General Information of the Ferroptosis Regulator (ID: REG10186)
Regulator Name 60S ribosomal protein L8 (RPL8)
Synonyms
Large ribosomal subunit protein uL2
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Gene Name RPL8
Gene ID 6132
Regulator Type Protein coding
Uniprot ID P62917
Sequence
MGRVIRGQRKGAGSVFRAHVKHRKGAARLRAVDFAERHGYIKGIVKDIIHDPGRGAPLAK
VVFRDPYRFKKRTELFIAAEGIHTGQFVYCGKKAQLNIGNVLPVGTMPEGTIVCCLEEKP
GDRGKLARASGNYATVISHNPETKKTRVKLPSGSKKVISSANRAVVGVVAGGGRIDKPIL
KAGRAYHKYKAKRNCWPRVRGVAMNPVEHPFGGGNHQHIGKPSTIRRDAPAGRKVGLIAA
RRTGRLRGTKTVQEKEN

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Family Universal ribosomal protein uL2 family
Function
Component of the large ribosomal subunit. The ribosome is a large ribonucleoprotein complex responsible for the synthesis of proteins in the cell.

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HGNC ID
HGNC:10368
KEGG ID hsa:6132
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
RPL8 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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Unspecific Target [Unspecific Target]
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Responsed Disease Intracerebral hemorrhage ICD-11: 8B00
Responsed Drug Rotenone Approved
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
hBCs (Brain cells)
In Vivo Model
Six-to-eight week old male ICR mice were purchased from the Experimental Animal Center of the Chinese Academy of Sciences (Shanghai, China). All animal procedures have been approved by the Institutional Animal Care and Use Committee of Ruijin hospital, Shanghai Jiao Tong University (Shanghai, China). Efforts were made as much as possible to reduce the number of mice used and to minimize suffering. Herein, a total of 51 mice were randomly divided into 3 groups: (i) sham group (n = 15), (ii) ICH group (n = 18), and (iii) ICH + Rot group (n = 18). To be specific, the current study was divided into two parts of the experimental design. Part 1: to observe the effects of Rot on the mitochondria-related genes, iron levels, MDA levels, SOD activity, hematoma volume, brain edema, and ultrastructural changes of mitochondria, animals were randomly divided into the sham group (n = 9), ICH group (n = 12), and ICH + Rot group (n = 12). All mice were euthanized at 3 d after operation and brain samples were harvested, as per our previously described reports. Part 2: to observe the effect of Rot on neurological deficits following ICH, 18 mice were randomly divided into additional 3 groups (sham group, ICH group, and ICH + Rot group). We evaluated mNSS scores at 1, 3, 7, and 14 days after ICH. We also assessed the memory function with the MWM test at 14 days after ICH.

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Response regulation Intracerebral hemorrhage induced significant mitochondrial dysfunction and that mitochondrial inhibitor rotenone can trigger and enhance neuronal ferroptosis. The ferroptosis protein markers ACSL4, COX-2, xCT, RPL8, and GPX4 were significantly upregulated in the hemin group. Rot treatment further enhanced hemin-induced upregulation of ACSL4, COX-2, xCT, RPL8, and GPX4 levels.
Intracerebral hemorrhage [ICD-11: 8B00]
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator 60S ribosomal protein L8 (RPL8) Protein coding
Responsed Drug Rotenone Approved
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
hBCs (Brain cells)
In Vivo Model
Six-to-eight week old male ICR mice were purchased from the Experimental Animal Center of the Chinese Academy of Sciences (Shanghai, China). All animal procedures have been approved by the Institutional Animal Care and Use Committee of Ruijin hospital, Shanghai Jiao Tong University (Shanghai, China). Efforts were made as much as possible to reduce the number of mice used and to minimize suffering. Herein, a total of 51 mice were randomly divided into 3 groups: (i) sham group (n = 15), (ii) ICH group (n = 18), and (iii) ICH + Rot group (n = 18). To be specific, the current study was divided into two parts of the experimental design. Part 1: to observe the effects of Rot on the mitochondria-related genes, iron levels, MDA levels, SOD activity, hematoma volume, brain edema, and ultrastructural changes of mitochondria, animals were randomly divided into the sham group (n = 9), ICH group (n = 12), and ICH + Rot group (n = 12). All mice were euthanized at 3 d after operation and brain samples were harvested, as per our previously described reports. Part 2: to observe the effect of Rot on neurological deficits following ICH, 18 mice were randomly divided into additional 3 groups (sham group, ICH group, and ICH + Rot group). We evaluated mNSS scores at 1, 3, 7, and 14 days after ICH. We also assessed the memory function with the MWM test at 14 days after ICH.

    Click to Show/Hide
Response regulation Intracerebral hemorrhage induced significant mitochondrial dysfunction and that mitochondrial inhibitor rotenone can trigger and enhance neuronal ferroptosis. The ferroptosis protein markers ACSL4, COX-2, xCT, RPL8, and GPX4 were significantly upregulated in the hemin group. Rot treatment further enhanced hemin-induced upregulation of ACSL4, COX-2, xCT, RPL8, and GPX4 levels.
Rotenone [Approved]
In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Inducer
Response Target Unspecific Target
Responsed Disease Intracerebral hemorrhage ICD-11: 8B00
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
hBCs (Brain cells)
In Vivo Model
Six-to-eight week old male ICR mice were purchased from the Experimental Animal Center of the Chinese Academy of Sciences (Shanghai, China). All animal procedures have been approved by the Institutional Animal Care and Use Committee of Ruijin hospital, Shanghai Jiao Tong University (Shanghai, China). Efforts were made as much as possible to reduce the number of mice used and to minimize suffering. Herein, a total of 51 mice were randomly divided into 3 groups: (i) sham group (n = 15), (ii) ICH group (n = 18), and (iii) ICH + Rot group (n = 18). To be specific, the current study was divided into two parts of the experimental design. Part 1: to observe the effects of Rot on the mitochondria-related genes, iron levels, MDA levels, SOD activity, hematoma volume, brain edema, and ultrastructural changes of mitochondria, animals were randomly divided into the sham group (n = 9), ICH group (n = 12), and ICH + Rot group (n = 12). All mice were euthanized at 3 d after operation and brain samples were harvested, as per our previously described reports. Part 2: to observe the effect of Rot on neurological deficits following ICH, 18 mice were randomly divided into additional 3 groups (sham group, ICH group, and ICH + Rot group). We evaluated mNSS scores at 1, 3, 7, and 14 days after ICH. We also assessed the memory function with the MWM test at 14 days after ICH.

    Click to Show/Hide
Response regulation Intracerebral hemorrhage induced significant mitochondrial dysfunction and that mitochondrial inhibitor rotenone can trigger and enhance neuronal ferroptosis. The ferroptosis protein markers ACSL4, COX-2, xCT, RPL8, and GPX4 were significantly upregulated in the hemin group. Rot treatment further enhanced hemin-induced upregulation of ACSL4, COX-2, xCT, RPL8, and GPX4 levels.
References
Ref 1 Mitochondrial Inhibitor Rotenone Triggers and Enhances Neuronal Ferroptosis Following Intracerebral Hemorrhage. ACS Chem Neurosci. 2023 Mar 15;14(6):1071-1079. doi: 10.1021/acschemneuro.2c00308. Epub 2023 Feb 27.