Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10346)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
PROK2
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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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 | [1] | ||||
| Target for Ferroptosis | Driver | ||||
| Responsed Disease | Traumatic brain injury | ICD-11: NA07 | |||
| Pathway Response | Ubiquitin mediated proteolysis | hsa04120 | |||
| Fatty acid metabolism | hsa01212 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
rPCNs (Rat primary cortical neurons) | ||||
| hBCs (Brain cells) | |||||
| In Vivo Model |
Eight-week-old male mice were subjected to severe CCI. Anesthesia was induced with 3% isoflurane in nitrous oxide: oxygen (7:3) and maintained with 1.5% isoflurane via nose cone. Temperature was maintained at 37 ± 0.5 using a heating blanket. After anesthesia, mice were placed in a stereotaxic frame (R.W.D. Shenzhen, China). A 4-mm-diameter craniotomy was performed over the left parietal bone and the bone flap was removed for trauma. A vertically directed CCI was applied (6.0 ± 0.2 m/s, 50 ms dwell time, 1.4 mm depth) using an impactor (R.W.D., Shenzhen, China). After the injury, the skin incision was closed. Mice were monitored with supplemental oxygen (100%) for 1h before returning to their cages. Fer-1 (1 mg/kg per day) was given i.p. at 7 days before CCI and once daily until euthanasia or the MWM test. Before the brain tissues were obtained, mice were perfused intracardially with 4 phosphate-buffer saline (PBS) solution.
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| Response regulation | Prok2 mediates neuronal cell deaths in traumatic brain injury via ferroptosis. Prok2 prevents neuronal cell death by suppressing the biosynthesis of lipid peroxidation substrates, arachidonic acid-phospholipids, via accelerated F-box only protein 10 (Fbxo10)-driven ubiquitination, degradation of long-chain-fatty-acid-CoA ligase 4 (Acsl4), and inhibition of lipid peroxidation. | ||||
Traumatic brain injury [ICD-11: NA07]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | Prokineticin-2 (PROK2) | Protein coding | |||
| Pathway Response | Ubiquitin mediated proteolysis | hsa04120 | |||
| Fatty acid metabolism | hsa01212 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
rPCNs (Rat primary cortical neurons) | ||||
| hBCs (Brain cells) | |||||
| In Vivo Model |
Eight-week-old male mice were subjected to severe CCI. Anesthesia was induced with 3% isoflurane in nitrous oxide: oxygen (7:3) and maintained with 1.5% isoflurane via nose cone. Temperature was maintained at 37 ± 0.5 using a heating blanket. After anesthesia, mice were placed in a stereotaxic frame (R.W.D. Shenzhen, China). A 4-mm-diameter craniotomy was performed over the left parietal bone and the bone flap was removed for trauma. A vertically directed CCI was applied (6.0 ± 0.2 m/s, 50 ms dwell time, 1.4 mm depth) using an impactor (R.W.D., Shenzhen, China). After the injury, the skin incision was closed. Mice were monitored with supplemental oxygen (100%) for 1h before returning to their cages. Fer-1 (1 mg/kg per day) was given i.p. at 7 days before CCI and once daily until euthanasia or the MWM test. Before the brain tissues were obtained, mice were perfused intracardially with 4 phosphate-buffer saline (PBS) solution.
Click to Show/Hide
|
||||
| Response regulation | Prok2 mediates neuronal cell deaths in traumatic brain injury via ferroptosis. Prok2 prevents neuronal cell death by suppressing the biosynthesis of lipid peroxidation substrates, arachidonic acid-phospholipids, via accelerated F-box only protein 10 (Fbxo10)-driven ubiquitination, degradation of long-chain-fatty-acid-CoA ligase 4 (Acsl4), and inhibition of lipid peroxidation. | ||||