Ferroptosis Target Information

General Information of the Ferroptosis Target (ID: TAR10036)
Target Name NADPH oxidase 1 (NOX1)
Synonyms
Mitogenic oxidase 1; NADH/NADPH mitogenic oxidase subunit P65-MOX; NOH-1
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Gene Name NOX1
Sequence
MGNWVVNHWFSVLFLVVWLGLNVFLFVDAFLKYEKADKYYYTRKILGSTLACARASALCL
NFNSTLILLPVCRNLLSFLRGTCSFCSRTLRKQLDHNLTFHKLVAYMICLHTAIHIIAHL
FNFDCYSRSRQATDGSLASILSSLSHDEKKGGSWLNPIQSRNTTVEYVTFTSIAGLTGVI
MTIALILMVTSATEFIRRSYFEVFWYTHHLFIFYILGLGIHGIGGIVRGQTEESMNESHP
RKCAESFEMWDDRDSHCRRPKFEGHPPESWKWILAPVILYICERILRFYRSQQKVVITKV
VMHPSKVLELQMNKRGFSMEVGQYIFVNCPSISLLEWHPFTLTSAPEEDFFSIHIRAAGD
WTENLIRAFEQQYSPIPRIEVDGPFGTASEDVFQYEVAVLVGAGIGVTPFASILKSIWYK
FQCADHNLKTKKIYFYWICRETGAFSWFNNLLTSLEQEMEELGKVGFLNYRLFLTGWDSN
IVGHAALNFDKATDIVTGLKQKTSFGRPMWDNEFSTIATSHPKSVVGVFLCGPRTLAKSL
RKCCHRYSSLDPRKVQFYFNKENF

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Function
NOH-1S is a voltage-gated proton channel that mediates the H(+) currents of resting phagocytes and other tissues. It participates in the regulation of cellular pH and is blocked by zinc. NOH-1L is a pyridine nucleotide-dependent oxidoreductase that generates superoxide and might conduct H(+) ions as part of its electron transport mechanism, whereas NOH-1S does not contain an electron transport chain.

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Gene ID 27035
Uniprot ID
Q9Y5S8
Target Type Driver Suppressor Marker
Mechanism Diagram Click to View the Original Diagram
Tissue Relative Abundances of This Target
Full List of Regulator(s) of This Ferroptosis Target and Corresponding Disease/Drug Response(s)
NOX1 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.
Browse Regulator related Disease
Browse Regulator related Drug
NAD-dependent protein deacetylase sirtuin-1 (SIRT1)
 Regulator Info 
Kidney injury [ICD-11: NB92]
In total 1 item(s) under this disease
 Disease Info 
Experiment 1 Reporting the Ferroptosis-centered Disease Response of This Regulator [1]
Regulator for Ferroptosis Suppressor
Responsed Drug Cadmium Investigative
 Drug Info 
Pathway Response Ferroptosis hsa04216
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model
 PC12 cells Adrenal gland pheochromocytoma Rattus norvegicus CVCL_0481
Response Description CdCl2-initiated injury was found to result from the induction of not only apoptosis but also ferroptosis, as evidenced by the increased iron content, ROS production, and mitochondrial membrane potential along with changes in the expressions of iron death-related genes (FTH1, GPX4, ASCL4, PTGS2, and NOX1) and levels of caspase9, Bax, and Bcl-2 proteins. It is possible that the damage caused by cadmium results from the induced ferroptosis and apoptosis via the miR-34a-5p/ Sirt1 axis.
hsa-miR-34a-5p (miRNA)
 Regulator Info 
Kidney injury [ICD-11: NB92]
In total 1 item(s) under this disease
 Disease Info 
Experiment 1 Reporting the Ferroptosis-centered Disease Response of This Regulator [1]
Regulator for Ferroptosis Driver
Responsed Drug Cadmium Investigative
 Drug Info 
Pathway Response Ferroptosis hsa04216
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model
 PC12 cells Adrenal gland pheochromocytoma Rattus norvegicus CVCL_0481
Response Description CdCl2-initiated injury was found to result from the induction of not only apoptosis but also ferroptosis, as evidenced by the increased iron content, ROS production, and mitochondrial membrane potential along with changes in the expressions of iron death-related genes (FTH1, GPX4, ASCL4, PTGS2, and NOX1) and levels of caspase9, Bax, and Bcl-2 proteins. It is possible that the damage caused by cadmium results from the induced ferroptosis and apoptosis via the miR-34a-5p/Sirt1 axis.
Unspecific Regulator
Rhabdomyosarcoma [ICD-11: 2B55]
In total 2 item(s) under this disease
 Disease Info 
Experiment 1 Reporting the Ferroptosis-centered Disease Response of This Regulator [2]
Responsed Drug Diphenyleneiodonium Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response Description Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC- and -selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
Experiment 2 Reporting the Ferroptosis-centered Disease Response of This Regulator [2]
Responsed Drug GKT137831 Phase 2
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response Description Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC- and -selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
NAD-dependent protein deacetylase sirtuin-1 (SIRT1)
 Regulator Info 
Cadmium [Investigative]
In total 1 item(s) under this drug
 Drug Info 
Experiment 1 Reporting the Ferroptosis-centered Drug Response of This Regulator [1]
Regulator for Ferroptosis Suppressor
Responsed Disease Kidney injury [ICD-11: NB92]
 Disease Info 
Pathway Response Ferroptosis hsa04216
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model PC12 cells Adrenal gland pheochromocytoma Rattus norvegicus CVCL_0481
Response Description CdCl2-initiated injury was found to result from the induction of not only apoptosis but also ferroptosis, as evidenced by the increased iron content, ROS production, and mitochondrial membrane potential along with changes in the expressions of iron death-related genes (FTH1, GPX4, ASCL4, PTGS2, and NOX1) and levels of caspase9, Bax, and Bcl-2 proteins. It is possible that the damage caused by cadmium results from the induced ferroptosis and apoptosis via the miR-34a-5p/ Sirt1 axis.
hsa-miR-34a-5p (miRNA)
 Regulator Info 
Cadmium [Investigative]
In total 1 item(s) under this drug
 Drug Info 
Experiment 1 Reporting the Ferroptosis-centered Drug Response of This Regulator [1]
Regulator for Ferroptosis Driver
Responsed Disease Kidney injury [ICD-11: NB92]
 Disease Info 
Pathway Response Ferroptosis hsa04216
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model PC12 cells Adrenal gland pheochromocytoma Rattus norvegicus CVCL_0481
Response Description CdCl2-initiated injury was found to result from the induction of not only apoptosis but also ferroptosis, as evidenced by the increased iron content, ROS production, and mitochondrial membrane potential along with changes in the expressions of iron death-related genes (FTH1, GPX4, ASCL4, PTGS2, and NOX1) and levels of caspase9, Bax, and Bcl-2 proteins. It is possible that the damage caused by cadmium results from the induced ferroptosis and apoptosis via the miR-34a-5p/Sirt1 axis.
Unspecific Regulator
Diphenyleneiodonium [Investigative]
In total 1 item(s) under this drug
 Drug Info 
Experiment 1 Reporting the Ferroptosis-centered Drug Response of This Regulator [2]
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response Description Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC- and -selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
GKT137831 [Phase 2]
In total 1 item(s) under this drug
 Drug Info 
Experiment 1 Reporting the Ferroptosis-centered Drug Response of This Regulator [2]
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response Description Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC- and -selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
References
Ref 1 Cadmium induces ferroptosis and apoptosis by modulating miR-34a-5p/Sirt1axis in PC12 cells. Environ Toxicol. 2022 Jan;37(1):41-51. doi: 10.1002/tox.23376. Epub 2021 Sep 24.
Ref 2 Targeting ferroptosis in rhabdomyosarcoma cells. Int J Cancer. 2020 Jan 15;146(2):510-520. doi: 10.1002/ijc.32496. Epub 2019 Jul 4.