Ferroptosis Target Information
General Information of the Ferroptosis Target (ID: TAR10043)
| Target Name | Diamine acetyltransferase 1 (SAT1) | ||||
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| Synonyms |
Polyamine N-acetyltransferase 1; Putrescine acetyltransferase ; Spermidine/spermine N(1)-acetyltransferase 1
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| Gene Name | SAT1 | ||||
| Sequence |
MAKFVIRPATAADCSDILRLIKELAKYEYMEEQVILTEKDLLEDGFGEHPFYHCLVAEVP
KEHWTPEGHSIVGFAMYYFTYDPWIGKLLYLEDFFVMSDYRGFGIGSEILKNLSQVAMRC RCSSMHFLVAEWNEPSINFYKRRGASDLSSEEGWRLFKIDKEYLLKMATEE Click to Show/Hide
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| Family | Acetyltransferase family | ||||
| Function |
Enzyme which catalyzes the acetylation of polyamines. Substrate specificity: norspermidine = spermidine >> spermine > N(1)- acetylspermine. This highly regulated enzyme allows a fine attenuation of the intracellular concentration of polyamines. Also involved in the regulation of polyamine transport out of cells. Also acts on 1,3- diaminopropane and 1,5-diaminopentane .
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| Gene ID | 6303 | ||||
| Uniprot ID | |||||
| Target Type | Driver Suppressor Marker | ||||
| Mechanism Diagram | Click to View the Original Diagram | ||||
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Tissue Relative Abundances of This Target
Full List of Regulator(s) of This Ferroptosis Target and Corresponding Disease/Drug Response(s)
SAT1 can be involved in and affect the ferroptosis by the following regulators, and result in corresponding disease/drug response(s). You can browse corresponding disease or drug response(s) resulting from the regulation of certain regulators.
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Cellular tumor antigen p53 (TP53)
Neurotoxicity [ICD-11: NE61]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response of This Regulator | [1] | ||||
| Regulator for Ferroptosis | Driver | ||||
| Responsed Drug | Sevoflurane | Approved | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
hBCs (Brain cells) | ||||
| In Vivo Model |
Pregnant rats were placed in a dedicated plastic chamber with ambient gas at a flow rate of 2L/min. Fer-1 solubilized in saline and 1% dimethyl sulfoxide (DMSO) and PD146176 (a specific 15LOX inhibitor) dissolved in corn oil containing 1% DMSO were administered intraperitoneally to rats at a dose of 5 mg/kg 1 h before each exposure, respectively. Similarly, 0.5 mg/kg Ku55933 (an ATM inhibitor), which is diluted in saline containing 1% DMSO, was intraperitoneally administered 2 h previously.
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| Response Description | Sevoflurane could enhance 15LO2-PEBP1 interaction and activate ATM and its downstream P53/SAT1 pathway, which might be attributed to excessive p-ATM nuclear translocation, indicating a potential therapeutic target for ameliorating sevoflurane-induced neurotoxicity. | ||||
E3 ubiquitin-protein ligase RNF113A (RNF113A)
Lung cancer [ICD-11: 2C25]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response of This Regulator | [2] | ||||
| Regulator for Ferroptosis | Suppressor | ||||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Apoptosis | hsa04210 | ||||
| Cell Process | Cell ferroptosis | ||||
| Cell apoptosis | |||||
| Cell proliferation | |||||
In Vitro Model |
A-549 cells | Lung adenocarcinoma | Homo sapiens | CVCL_0023 | |
| NCI-H1975 cells | Lung adenocarcinoma | Homo sapiens | CVCL_1511 | ||
| HEK293 cells | Normal | Homo sapiens | CVCL_0045 | ||
| PCS-201-012 (Human normal dermal fibroblasts) | |||||
| In Vivo Model |
Five millions of control or RNF113A-depleted Cisplatin-resistant A549 cells were transplanted into immunodeficient NOD/SCID 8 weeks old mice. Tumors were grown up to 0.1-0.2 mm3 and mice were then treated with Cisplatin (1 mg/kg) six times every 3 days. Seven mice were used per experimental conditions. No randomization of mice was used.
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| Response Description | RNF113A, whose loss-of-function causes the X-linked trichothiodystrophy, is overexpressed in lung cancer and protects from Cisplatin-dependent cell death. RNF113A deficiency triggers cell death upon DNA damage through multiple mechanisms, including apoptosis via the destabilization of the prosurvival protein MCL-1, ferroptosis due to enhanced SAT1 expression, and increased production of ROS due to altered Noxa1 expression. | ||||
Cellular tumor antigen p53 (TP53)
Sevoflurane
[Approved]
| In total 1 item(s) under this drug | |||||
| Experiment 1 Reporting the Ferroptosis-centered Drug Response of This Regulator | [1] | ||||
| Regulator for Ferroptosis | Driver | ||||
| Responsed Disease | Neurotoxicity [ICD-11: NE61] | ||||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
| In Vitro Model | hBCs (Brain cells) | ||||
| In Vivo Model |
Pregnant rats were placed in a dedicated plastic chamber with ambient gas at a flow rate of 2L/min. Fer-1 solubilized in saline and 1% dimethyl sulfoxide (DMSO) and PD146176 (a specific 15LOX inhibitor) dissolved in corn oil containing 1% DMSO were administered intraperitoneally to rats at a dose of 5 mg/kg 1 h before each exposure, respectively. Similarly, 0.5 mg/kg Ku55933 (an ATM inhibitor), which is diluted in saline containing 1% DMSO, was intraperitoneally administered 2 h previously.
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| Response Description | Sevoflurane could enhance 15LO2-PEBP1 interaction and activate ATM and its downstream P53/SAT1 pathway, which might be attributed to excessive p-ATM nuclear translocation, indicating a potential therapeutic target for ameliorating sevoflurane-induced neurotoxicity. | ||||
References