PTGES
Prostaglandin E synthase
Also known as: MGST-IV, MGST1-L1, MGST1L1, PIG12, PTGES_HUMAN, TP53I12
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- O14684
- Gene
- PTGES
- Ensembl
- ENSG00000148344
- Chromosome
- 9
- Canonical length
- 152 aa
- Protein class
- Enzymes, Metabolic proteins, Predicted membrane proteins
- Subcellular location
- Endoplasmic reticulum
- Quaternary structure
- Homotrimer
OverviewNCBI Gene
The protein encoded by this gene is a glutathione-dependent prostaglandin E synthase. The expression of this gene has been shown to be induced by proinflammatory cytokine interleukin 1 beta (IL1B). Its expression can also be induced by tumor suppressor protein TP53, and may be involved in TP53 induced apoptosis. Knockout studies in mice suggest that this gene may contribute to the pathogenesis of collagen-induced arthritis and mediate acute pain during inflammatory responses. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
152 residues, UniProt reviewed canonical sequence.
>O14684|PTGES
1 MPAHSLVMSS PALPAFLLCS TLLVIKMYVV AIITGQVRLR KKAFANPEDA LRHGGPQYCR
61 SDPDVERCLR AHRNDMETIY PFLFLGFVYS FLGPNPFVAW MHFLVFLVGR VAHTVAYLGK
121 LRAPIRSVTY TLAQLPCASM ALQILWEAAR HLLocalizationUniProt · AlphaFold · HPA
Whether an antibody against PTGES 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
- 4
- Mean surface accessibility (rSASA)
- 0.31
- Highest tissue expression
- 80 nTPM
Expression across tissuesHPA
Tissue
- seminal vesicle: 80 nTPM
- urinary bladder: 73 nTPM
- placenta: 55 nTPM
- parathyroid gland: 40 nTPM
- skin: 39 nTPM
- adipose tissue: 35 nTPM
Single-cell type
- extravillous trophoblasts: 406 nCPM
- migrating cytotrophoblasts: 327 nCPM
- syncytiotrophoblasts: 318 nCPM
- cytotrophoblasts: 144 nCPM
- ocular epithelial cells: 121 nCPM
- salivary duct cells: 119 nCPM
Immune cell
- basophil: 29 nTPM
- non-classical monocyte: 4.1 nTPM
- intermediate monocyte: 2.2 nTPM
- neutrophil: 1.9 nTPM
- total PBMC: 0.3 nTPM
- myeloid DC: 0.1 nTPM
Brain region
- pons: 9.4 nTPM
- midbrain: 6.9 nTPM
- medulla oblongata: 6.1 nTPM
- hypothalamus: 4.9 nTPM
- cerebral cortex: 4.2 nTPM
- thalamus: 4.2 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)
- 0.73
- gnomAD pLI
- 0.71
- gnomAD missense Z
- 1.31
- DepMap mean gene effect
- 0.16
- DepMap dependency class
- none
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
- cell population proliferation
- cyclooxygenase pathway
- negative regulation of cell population proliferation
- positive regulation of prostaglandin secretion
- prostaglandin biosynthetic process
- prostaglandin metabolic process
- regulation of fever generation
- regulation of inflammatory response
- sensory perception of pain
- signal transduction
Molecular functions
- glutathione binding
- glutathione peroxidase activity
- glutathione transferase activity
- prostaglandin-D synthase activity
- prostaglandin-E synthase activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads PTGES as an antibody target. Whether an autoantibody or antibody against PTGES could matter depends on whether native PTGES is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
PTGES 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 PTGES as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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