TXNRD2
Thioredoxin reductase 2, mitochondrial
Also known as: SELZ, TR, TR3, TRXR2, TRXR2_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q9NNW7
- Gene
- TXNRD2
- Ensembl
- ENSG00000184470
- Chromosome
- 22
- Canonical length
- 524 aa
- Protein class
- Disease related genes, Enzymes, Human disease related genes, Metabolic proteins, Plasma proteins, Potential drug targets, Predicted intracellular proteins
- Subcellular location
- Mitochondria,Cytosol
- Quaternary structure
- Homodimer
OverviewNCBI Gene
The protein encoded by this gene belongs to the pyridine nucleotide-disulfide oxidoreductase family, and is a member of the thioredoxin (Trx) system. Three thioredoxin reductase (TrxR) isozymes are found in mammals. TrxRs are selenocysteine-containing flavoenzymes, which reduce thioredoxins, as well as other substrates, and play a key role in redox homoeostasis. This gene encodes a mitochondrial form important for scavenging reactive oxygen species in mitochondria. It functions as a homodimer containing FAD, and selenocysteine (Sec) at the active site. Sec is encoded by UGA codon that normally signals translation termination. The 3' UTRs of selenoprotein mRNAs contain a conserved stem-loop structure, the Sec insertion sequence (SECIS) element, which is necessary for the recognition of UGA as a Sec codon rather than as a stop signal. Alternatively spliced transcript variants encoding different isoforms, including a few localized in the cytosol and some lacking the C-terminal Sec residue, have been found for this gene. [provided by RefSeq, Jun 2017]
Canonical amino-acid sequenceUniProt
524 residues, UniProt reviewed canonical sequence.
>Q9NNW7|TXNRD2
1 MAAMAVALRG LGGRFRWRTQ AVAGGVRGAA RGAAAGQRDY DLLVVGGGSG GLACAKEAAQ
61 LGRKVAVVDY VEPSPQGTRW GLGGTCVNVG CIPKKLMHQA ALLGGLIQDA PNYGWEVAQP
121 VPHDWRKMAE AVQNHVKSLN WGHRVQLQDR KVKYFNIKAS FVDEHTVCGV AKGGKEILLS
181 ADHIIIATGG RPRYPTHIEG ALEYGITSDD IFWLKESPGK TLVVGASYVA LECAGFLTGI
241 GLDTTIMMRS IPLRGFDQQM SSMVIEHMAS HGTRFLRGCA PSRVRRLPDG QLQVTWEDST
301 TGKEDTGTFD TVLWAIGRVP DTRSLNLEKA GVDTSPDTQK ILVDSREATS VPHIYAIGDV
361 VEGRPELTPI AIMAGRLLVQ RLFGGSSDLM DYDNVPTTVF TPLEYGCVGL SEEEAVARHG
421 QEHVEVYHAH YKPLEFTVAG RDASQCYVKM VCLREPPQLV LGLHFLGPNA GEVTQGFALG
481 IKCGASYAQV MRTVGIHPTC SEEVVKLRIS KRSGLDPTVT GCUGLocalizationUniProt · AlphaFold · HPA
Whether an antibody against TXNRD2 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
- Highest tissue expression
- 63 nTPM
Expression across tissuesHPA
Tissue
- liver: 63 nTPM
- adrenal gland: 44 nTPM
- choroid plexus: 31 nTPM
- cerebellum: 29 nTPM
- heart muscle: 29 nTPM
- prostate: 26 nTPM
Single-cell type
- prostatic glandular cells: 94 nCPM
- cytotrophoblasts: 85 nCPM
- myonuclei: 71 nCPM
- hepatocytes: 66 nCPM
- parietal cells: 65 nCPM
- podocytes: 62 nCPM
Immune cell
- classical monocyte: 11 nTPM
- intermediate monocyte: 8.2 nTPM
- non-classical monocyte: 8 nTPM
- myeloid DC: 7.8 nTPM
- eosinophil: 5.8 nTPM
- total PBMC: 4.6 nTPM
Brain region
- choroid plexus: 35 nTPM
- cerebellum: 27 nTPM
- hippocampal formation: 17 nTPM
- cerebral cortex: 17 nTPM
- thalamus: 16 nTPM
- midbrain: 16 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about TXNRD2.
Disease | AllUniProt
Conditions TXNRD2 is implicated in, by any mechanism.
- Glucocorticoid deficiency 5 (GCCD5) MIM:617825
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)
- 0.99
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.64
- DepMap mean gene effect
- -0.1
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 5% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- cell redox homeostasis
- response to hyperoxia
- response to selenium ion
- response to oxygen radical
Molecular functions
- flavin adenine dinucleotide binding
- protein homodimerization activity
- protein-containing complex binding
- thioredoxin-disulfide reductase (NADPH) activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Pyridine nucleotide-disulphide oxidoreductase, class I
- Pyridine nucleotide-disulphide oxidoreductase, dimerisation domain
- Thioredoxin/glutathione reductase selenoprotein
- Pyridine nucleotide-disulphide oxidoreductase, class I, active site
- FAD/NAD-linked reductase, dimerisation domain superfamily
- FAD/NAD(P)-binding domain
- FAD/NAD(P)-binding domain superfamily
- Glutathione reductase/thioredoxin reductase-like
- Pyridine nucleotide-disulphide oxidoreductase, dimerisation domain
- Pyridine nucleotide-disulphide oxidoreductase
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads TXNRD2 as an antibody target. Whether an autoantibody or antibody against TXNRD2 could matter depends on whether native TXNRD2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
TXNRD2 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 TXNRD2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
Loading the interactive Seroatlas protein explorer...