REXO2
Oligoribonuclease, mitochondrial
Also known as: CGI-114, DKFZP566E144, ORN_HUMAN, SFN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q9Y3B8
- Gene
- REXO2
- Ensembl
- ENSG00000076043
- Chromosome
- 11
- Canonical length
- 237 aa
- Protein class
- Predicted intracellular proteins
- Subcellular location
- Nucleoli,Focal adhesion sites,Mitochondria
- Quaternary structure
- Homotetramer
OverviewNCBI Gene
This gene encodes a 3'-to-5' exonuclease specific for small (primarily 5 nucleotides or less in length) single-stranded RNA and DNA oligomers. This protein may have a role in DNA repair, replication, and recombination, and in RNA processing and degradation. It may also be involved in resistance of human cells to UV-C-induced cell death through its role in the DNA repair process. [provided by RefSeq, Nov 2011]
Canonical amino-acid sequenceUniProt
237 residues, UniProt reviewed canonical sequence.
>Q9Y3B8|REXO2
1 MLGGSLGSRL LRGVGGSHGR FGARGVREGG AAMAAGESMA QRMVWVDLEM TGLDIEKDQI
61 IEMACLITDS DLNILAEGPN LIIKQPDELL DSMSDWCKEH HGKSGLTKAV KESTITLQQA
121 EYEFLSFVRQ QTPPGLCPLA GNSVHEDKKF LDKYMPQFMK HLHYRIIDVS TVKELCRRWY
181 PEEYEFAPKK AASHRALDDI SESIKELQFY RNNIFKKKID EKKRKIIENG ENEKTVSLocalizationUniProt · AlphaFold · HPA
Whether an antibody against REXO2 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
- Other membrane
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.35
- Highest tissue expression
- 145 nTPM
Expression across tissuesHPA
Tissue
- parathyroid gland: 145 nTPM
- heart muscle: 135 nTPM
- salivary gland: 109 nTPM
- smooth muscle: 100 nTPM
- kidney: 96 nTPM
- blood vessel: 94 nTPM
Single-cell type
- esophageal apical cells: 1,142 nCPM
- oocytes: 1,068 nCPM
- parietal cells: 573 nCPM
- decidual stromal cells: 494 nCPM
- late primary spermatocytes: 378 nCPM
- syncytiotrophoblasts: 374 nCPM
Immune cell
- T-reg: 76 nTPM
- plasmacytoid DC: 70 nTPM
- basophil: 64 nTPM
- memory CD4 T-cell: 48 nTPM
- NK-cell: 45 nTPM
- naive CD4 T-cell: 43 nTPM
Brain region
- medulla oblongata: 32 nTPM
- hypothalamus: 30 nTPM
- pons: 30 nTPM
- white matter: 29 nTPM
- choroid plexus: 28 nTPM
- midbrain: 27 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)
- 0.77
- gnomAD pLI
- 0.02
- gnomAD missense Z
- 1.01
- DepMap mean gene effect
- -0.16
- 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
- mitochondrial RNA surveillance
- nucleobase-containing compound metabolic process
- nucleotide metabolic process
Molecular functions
- 3'-5' exonuclease activity
- 3'-5'-DNA exonuclease activity
- 3'-5'-RNA exonuclease activity
- magnesium ion binding
- nucleic acid binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads REXO2 as an antibody target. Whether an autoantibody or antibody against REXO2 could matter depends on whether native REXO2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
REXO2 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 REXO2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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