Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10182)
Regulator Name Coatomer subunit zeta-1 (COPZ1)
Synonyms
COPZ; Zeta-1-coat protein
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Gene Name COPZ1
Gene ID 22818
Regulator Type Protein coding
Uniprot ID P61923
Sequence
MEALILEPSLYTVKAILILDNDGDRLFAKYYDDTYPSVKEQKAFEKNIFNKTHRTDSEIA
LLEGLTVVYKSSIDLYFYVIGSSYENELMLMAVLNCLFDSLSQMLRKNVEKRALLENMEG
LFLAVDEIVDGGVILESDPQQVVHRVALRGEDVPLTEQTVSQVLQSAKEQIKWSLLR

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Family Adaptor complexes small subunit family
Function
The coatomer is a cytosolic protein complex that binds to dilysine motifs and reversibly associates with Golgi non-clathrin- coated vesicles, which further mediate biosynthetic protein transport from the ER, via the Golgi up to the trans Golgi network. Coatomer complex is required for budding from Golgi membranes, and is essential for the retrograde Golgi-to-ER transport of dilysine-tagged proteins. The zeta subunit may be involved in regulating the coat assembly and, hence, the rate of biosynthetic protein transport due to its association-dissociation properties with the coatomer complex.

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HGNC ID
HGNC:2243
KEGG ID hsa:22818
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
COPZ1 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
Nuclear receptor coactivator 4 (NCOA4) [Driver]
 Target Info 
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Driver
Responsed Disease Glioblastoma ICD-11: 2A00
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
Cell proliferation
In Vitro Model
 U-87MG cells Glioblastoma Homo sapiens CVCL_GP63
U-251MG cells Astrocytoma Homo sapiens CVCL_0021
A-172 cells Glioblastoma Homo sapiens CVCL_0131
LN-229 cells Glioblastoma Homo sapiens CVCL_0393
T98 cells Glioblastoma Homo sapiens CVCL_B368
In Vivo Model
Mice were divided into two groups (10 mice per group) and anesthetized with an intraperitoneal injection (80 uL) containing ketamine HCl (25 mg/mL), xylazine (2.5 mg/mL), and 14.25% ethyl alcohol (diluted 1:3 in 0.9% NaCl). U87MG-NC and U87MG-sh-COPZ1#1 glioma cells (106 cells diluted in 10 uL PBS per animal) were injected into the right frontal lobes of each mouse using the following coordinates: 1 mm anterior and 2.5 mm lateral to the bregma, at a depth of 2 mm.

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Response regulation COPZ1 knockdown also led to the increase in nuclear receptor coactivator 4 (NCOA4), resulting in the degradation of ferritin, and a subsequent increase in the intracellular levels of ferrous iron and ultimately ferroptosis.The COPZ1/NCOA4/FTH1 axis is therefore a novel therapeutic target for the treatment of human glioblastoma.
Glioblastoma [ICD-11: 2A00]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Coatomer subunit zeta-1 (COPZ1) Protein coding
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
Cell proliferation
In Vitro Model
 U-87MG cells Glioblastoma Homo sapiens CVCL_GP63
U-251MG cells Astrocytoma Homo sapiens CVCL_0021
A-172 cells Glioblastoma Homo sapiens CVCL_0131
LN-229 cells Glioblastoma Homo sapiens CVCL_0393
T98 cells Glioblastoma Homo sapiens CVCL_B368
In Vivo Model
Mice were divided into two groups (10 mice per group) and anesthetized with an intraperitoneal injection (80 uL) containing ketamine HCl (25 mg/mL), xylazine (2.5 mg/mL), and 14.25% ethyl alcohol (diluted 1:3 in 0.9% NaCl). U87MG-NC and U87MG-sh-COPZ1#1 glioma cells (106 cells diluted in 10 uL PBS per animal) were injected into the right frontal lobes of each mouse using the following coordinates: 1 mm anterior and 2.5 mm lateral to the bregma, at a depth of 2 mm.

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Response regulation COPZ1 knockdown also led to the increase in nuclear receptor coactivator 4 (NCOA4), resulting in the degradation of ferritin, and a subsequent increase in the intracellular levels of ferrous iron and ultimately ferroptosis.The COPZ1/NCOA4/FTH1 axis is therefore a novel therapeutic target for the treatment of human glioblastoma.
References
Ref 1 Loss of COPZ1 induces NCOA4 mediated autophagy and ferroptosis in glioblastoma cell lines. Oncogene. 2021 Feb;40(8):1425-1439. doi: 10.1038/s41388-020-01622-3. Epub 2021 Jan 8.