General Information of the Ferroptosis Regulator (ID: REG10097)
Regulator Name Beta-enolase (ENO3)
Synonyms
2-phospho-D-glycerate hydro-lyase; Enolase 3; Muscle-specific enolase; Skeletal muscle enolase
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Gene Name ENO3
Gene ID 2027
Regulator Type Protein coding
Uniprot ID P13929
Sequence
MAMQKIFAREILDSRGNPTVEVDLHTAKGRFRAAVPSGASTGIYEALELRDGDKGRYLGK
GVLKAVENINNTLGPALLQKKLSVVDQEKVDKFMIELDGTENKSKFGANAILGVSLAVCK
AGAAEKGVPLYRHIADLAGNPDLILPVPAFNVINGGSHAGNKLAMQEFMILPVGASSFKE
AMRIGAEVYHHLKGVIKAKYGKDATNVGDEGGFAPNILENNEALELLKTAIQAAGYPDKV
VIGMDVAASEFYRNGKYDLDFKSPDDPARHITGEKLGELYKSFIKNYPVVSIEDPFDQDD
WATWTSFLSGVNIQIVGDDLTVTNPKRIAQAVEKKACNCLLLKVNQIGSVTESIQACKLA
QSNGWGVMVSHRSGETEDTFIADLVVGLCTGQIKTGAPCRSERLAKYNQLMRIEEALGDK
AIFAGRKFRNPKAK

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Family Enolase family
Function
Glycolytic enzyme that catalyzes the conversion of 2- phosphoglycerate to phosphoenolpyruvate. Appears to have a function in striated muscle development and regeneration.

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HGNC ID
HGNC:3354
KEGG ID hsa:2027
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
ENO3 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).
Browse Target
Browse Disease
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 Marker/Suppressor
Responsed Disease Nonalcoholic fatty liver disease ICD-11: DB92
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
L-02 cells Endocervical adenocarcinoma Homo sapiens CVCL_6926
In Vivo Model
Eight-week-old C57BL/6 mice, body weight about 22-24 g, male (n = 24) were purchased from Beijing Vital River Laboratory Animal Technology Co. Ltd China. The mice were randomly divided into four groups and were maintained on a MCD diet (Medicience, Yangzhou, China) for 4, 8, and 12 weeks to induce NASH. Liver tissue and blood samples (from the eyeballs of the mice) were harvested for further analyses. Mice on a normal diet were used as the control.

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Response regulation ENO3 promoted the progression of NASH by negatively regulating ferroptosis via elevating GPX4 expression and lipid accumulation. These findings provided solid foundation for the mechanism of ferroptosis on the progression of NASH regulated by ENO3, suggesting that ENO3 may be a potential therapeutic target for non-alcoholic fatty liver disease.
Nonalcoholic fatty liver disease [ICD-11: DB92]
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Beta-enolase (ENO3) Protein coding
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
L-02 cells Endocervical adenocarcinoma Homo sapiens CVCL_6926
In Vivo Model
Eight-week-old C57BL/6 mice, body weight about 22-24 g, male (n = 24) were purchased from Beijing Vital River Laboratory Animal Technology Co. Ltd China. The mice were randomly divided into four groups and were maintained on a MCD diet (Medicience, Yangzhou, China) for 4, 8, and 12 weeks to induce NASH. Liver tissue and blood samples (from the eyeballs of the mice) were harvested for further analyses. Mice on a normal diet were used as the control.

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Response regulation ENO3 promoted the progression of NASH by negatively regulating ferroptosis via elevating GPX4 expression and lipid accumulation. These findings provided solid foundation for the mechanism of ferroptosis on the progression of NASH regulated by ENO3, suggesting that ENO3 may be a potential therapeutic target for non-alcoholic fatty liver disease.
References
Ref 1 ENO3 promoted the progression of NASH by negatively regulating ferroptosis via elevation of GPX4 expression and lipid accumulation. Ann Transl Med. 2021 Apr;9(8):661. doi: 10.21037/atm-21-471.