PRDX3
Thioredoxin-dependent peroxide reductase, mitochondrial
Also known as: AOP-1, AOP1, MER5, PRDX3_HUMAN, SP-22
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P30048
- Gene
- PRDX3
- Ensembl
- ENSG00000165672
- Chromosome
- 10
- Canonical length
- 256 aa
- Protein class
- Disease related genes, Enzymes, Human disease related genes, Metabolic proteins, Plasma proteins, Potential drug targets, Predicted intracellular proteins
- Subcellular location
- Vesicles,Mitochondria
- Quaternary structure
- Homodimer
OverviewNCBI Gene
This gene encodes a mitochondrial protein with antioxidant function. The protein is similar to the C22 subunit of Salmonella typhimurium alkylhydroperoxide reductase, and it can rescue bacterial resistance to alkylhydroperoxide in E. coli that lack the C22 subunit. The human and mouse genes are highly conserved, and they map to the regions syntenic between mouse and human chromosomes. Sequence comparisons with recently cloned mammalian homologs suggest that these genes consist of a family that is responsible for the regulation of cellular proliferation, differentiation and antioxidant functions. This family member can protect cells from oxidative stress, and it can promote cell survival in prostate cancer. Alternative splicing of this gene results in multiple transcript variants. Related pseudogenes have been identified on chromosomes 1, 3, 13 and 22. [provided by RefSeq, Oct 2014]
Canonical amino-acid sequenceUniProt
256 residues, UniProt reviewed canonical sequence.
>P30048|PRDX3
1 MAAAVGRLLR ASVARHVSAI PWGISATAAL RPAACGRTSL TNLLCSGSSQ AKLFSTSSSC
61 HAPAVTQHAP YFKGTAVVNG EFKDLSLDDF KGKYLVLFFY PLDFTFVCPT EIVAFSDKAN
121 EFHDVNCEVV AVSVDSHFSH LAWINTPRKN GGLGHMNIAL LSDLTKQISR DYGVLLEGSG
181 LALRGLFIID PNGVIKHLSV NDLPVGRSVE ETLRLVKAFQ YVETHGEVCP ANWTPDSPTI
241 KPSPAASKEY FQKVNQLocalizationUniProt · AlphaFold · HPA
Whether an antibody against PRDX3 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)
- 0.38
- Highest tissue expression
- 534 nTPM
Expression across tissuesHPA
Tissue
- liver: 534 nTPM
- tongue: 376 nTPM
- kidney: 360 nTPM
- skeletal muscle: 352 nTPM
- adrenal gland: 323 nTPM
- heart muscle: 260 nTPM
Single-cell type
- parietal cells: 612 nCPM
- hepatocytes: 436 nCPM
- cytotrophoblasts: 372 nCPM
- gastric progenitor cells: 353 nCPM
- migrating cytotrophoblasts: 347 nCPM
- hofbauer cells: 280 nCPM
Immune cell
- total PBMC: 510 nTPM
- classical monocyte: 430 nTPM
- myeloid DC: 382 nTPM
- intermediate monocyte: 370 nTPM
- non-classical monocyte: 335 nTPM
- eosinophil: 248 nTPM
Brain region
- choroid plexus: 153 nTPM
- hypothalamus: 79 nTPM
- white matter: 75 nTPM
- cerebellum: 72 nTPM
- spinal cord: 70 nTPM
- thalamus: 68 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about PRDX3.
Disease | AllUniProt
Conditions PRDX3 is implicated in, by any mechanism.
- Spinocerebellar ataxia, autosomal recessive, 32 (SCAR32) MIM:619862
- Corneal dystrophy, punctiform and polychromatic pre-Descemet (PPPCD) MIM:619871
Disease | GeneticClinVar
10 pathogenic / likely-pathogenic of 68 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Spinocerebellar ataxia, autosomal recessive 32
- Corneal dystrophy, punctiform and polychromatic pre-descemet
- Autosomal recessive cerebellar ataxia
Disease | ImmuneIEDB
Conditions an epitope on PRDX3 was assayed in.
- skin melanoma T cell
ReferencesPubMed · IEDB
Publications for PRDX3 from three distinct lines of evidence, kept separate because they answer different questions: whether antibodies are directed at the protein, whether a B-cell epitope has been mapped on it, and whether a T-cell epitope has. Each is labelled with its source.
Reference: AutoantibodyPubMed
1 publication
- Anti-retinal pigment epithelium antibodies in acute exudative polymorphous vitelliform maculopathy: a new hypothesis about disease pathogenesis.
2011 · Arch Ophthalmol · RCR 2.4 · 55 citations
Reference: T cellIEDB
1 publication
- Durable Complete Response from Metastatic Melanoma after Transfer of Autologous T Cells Recognizing 10 Mutated Tumor Antigens.
2016 · Cancer Immunol Res · RCR 2.8 · 107 citations
Sources: PubMed — antigen-level antibody evidence from a custom retrieval. Records matching a controlled set of autoantibody terms (the MeSH descriptors Autoantibodies and Autoantigens, with title and abstract term variants) were obtained through NCBI E-utilities, and their titles and abstracts parsed for constructions that direct an antibody at a named protein rather than for co-occurrence. Captured names were resolved against UniProt nomenclature and each antigen adjudicated individually against the source text. IEDB — curated epitope assays from the Immune Epitope Database (Vita et al., Nucleic Acids Research 2019). Bibliographic records from PubMed and MeSH, U.S. National Library of Medicine; citation metrics from NIH iCite (Hutchins et al., PLoS Biology 2016). Titles link to PubMed; abstracts are not reproduced here. The NLM does not endorse this analysis.
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)
- 0.88
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.06
- DepMap mean gene effect
- -0.2
- 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
- cell redox homeostasis
- cellular response to oxidative stress
- cellular response to reactive oxygen species
- hydrogen peroxide catabolic process
- maternal placenta development
- mitochondrion organization
- myeloid cell differentiation
- negative regulation of apoptotic process
- negative regulation of kinase activity
- positive regulation of cell population proliferation
- positive regulation of NF-kappaB transcription factor activity
- regulation of mitochondrial membrane potential
- response to hydrogen peroxide
- response to lipopolysaccharide
- response to oxidative stress
Molecular functions
- cysteine-type endopeptidase inhibitor activity involved in apoptotic process
- identical protein binding
- protein kinase binding
- thioredoxin peroxidase activity
- NADH-dependent peroxiredoxin activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of PRDX3 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 PRDX3 as an antibody target. Whether an autoantibody or antibody against PRDX3 could matter depends on whether native PRDX3 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
PRDX3 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 PRDX3 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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