021 | ||
| hACs (Normal human astrocyte cells) | |||||
| In Vivo Model |
BALB/c nude mice (female, four-week-old) were purchased from the Nanjing Medical University Experimental Animal Department. Female mice were randomly divided into test group and control group. 2.5 x 105 LN229/TMZ cells transfected with sh-MAPK8-1 or sh-LINC01564-1 were injected into the brain of mice in test group, taking the mice injected with sh-NC-transfected ones as control. Seven days later, the mice were treated with TMZ (66 mg/kg per day, 5 days/cycle, 4 cycles in total) as a monotherapy. Tumor volume was monitored every three days in the period of TMZ treatment. The mice were killed 28 days after the injection. Tumors were excised from mice for observation and weighing as well as the detection of the level of ROS, iron (Fe2+) and proteins (i.e., NFE2L2, NQO1, FTH1 and HO-1).
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| Response regulation | LINC01564 promotes the temozolomide (TMZ) resistance of glioma cells by upregulating NFE2L2 expression to inhibit ferroptosis. LINC01564 promotes MAPK8 mRNA stability by recruiting SRSF1, and MAPK8 was positively correlated with NFE2L2 and its targets, proving its mediation of NFE2L2. | ||||
Long-chain-fatty-acid--CoA ligase 4 (ACSL4) [Driver]
| In total 1 item(s) under this target | |||||
| Experiment 1 Reporting the Ferroptosis Target of This Regulator | [2] | ||||
| Target for Ferroptosis | Driver | ||||
| Responsed Disease | Ischemia/reperfusion injury | ICD-11: DB98 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
HK-2 cells | Normal | Homo sapiens | CVCL_0302 | |
| In Vivo Model |
Mouse renal I/R model was performed in male C57BL/6 mice (8-12 weeks old). Briefly, the mice were anesthetized with pentobarbital sodium by intraperitoneal injection and lay on the right side. Dorsal incisions of both left and right sides were made to expose kidneys. The right kidney artery was gently separated with cotton swabs and occluded with a microvascular clamp to induce renal ischemia for 45 min. The left renal pedicle clamping and ischemia were the same as right. After ischemia, the micro-aneurysm clips were removed to start the reperfusion. The wounds were sutured and resuscitated with warm sterile saline intraperitoneally. All operations were the same in the sham group except for clamping and ischemia.
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| Response regulation | Human urine-derived stem cells (USCs)-derived exosomes (USC-Exo) could improve kidney ischemia/reperfusion injury (IRI). Mechanistically, LncRNA TUG1 was carried by USC-Exo downregulation of ACSL4 expression in kidney cells by interacting with SRSF1, then inhibited ACSL4-mediated cell ferroptosis, and thus improved kidney injury in IRI-induced AKI. | ||||
Glioblastoma [ICD-11: 2A00]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | Serine/arginine-rich splicing factor 1 (SRSF1) | Protein coding | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
LN-229 cells | Glioblastoma | Homo sapiens | CVCL_0393 | |
| U-251MG cells | Astrocytoma | Homo sapiens | CVCL_0021 | ||
| hACs (Normal human astrocyte cells) | |||||
| In Vivo Model |
BALB/c nude mice (female, four-week-old) were purchased from the Nanjing Medical University Experimental Animal Department. Female mice were randomly divided into test group and control group. 2.5 x 105 LN229/TMZ cells transfected with sh-MAPK8-1 or sh-LINC01564-1 were injected into the brain of mice in test group, taking the mice injected with sh-NC-transfected ones as control. Seven days later, the mice were treated with TMZ (66 mg/kg per day, 5 days/cycle, 4 cycles in total) as a monotherapy. Tumor volume was monitored every three days in the period of TMZ treatment. The mice were killed 28 days after the injection. Tumors were excised from mice for observation and weighing as well as the detection of the level of ROS, iron (Fe2+) and proteins (i.e., NFE2L2, NQO1, FTH1 and HO-1).
Click to Show/Hide
|
||||
| Response regulation | LINC01564 promotes the temozolomide (TMZ) resistance of glioma cells by upregulating NFE2L2 expression to inhibit ferroptosis. LINC01564 promotes MAPK8 mRNA stability by recruiting SRSF1, and MAPK8 was positively correlated with NFE2L2 and its targets, proving its mediation of NFE2L2. | ||||
Ischemia/reperfusion injury [ICD-11: DB98]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [2] | ||||
| Target Regulator | Serine/arginine-rich splicing factor 1 (SRSF1) | Protein coding | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
HK-2 cells | Normal | Homo sapiens | CVCL_0302 | |
| In Vivo Model |
Mouse renal I/R model was performed in male C57BL/6 mice (8-12 weeks old). Briefly, the mice were anesthetized with pentobarbital sodium by intraperitoneal injection and lay on the right side. Dorsal incisions of both left and right sides were made to expose kidneys. The right kidney artery was gently separated with cotton swabs and occluded with a microvascular clamp to induce renal ischemia for 45 min. The left renal pedicle clamping and ischemia were the same as right. After ischemia, the micro-aneurysm clips were removed to start the reperfusion. The wounds were sutured and resuscitated with warm sterile saline intraperitoneally. All operations were the same in the sham group except for clamping and ischemia.
Click to Show/Hide
|
||||
| Response regulation | Human urine-derived stem cells (USCs)-derived exosomes (USC-Exo) could improve kidney ischemia/reperfusion injury (IRI). Mechanistically, LncRNA TUG1 was carried by USC-Exo downregulation of ACSL4 expression in kidney cells by interacting with SRSF1, then inhibited ACSL4-mediated cell ferroptosis, and thus improved kidney injury in IRI-induced AKI. | ||||
References