Ferroptosis Target Information
General Information of the Ferroptosis Target (ID: TAR10026)
Target Name | Glutaminase liver isoform, mitochondrial (GLS2) | ||||
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Synonyms |
L-glutaminase; L-glutamine amidohydrolase
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Gene Name | GLS2 | ||||
Sequence |
MRSMKALQKALSRAGSHCGRGGWGHPSRSPLLGGGVRHHLSEAAAQGRETPHSHQPQHQD
HDSSESGMLSRLGDLLFYTIAEGQERIPIHKFTTALKATGLQTSDPRLRDCMSEMHRVVQ ESSSGGLLDRDLFRKCVSSNIVLLTQAFRKKFVIPDFEEFTGHVDRIFEDVKELTGGKVA AYIPQLAKSNPDLWGVSLCTVDGQRHSVGHTKIPFCLQSCVKPLTYAISISTLGTDYVHK FVGKEPSGLRYNKLSLNEEGIPHNPMVNAGAIVVSSLIKMDCNKAEKFDFVLQYLNKMAG NEYMGFSNATFQSEKETGDRNYAIGYYLKEKKCFPKGVDMMAALDLYFQLCSVEVTCESG SVMAATLANGGICPITGESVLSAEAVRNTLSLMHSCGMYDFSGQFAFHVGLPAKSAVSGA ILLVVPNVMGMMCLSPPLDKLGNSHRGTSFCQKLVSLFNFHNYDNLRHCARKLDPRREGA EIRNKTVVNLLFAAYSGDVSALRRFALSAMDMEQKDYDSRTALHVAAAEGHIEVVKFLIE ACKVNPFAKDRWGNIPLDDAVQFNHLEVVKLLQDYQDSYTLSETQAEAAAEALSKENLES MV Click to Show/Hide
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Family | Glutaminase family | ||||
Function |
Plays an important role in the regulation of glutamine catabolism. Promotes mitochondrial respiration and increases ATP generation in cells by catalyzing the synthesis of glutamate and alpha- ketoglutarate. Increases cellular anti-oxidant function via NADH and glutathione production. May play a role in preventing tumor proliferation.
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Gene ID | 27165 | ||||
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)
GLS2 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
hsa-miR-190a-5p (miRNA)
Acute myocardial infarction [ICD-11: BA41]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response of This Regulator | [1] | |||
Regulator for Ferroptosis | Suppressor | |||
Pathway Response | Glutathione metabolism | hsa00480 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
Cell proliferation | ||||
In Vitro Model |
CHO-S/H9C2 cells | Normal | Cricetulus griseus | CVCL_A0TS |
HEK-293T cells | Normal | Homo sapiens | CVCL_0063 | |
Response Description | MiR-190a-5p negatively regulate ferroptosis via directly targeting GLS2 in rat cardiomyocyte H9c2 cells. Forced expression of miR-190a-5p inhibited GLS2, resulting in downregulation of ROS, MDA and Fe2+accumulation. In summary, miR-190a-5p plays an essential role in regulation of ferroptosis of cardiomyocytes and suggest a potential therapeutic target for myocardial infarction. | |||
Double-stranded RNA-specific adenosine deaminase (ADAR)
Glioblastoma [ICD-11: 2A00]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response of This Regulator | [2] | ||||
Regulator for Ferroptosis | Driver | ||||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
U251-TR3 cells | Astrocytoma | Homo sapiens | CVCL_1G29 | |
U-251MG cells | Astrocytoma | Homo sapiens | CVCL_0021 | ||
In Vivo Model |
Nude mice (four-week-old, female, 3/group) were purchased from Model Animal Research Center of Nanjing University. 2.5 x 105 luciferase labeled pcDNA3.1-ATXN8OS/GLS2 were transfected into U251 cells. After 48 h, transfected cells were injected stereotactically into thebrainof nude mice. In the first week after operation, TMZ was given to treat nude mice by oral gavage (66 mg/kg per day for 5 days), with vehicle as control. Bioluminescence imaging (IVIS Spectrum; PerkinElmer, USA) was applied for confirming the formation of intracranial tumor. 28 days late, all the mice were sacrificed. The resected tumors were measure at Lipid ROS and intracellular iron level. The whole experiments were approved by ethic committee of Shanxi Provincial Peoples Hospital.
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Response Description | Rescue experiments indicated that ATXN8OS modulated TMZ-resistance of glioma through GLS2. In conclusion, ATXN8OS mediated ferroptosis and regulated the TMZ-resistance of glioma via ADAR/GLS2 pathway. | ||||
ATXN8OS (IncRNA)
Glioblastoma [ICD-11: 2A00]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response of This Regulator | [2] | ||||
Regulator for Ferroptosis | Driver | ||||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
U251-TR3 cells | Astrocytoma | Homo sapiens | CVCL_1G29 | |
U-251MG cells | Astrocytoma | Homo sapiens | CVCL_0021 | ||
In Vivo Model |
Nude mice (four-week-old, female, 3/group) were purchased from Model Animal Research Center of Nanjing University. 2.5 x 105 luciferase labeled pcDNA3.1-ATXN8OS/GLS2 were transfected into U251 cells. After 48 h, transfected cells were injected stereotactically into thebrainof nude mice. In the first week after operation, TMZ was given to treat nude mice by oral gavage (66 mg/kg per day for 5 days), with vehicle as control. Bioluminescence imaging (IVIS Spectrum; PerkinElmer, USA) was applied for confirming the formation of intracranial tumor. 28 days late, all the mice were sacrificed. The resected tumors were measure at Lipid ROS and intracellular iron level. The whole experiments were approved by ethic committee of Shanxi Provincial Peoples Hospital.
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Response Description | Rescue experiments indicated that ATXN8OS modulated TMZ-resistance of glioma through GLS2. In conclusion, ATXN8OS mediated ferroptosis and regulated the TMZ-resistance of glioma via ADAR/GLS2 pathway. | ||||
Unspecific Regulator
Neurotoxicity [ICD-11: NE61]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response of This Regulator | [3] | ||||
Responsed Drug | Formaldehyde | Investigative | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
HT22 cells | Normal | Mus musculus | CVCL_0321 | |
In Vivo Model |
Sprague-Dawley (SD, weight: 200-220 g) rats were obtained from Hunan SJA laboratory animal company (Changsha, Hunan, China). SD rats were anaesthetized by sodium pentobarbital (45 mg/kg, i.p.) and secured in a stereotaxic frame. The aseptically cannula was implanted into lateral ventricle according to the following coordinates: AP: -1mm; ML: 2 mm; DV: 4 mm. During experiment, the unilateral ventricle of rats was received 2.5 ul FA (0.1, 1, 10 umol) according to the experiment scheme in vivo.
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Response Description | Formaldehyde (FA)-induced neurotoxicity is implicated in neuronal ferroptosis. FA induced cell death in HT22 cells, and upregulated the ferroptosis-associated genes, including Ptgs2 (prostaglandin-endoperoxide synthase 2), GLS2 (glutaminase 2), solute carrier family 1 member 5 (SLC1A5), and solute carrier family 38 member 1 (SLC38A1) in HT22 cells, indicating the inductive role of FA in the ferroptosis of HT22 cells for the formaldehyde-induced neurotoxicity. | ||||
Unspecific Regulator
Formaldehyde
[Investigative]
In total 1 item(s) under this drug | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Response of This Regulator | [3] | ||||
Responsed Disease | Neurotoxicity [ICD-11: NE61] | ||||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model | HT22 cells | Normal | Mus musculus | CVCL_0321 | |
In Vivo Model |
Sprague-Dawley (SD, weight: 200-220 g) rats were obtained from Hunan SJA laboratory animal company (Changsha, Hunan, China). SD rats were anaesthetized by sodium pentobarbital (45 mg/kg, i.p.) and secured in a stereotaxic frame. The aseptically cannula was implanted into lateral ventricle according to the following coordinates: AP: -1mm; ML: 2 mm; DV: 4 mm. During experiment, the unilateral ventricle of rats was received 2.5 ul FA (0.1, 1, 10 umol) according to the experiment scheme in vivo.
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Response Description | Formaldehyde (FA)-induced neurotoxicity is implicated in neuronal ferroptosis. FA induced cell death in HT22 cells, and upregulated the ferroptosis-associated genes, including Ptgs2 (prostaglandin-endoperoxide synthase 2), GLS2 (glutaminase 2), solute carrier family 1 member 5 (SLC1A5), and solute carrier family 38 member 1 (SLC38A1) in HT22 cells, indicating the inductive role of FA in the ferroptosis of HT22 cells for the formaldehyde-induced neurotoxicity. | ||||
References