General Information of the Ferroptosis Regulator (ID: REG10088)
Regulator Name Thioredoxin (TXN)
Synonyms
TRDX, TRX, TRX1; ATL-derived factor; Surface-associated sulphydryl protein; Allergen=Hom s Trx
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Gene Name TXN
Gene ID 7295
Regulator Type Protein coding
Uniprot ID P10599
Sequence
MVKQIESKTAFQEALDAAGDKLVVVDFSATWCGPCKMIKPFFHSLSEKYSNVIFLEVDVD
DCQDVASECEVKCMPTFQFFKKGQKVGEFSGANKEKLEATINELV

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Family Thioredoxin family
Function
Participates in various redox reactions through the reversible oxidation of its active center dithiol to a disulfide and catalyzes dithiol-disulfide exchange reactions. Plays a role in the reversible S- nitrosylation of cysteine residues in target proteins, and thereby contributes to the response to intracellular nitric oxide. Nitrosylates the active site Cys of CASP3 in response to nitric oxide (NO), and thereby inhibits caspase-3 activity. Induces the FOS/JUN AP-1 DNA-binding activity in ionizing radiation (IR) cells through its oxidation/reduction status and stimulates AP-1 transcriptional activity. { | | | | | | | }.; ADF augments the expression of the interleukin-2 receptor TAC (IL2R/P55).

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HGNC ID
HGNC:12435
KEGG ID hsa:7295
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
TXN 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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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 Parkinson disease ICD-11: 8A00
Responsed Drug Cyperquat Investigative
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model
PC12 cells Adrenal gland pheochromocytoma Rattus norvegicus CVCL_0481
SH-SY5Y cells Neuroblastoma Homo sapiens CVCL_0019
In Vivo Model
Male C57BL/6 mice wild-type (WT), 8 weeks of age, were from Chongqing Medical University, China. Mice were divided into four groups (n = 10-13 per group), control group, MPTP group, h-Trx-1 Tg group, and h-Trx-1 Tg + MPTP group. Control and h-Trx-1 Tg groups were administered saline only. For the Trx-1 knockdown experiment, mice were divided into six groups (n = 10-13 per group), control + saline group, control + MPTP group, AAV9-vehicle + saline group, AAV9-vehicle + MPTP group, AAV9-shRNA-mTrx-1 + saline group, and AAV9-shRNA-mTrx-1 + MPTP.

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Response regulation 1-methyl-4-phenylpyridinium (Cyperquat) decreased cell viability, GPX4, and Trx-1 (TXN). The decreased GPX4 and GSH, and increased ROS were inhibited by Fer-1 and Trx-1 overexpression. Trx-1 reversed the decreases of GPX4 and tyrosine hydroxylase (TH) induced by MPTP in the substantia nigra pars compacta (SNpc). Trx-1 inhibits ferroptosis in parkinson's disease through regulating GPX4 and GSH.
Parkinson disease [ICD-11: 8A00]
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Thioredoxin (TXN) Protein coding
Responsed Drug Cyperquat Investigative
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model
PC12 cells Adrenal gland pheochromocytoma Rattus norvegicus CVCL_0481
SH-SY5Y cells Neuroblastoma Homo sapiens CVCL_0019
In Vivo Model
Male C57BL/6 mice wild-type (WT), 8 weeks of age, were from Chongqing Medical University, China. Mice were divided into four groups (n = 10-13 per group), control group, MPTP group, h-Trx-1 Tg group, and h-Trx-1 Tg + MPTP group. Control and h-Trx-1 Tg groups were administered saline only. For the Trx-1 knockdown experiment, mice were divided into six groups (n = 10-13 per group), control + saline group, control + MPTP group, AAV9-vehicle + saline group, AAV9-vehicle + MPTP group, AAV9-shRNA-mTrx-1 + saline group, and AAV9-shRNA-mTrx-1 + MPTP.

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Response regulation 1-methyl-4-phenylpyridinium (Cyperquat) decreased cell viability, GPX4, and Trx-1 (TXN). The decreased GPX4 and GSH, and increased ROS were inhibited by Fer-1 and Trx-1 overexpression. Trx-1 reversed the decreases of GPX4 and tyrosine hydroxylase (TH) induced by MPTP in the substantia nigra pars compacta (SNpc). Trx-1 inhibits ferroptosis in parkinson's disease through regulating GPX4 and GSH.
Cyperquat [Investigative]
In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Inducer
Response Target Phospholipid hydroperoxide glutathione peroxidase (GPX4) Suppressor
Responsed Disease Parkinson disease ICD-11: 8A00
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model
PC12 cells Adrenal gland pheochromocytoma Rattus norvegicus CVCL_0481
SH-SY5Y cells Neuroblastoma Homo sapiens CVCL_0019
In Vivo Model
Male C57BL/6 mice wild-type (WT), 8 weeks of age, were from Chongqing Medical University, China. Mice were divided into four groups (n = 10-13 per group), control group, MPTP group, h-Trx-1 Tg group, and h-Trx-1 Tg + MPTP group. Control and h-Trx-1 Tg groups were administered saline only. For the Trx-1 knockdown experiment, mice were divided into six groups (n = 10-13 per group), control + saline group, control + MPTP group, AAV9-vehicle + saline group, AAV9-vehicle + MPTP group, AAV9-shRNA-mTrx-1 + saline group, and AAV9-shRNA-mTrx-1 + MPTP.

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Response regulation 1-methyl-4-phenylpyridinium (Cyperquat) decreased cell viability, GPX4, and Trx-1 (TXN). The decreased GPX4 and GSH, and increased ROS were inhibited by Fer-1 and Trx-1 overexpression. Trx-1 reversed the decreases of GPX4 and tyrosine hydroxylase (TH) induced by MPTP in the substantia nigra pars compacta (SNpc). Trx-1 inhibits ferroptosis in parkinson's disease through regulating GPX4 and GSH.
References
Ref 1 Thioredoxin-1 Rescues MPP(+)/MPTP-Induced Ferroptosis by Increasing Glutathione Peroxidase 4. Mol Neurobiol. 2021 Jul;58(7):3187-3197. doi: 10.1007/s12035-021-02320-1. Epub 2021 Feb 26.