Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10425)
Regulator Name NADPH oxidase 5 (NOX5)
Gene Name NOX5
Gene ID 79400
Regulator Type Protein coding
Uniprot ID Q96PH1
Sequence
MNTSGDPAQTGPEGCRGTMSAEEDARWLRWVTQQFKTIAGEDGEISLQEFKAALHVKESF
FAERFFALFDSDRSGTITLQELQEALTLLIHGSPMDKLKFLFQVYDIDVCARQGASAGTE
WGAGAGPHWASSPLGTGSGSIDPDELRTVLQSCLRESAISLPDEKLDQLTLALFESADAD
GNGAITFEELRDELQRFPGVMENLTISAAHWLTAPAPRPRPRRPRQLTRAYWHNHRSQLF
CLATYAGLHVLLFGLAASAHRDLGASVMVAKGCGQCLNFDCSFIAVLMLRRCLTWLRATW
LAQVLPLDQNIQFHQLMGYVVVGLSLVHTVAHTVNFVLQAQAEASPFQFWELLLTTRPGI
GWVHGSASPTGVALLLLLLLMFICSSSCIRRSGHFEVFYWTHLSYLLVWLLLIFHGPNFW
KWLLVPGILFFLEKAIGLAVSRMAAVCIMEVNLLPSKVTHLLIKRPPFFHYRPGDYLYLN
IPTIARYEWHPFTISSAPEQKDTIWLHIRSQGQWTNRLYESFKASDPLGRGSKRLSRSVT
MRKSQRSSKGSEILLEKHKFCNIKCYIDGPYGTPTRRIFASEHAVLIGAGIGITPFASIL
QSIMYRHQKRKHTCPSCQHSWIEGVQDNMKLHKVDFIWINRDQRSFEWFVSLLTKLEMDQ
AEEAQYGRFLELHMYMTSALGKNDMKAIGLQMALDLLANKEKKDSITGLQTRTQPGRPDW
SKVFQKVAAEKKGKVQVFFCGSPALAKVLKGHCEKFGFRFFQENF

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Function
Calcium-dependent NADPH oxidase that generates superoxide. Also functions as a calcium-dependent proton channel and may regulate redox-dependent processes in lymphocytes and spermatozoa. May play a role in cell growth and apoptosis. Isoform v2 and isoform v5 are involved in endothelial generation of reactive oxygen species (ROS), proliferation and angiogenesis and contribute to endothelial response to thrombin.

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HGNC ID
HGNC:14874
KEGG ID hsa:79400
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
NOX5 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
Browse Drug
Unspecific Target [Unspecific Target]
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Responsed Disease Rhabdomyosarcoma ICD-11: 2B55
 Disease Info 
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 regulation 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-a and b-selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX, including NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
Rhabdomyosarcoma [ICD-11: 2B55]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator NADPH oxidase 5 (NOX5) Protein coding
 Regulator Info 
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 regulation 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-a and b-selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX, including NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
Diphenyleneiodonium [Investigative]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Suppressor
Response Target Unspecific Target
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 regulation 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-a and b-selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX, including NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
References
Ref 1 Targeting ferroptosis in rhabdomyosarcoma cells. Int J Cancer. 2020 Jan 15;146(2):510-520. doi: 10.1002/ijc.32496. Epub 2019 Jul 4.