General Information of the Ferroptosis Regulator (ID: REG10435)
Regulator Name Aquaporin-11 (AQP11)
Gene Name AQP11
Gene ID 282679
Regulator Type Protein coding
Uniprot ID Q8NBQ7
Sequence
MSPLLGLRSELQDTCTSLGLMLSVVLLMGLARVVARQQLHRPVAHAFVLEFLATFQLCCC
THELQLLSEQHPAHPTWTLTLVYFFSLVHGLTLVGTSSNPCGVMMQMMLGGMSPETGAVR
LLAQLVSALCSRYCTSALWSLGLTQYHVSERSFACKNPIRVDLLKAVITEAVCSFLFHSA
LLHFQEVRTKLRIHLLAALITFLVYAGGSLTGAVFNPALALSLHFMCFDEAFPQFFIVYW
LAPSLGILLMILMFSFFLPWLHNNHTINKKE

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Family MIP/aquaporin family
Function
Channel protein that facilitates the transport of water, glycerol and hydrogen peroxide across membrane of cell or organelles guaranteeing intracellular homeostasis in several organes like liver, kidney and brain. In situation of stress, participates in endoplasmic reticulum (ER) homeostasis by regulating redox homeostasis through the transport of hydrogen peroxide across the endoplasmic reticulum membrane thereby regulating the oxidative stress through the NADPH oxidase 2 pathway. Plays a role by maintaining an environment suitable for translation or protein foldings in the ER lumen namely by participating in the PKD1 glycosylation processing resulting in regulation of PKD1 membrane trafficking thereby preventing the accumulation of unfolding protein in ER (By similarity). Plays a role in the proximal tubule function by regulating its endosomal acidification (By similarity). May play a role in postnatal kidney development (By similarity).

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HGNC ID
HGNC:19940
KEGG ID hsa:282679
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
AQP11 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
Prostaglandin G/H synthase 2 (PTGS2) [Driver; Marker]
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Marker
Responsed Disease Status epilepticus ICD-11: 8A66
Responsed Drug Penicillamine Approved
Pathway Response Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model
HT22 cells Normal Mus musculus CVCL_0321
In Vivo Model
Male C57BL/6J mice (6-8 weeks of age, weighing 18-22 g) were provided by at the Centre for Animals of Central South University (Changsha, China). To prepare the seizure mouse model, the mice underwent the intrahippocampal injection of KA as described in our previous investigation. For short, mice were anesthetized with sodium phenobarbital (50 mg/kg, i.p.) and carefully placed on a stereotaxic apparatus. Then, KA (1 uL, 250 ng/uL dissolved in saline) was stereotactically injected into the hippocampus according to the following coordinates: anteroposterior -2.0 mm; lateral -1.3 mm; dorsoventral -1.2 mm. After injection, the infusion needle was kept in place for 5-10 min to avoid liquid reflux. Mice in the control group underwent the same surgical procedure but received injection with an equal volume of phosphate buffered saline (PBS) instead of KA.

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Response regulation D-penicillamine (DPA) can be repurposed to cure seizure disorders such as epilepsy. Furthermore, ferroptosis-associated indices including acyl-coA synthetase long chain family member 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (Ptgs2) gene and lipid peroxide (LPO) level were significantly decreased in KA mouse model after DPA treatment. The effects of DPA on ferroptosis process are dependent upon Aqp11.
Long-chain-fatty-acid--CoA ligase 4 (ACSL4) [Driver]
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Driver
Responsed Disease Status epilepticus ICD-11: 8A66
Responsed Drug Penicillamine Approved
Pathway Response Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model
HT22 cells Normal Mus musculus CVCL_0321
In Vivo Model
Male C57BL/6J mice (6-8 weeks of age, weighing 18-22 g) were provided by at the Centre for Animals of Central South University (Changsha, China). To prepare the seizure mouse model, the mice underwent the intrahippocampal injection of KA as described in our previous investigation. For short, mice were anesthetized with sodium phenobarbital (50 mg/kg, i.p.) and carefully placed on a stereotaxic apparatus. Then, KA (1 uL, 250 ng/uL dissolved in saline) was stereotactically injected into the hippocampus according to the following coordinates: anteroposterior -2.0 mm; lateral -1.3 mm; dorsoventral -1.2 mm. After injection, the infusion needle was kept in place for 5-10 min to avoid liquid reflux. Mice in the control group underwent the same surgical procedure but received injection with an equal volume of phosphate buffered saline (PBS) instead of KA.

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Response regulation D-penicillamine can be repurposed to cure seizure disorders such as epilepsy. D-penicillamine reveals the amelioration of seizure-induced neuronal injury via inhibiting Aqp11-dependent ferroptosis. Furthermore, ferroptosis-associated indices including acyl-coA synthetase long chain family member 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (Ptgs2) gene and lipid peroxide (LPO) level were significantly decreased in KA mouse model after DPA treatment.
Status epilepticus [ICD-11: 8A66]
In total 2 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Aquaporin-11 (AQP11) Protein coding
Responsed Drug Penicillamine Approved
Pathway Response Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model
HT22 cells Normal Mus musculus CVCL_0321
In Vivo Model
Male C57BL/6J mice (6-8 weeks of age, weighing 18-22 g) were provided by at the Centre for Animals of Central South University (Changsha, China). To prepare the seizure mouse model, the mice underwent the intrahippocampal injection of KA as described in our previous investigation. For short, mice were anesthetized with sodium phenobarbital (50 mg/kg, i.p.) and carefully placed on a stereotaxic apparatus. Then, KA (1 uL, 250 ng/uL dissolved in saline) was stereotactically injected into the hippocampus according to the following coordinates: anteroposterior -2.0 mm; lateral -1.3 mm; dorsoventral -1.2 mm. After injection, the infusion needle was kept in place for 5-10 min to avoid liquid reflux. Mice in the control group underwent the same surgical procedure but received injection with an equal volume of phosphate buffered saline (PBS) instead of KA.

    Click to Show/Hide
Response regulation D-penicillamine (DPA) can be repurposed to cure seizure disorders such as epilepsy. Furthermore, ferroptosis-associated indices including acyl-coA synthetase long chain family member 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (Ptgs2) gene and lipid peroxide (LPO) level were significantly decreased in KA mouse model after DPA treatment. The effects of DPA on ferroptosis process are dependent upon Aqp11.
Experiment 2 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Aquaporin-11 (AQP11) Protein coding
Responsed Drug Penicillamine Approved
Pathway Response Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model
HT22 cells Normal Mus musculus CVCL_0321
In Vivo Model
Male C57BL/6J mice (6-8 weeks of age, weighing 18-22 g) were provided by at the Centre for Animals of Central South University (Changsha, China). To prepare the seizure mouse model, the mice underwent the intrahippocampal injection of KA as described in our previous investigation. For short, mice were anesthetized with sodium phenobarbital (50 mg/kg, i.p.) and carefully placed on a stereotaxic apparatus. Then, KA (1 uL, 250 ng/uL dissolved in saline) was stereotactically injected into the hippocampus according to the following coordinates: anteroposterior -2.0 mm; lateral -1.3 mm; dorsoventral -1.2 mm. After injection, the infusion needle was kept in place for 5-10 min to avoid liquid reflux. Mice in the control group underwent the same surgical procedure but received injection with an equal volume of phosphate buffered saline (PBS) instead of KA.

    Click to Show/Hide
Response regulation D-penicillamine can be repurposed to cure seizure disorders such as epilepsy. D-penicillamine reveals the amelioration of seizure-induced neuronal injury via inhibiting Aqp11-dependent ferroptosis. Furthermore, ferroptosis-associated indices including acyl-coA synthetase long chain family member 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (Ptgs2) gene and lipid peroxide (LPO) level were significantly decreased in KA mouse model after DPA treatment.
Penicillamine [Approved]
In total 2 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Suppressor
Response Target Prostaglandin G/H synthase 2 (PTGS2) Driver; Marker
Responsed Disease Status epilepticus ICD-11: 8A66
Pathway Response Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model
HT22 cells Normal Mus musculus CVCL_0321
In Vivo Model
Male C57BL/6J mice (6-8 weeks of age, weighing 18-22 g) were provided by at the Centre for Animals of Central South University (Changsha, China). To prepare the seizure mouse model, the mice underwent the intrahippocampal injection of KA as described in our previous investigation. For short, mice were anesthetized with sodium phenobarbital (50 mg/kg, i.p.) and carefully placed on a stereotaxic apparatus. Then, KA (1 uL, 250 ng/uL dissolved in saline) was stereotactically injected into the hippocampus according to the following coordinates: anteroposterior -2.0 mm; lateral -1.3 mm; dorsoventral -1.2 mm. After injection, the infusion needle was kept in place for 5-10 min to avoid liquid reflux. Mice in the control group underwent the same surgical procedure but received injection with an equal volume of phosphate buffered saline (PBS) instead of KA.

    Click to Show/Hide
Response regulation D-penicillamine (DPA) can be repurposed to cure seizure disorders such as epilepsy. Furthermore, ferroptosis-associated indices including acyl-coA synthetase long chain family member 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (Ptgs2) gene and lipid peroxide (LPO) level were significantly decreased in KA mouse model after DPA treatment. The effects of DPA on ferroptosis process are dependent upon Aqp11.
Experiment 2 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Suppressor
Response Target Long-chain-fatty-acid--CoA ligase 4 (ACSL4) Driver
Responsed Disease Status epilepticus ICD-11: 8A66
Pathway Response Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model
HT22 cells Normal Mus musculus CVCL_0321
In Vivo Model
Male C57BL/6J mice (6-8 weeks of age, weighing 18-22 g) were provided by at the Centre for Animals of Central South University (Changsha, China). To prepare the seizure mouse model, the mice underwent the intrahippocampal injection of KA as described in our previous investigation. For short, mice were anesthetized with sodium phenobarbital (50 mg/kg, i.p.) and carefully placed on a stereotaxic apparatus. Then, KA (1 uL, 250 ng/uL dissolved in saline) was stereotactically injected into the hippocampus according to the following coordinates: anteroposterior -2.0 mm; lateral -1.3 mm; dorsoventral -1.2 mm. After injection, the infusion needle was kept in place for 5-10 min to avoid liquid reflux. Mice in the control group underwent the same surgical procedure but received injection with an equal volume of phosphate buffered saline (PBS) instead of KA.

    Click to Show/Hide
Response regulation D-penicillamine can be repurposed to cure seizure disorders such as epilepsy. D-penicillamine reveals the amelioration of seizure-induced neuronal injury via inhibiting Aqp11-dependent ferroptosis. Furthermore, ferroptosis-associated indices including acyl-coA synthetase long chain family member 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (Ptgs2) gene and lipid peroxide (LPO) level were significantly decreased in KA mouse model after DPA treatment.
References
Ref 1 D-Penicillamine Reveals the Amelioration of Seizure-Induced Neuronal Injury via Inhibiting Aqp11-Dependent Ferroptosis. Antioxidants (Basel). 2022 Aug 19;11(8):1602. doi: 10.3390/antiox11081602.