Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10257)
Regulator Name Acyl-coenzyme A thioesterase 1 (ACOT1)
Synonyms
CTE1; CTE-I; CTE-Ib; Inducible cytosolic acyl-coenzyme A thioester hydrolase; Long chain acyl-CoA thioester hydrolase; Palmitoyl-coenzyme A thioesterase
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Gene Name ACOT1
Gene ID 641371
Regulator Type Protein coding
Uniprot ID Q86TX2
Sequence
MAATLILEPAGRCCWDEPVRIAVRGLAPEQPVTLRASLRDEKGALFQAHARYRADTLGEL
DLERAPALGGSFAGLEPMGLLWALEPEKPLVRLVKRDVRTPLAVELEVLDGHDPDPGRLL
CRVRHERYFLPPGVRREPVRAGRVRGTLFLPPEPGPFPGIVDMFGTGGGLLEYRASLLAG
KGFAVMALAYYNYEDLPKTMETLHLEYFEEAVNYLLSHPEVKGPGVGLLGISKGGELCLS
MASFLKGITAAVVINGSVANVGGTLRYKGETLPPVGVNRNRIKVTKDGYADIVDVLNSPL
EGPDQKSFIPVERAESTFLFLVGQDDHNWKSEFYANEACKRLQAHGRRKPQIICYPETGH
YIEPPYFPLCRASLHALVGSPIIWGGEPRAHAMAQVDAWKQLQTFFHKHLGGHEGTIPSK
V

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Family C/M/P thioester hydrolase family
Function
Catalyzes the hydrolysis of acyl-CoAs into free fatty acids and coenzyme A (CoASH), regulating their respective intracellular levels. More active towards saturated and unsaturated long chain fatty acyl-CoAs (C12-C20).

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HGNC ID
HGNC:33128
KEGG ID hsa:641371
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
ACOT1 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 Cardiomyopathy ICD-11: BC43
 Disease Info 
Responsed Drug Doxorubicin Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 HL-1 cells Normal Mus musculus CVCL_0303
In Vivo Model
C57BL/6 male mice (20-25 g) at 7 weeks were purchased from the Vital River Laboratory Animal Technology Co., Ltd. Two doses of DOX was administrated by intraperitoneal injection, 15 mg/kg at Day 1, and 10 mg/kg at Day 8. Mice were then killed at Day 15 after transthoracic echocardiography examination.

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Response regulation Both in vitro and in vivo experiments proved the downregulation of Acot1 in doxorubicin-induced cardiotoxicity (DIC), which can be partially prevented with Fer-1 treatment. Acot1 may become a potential treating target in preventing doxorubicin-induced cardiotoxicity by anti-ferroptosis.
Cardiomyopathy [ICD-11: BC43]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Acyl-coenzyme A thioesterase 1 (ACOT1) Protein coding
 Regulator Info 
Responsed Drug Doxorubicin Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 HL-1 cells Normal Mus musculus CVCL_0303
In Vivo Model
C57BL/6 male mice (20-25 g) at 7 weeks were purchased from the Vital River Laboratory Animal Technology Co., Ltd. Two doses of DOX was administrated by intraperitoneal injection, 15 mg/kg at Day 1, and 10 mg/kg at Day 8. Mice were then killed at Day 15 after transthoracic echocardiography examination.

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Response regulation Both in vitro and in vivo experiments proved the downregulation of Acot1 in doxorubicin-induced cardiotoxicity (DIC), which can be partially prevented with Fer-1 treatment. Acot1 may become a potential treating target in preventing doxorubicin-induced cardiotoxicity by anti-ferroptosis.
Doxorubicin [Investigative]
 Drug Info 
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 Cardiomyopathy ICD-11: BC43
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 HL-1 cells Normal Mus musculus CVCL_0303
In Vivo Model
C57BL/6 male mice (20-25 g) at 7 weeks were purchased from the Vital River Laboratory Animal Technology Co., Ltd. Two doses of DOX was administrated by intraperitoneal injection, 15 mg/kg at Day 1, and 10 mg/kg at Day 8. Mice were then killed at Day 15 after transthoracic echocardiography examination.

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Response regulation Both in vitro and in vivo experiments proved the downregulation of Acot1 in doxorubicin-induced cardiotoxicity (DIC), which can be partially prevented with Fer-1 treatment. Acot1 may become a potential treating target in preventing doxorubicin-induced cardiotoxicity by anti-ferroptosis.
References
Ref 1 Acyl-CoA thioesterase 1 prevents cardiomyocytes from Doxorubicin-induced ferroptosis via shaping the lipid composition. Cell Death Dis. 2020 Sep 15;11(9):756. doi: 10.1038/s41419-020-02948-2.