GSTA5
Glutathione S-transferase A5
Also known as: GSTA5_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q7RTV2
- Gene
- GSTA5
- Ensembl
- ENSG00000182793
- Chromosome
- 6
- Canonical length
- 222 aa
- Protein class
- Enzymes, Metabolic proteins, Predicted intracellular proteins
- Subcellular location
- Cytosol
- Quaternary structure
- Homodimer
OverviewNCBI Gene
The glutathione S-transferases (GST; EC 2.5.1.18) catalyze the conjugation of reduced glutathiones and a variety of electrophiles, including many known carcinogens and mutagens. The cytosolic GSTs belong to a large superfamily, with members located on different chromosomes. For additional information on GSTs, see GSTA1 (MIM 138359).[supplied by OMIM, Sep 2008]
Canonical amino-acid sequenceUniProt
222 residues, UniProt reviewed canonical sequence.
>Q7RTV2|GSTA5
1 MAEKPKLHYS NARGSMESIR WLLAAAGVEL EEKFLESAED LDKLRNDGSL LFQQVPMVEI
61 DGMKLVQTRA ILNYIASKYN LYGKDMKERA LIDMYTEGIV DLTEMILLLL ICQPEERDAK
121 TALVKEKIKN RYFPAFEKVL KSHRQDYLVG NKLSWADIHL VELFYYVEEL DSSLISSFPL
181 LKALKTRISN LPTVKKFLQP GSQRKPPMDE KSLEEARKIF RFLocalizationUniProt · AlphaFold · HPA
Whether an antibody against GSTA5 can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Intracellular
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.28
- Highest tissue expression
- 0 nTPM
Expression across tissuesHPA
Tissue
- adipose tissue: 0 nTPM
- adrenal gland: 0 nTPM
- amygdala: 0 nTPM
- appendix: 0 nTPM
- basal ganglia: 0 nTPM
- blood vessel: 0 nTPM
Single-cell type
- conjunctival goblet cells: 2.9 nCPM
- endometrial secretory cells: 1 nCPM
- breast lactating cells: 0.8 nCPM
- early primary spermatocytes: 0.8 nCPM
- ocular epithelial cells: 0.5 nCPM
- transitional alveolar cells: 0.4 nCPM
Immune cell
- basophil: 0 nTPM
- classical monocyte: 0 nTPM
- eosinophil: 0 nTPM
- gdT-cell: 0 nTPM
- intermediate monocyte: 0 nTPM
- MAIT T-cell: 0 nTPM
Brain region
- amygdala: 0 nTPM
- basal ganglia: 0 nTPM
- cerebellum: 0 nTPM
- cerebral cortex: 0 nTPM
- choroid plexus: 0 nTPM
- hippocampal formation: 0 nTPM
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 1.91
- gnomAD pLI
- 0
- gnomAD missense Z
- -1.36
- DepMap mean gene effect
- -0.05
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Glutathione S-transferase, alpha class
- Glutathione S-transferase, N-terminal
- Glutathione S-transferase, C-terminal
- Glutathione S-transferase, C-terminal-like
- Thioredoxin-like superfamily
- Glutathione S-transferase, C-terminal domain superfamily
- Glutathione transferase family
- Glutathione S-transferase superfamily
- Glutathione S-transferase, C-terminal domain
- Glutathione S-transferase, N-terminal domain
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of GSTA5 in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads GSTA5 as an antibody target. Whether an autoantibody or antibody against GSTA5 could matter depends on whether native GSTA5 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
GSTA5 is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.
Annotation status
The present source text does not explicitly label GSTA5 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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