Entity Details

Primary name GPX7_HUMAN
Entity type UniProt
Source Source Link

Details

AccessionQ96SL4
EntryNameGPX7_HUMAN
FullNameGlutathione peroxidase 7
TaxID9606
Evidenceevidence at protein level
Length187
SequenceStatuscomplete
DateCreated2003-08-04
DateModified2021-06-02

Ontological Relatives

GenesGPX7

GO terms

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GOName
GO:0004096 catalase activity
GO:0004601 peroxidase activity
GO:0004602 glutathione peroxidase activity
GO:0005576 extracellular region
GO:0005783 endoplasmic reticulum
GO:0005788 endoplasmic reticulum lumen
GO:0034599 cellular response to oxidative stress

Subcellular Location

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Subcellular Location
Secreted

Domains

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DomainNameCategoryType
IPR000889 Glutathione peroxidaseFamilyFamily
IPR013376 Glutathione peroxidase Gpx7, putativeFamilyFamily
IPR029759 Glutathione peroxidase active siteSiteActive site
IPR029760 Glutathione peroxidase conserved siteSiteConserved site
IPR036249 Thioredoxin-like superfamilyFamilyHomologous superfamily

Diseases

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Disease IDSourceNameDescription
614266 OMIMBarrett esophagus (BE)A condition characterized by a metaplastic change in which normal esophageal squamous epithelium is replaced by a columnar and intestinal-type epithelium. Patients with Barrett esophagus have an increased risk of esophageal adenocarcinoma. The main cause of Barrett esophagus is gastroesophageal reflux. The retrograde movement of acid and bile salts from the stomach into the esophagus causes prolonged injury to the esophageal epithelium and induces chronic esophagitis, which in turn is believed to trigger the pathologic changes. The disease is caused by variants affecting the gene represented in this entry. The pathologic mechanisms leading to Barrett esophagus involve GPX7 dysfunction that results in higher levels of hydrogen peroxide and ROS-induced oxidative stress and DNA damage in esophageal cells.

Drugs

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DrugNameSourceType
DB00143 GlutathioneDrugbanksmall molecule
DB03310 Glutathione disulfideDrugbanksmall molecule