NR2F2
COUP transcription factor 2
Also known as: ARP1, COT2_HUMAN, COUP-TFII, COUPTF2, COUPTFB, NF-E3, SVP40, TFCOUP2
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P24468
- Gene
- NR2F2
- Ensembl
- ENSG00000185551
- Chromosome
- 15
- Canonical length
- 414 aa
- Protein class
- Disease related genes, Human disease related genes, Nuclear receptors, Predicted intracellular proteins, Transcription factors
- Subcellular location
- Nucleoplasm,Cytosol
- Quaternary structure
- Homodimer
OverviewNCBI Gene
This gene encodes a member of the steroid thyroid hormone superfamily of nuclear receptors. The encoded protein is a ligand inducible transcription factor that is involved in the regulation of many different genes. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Mar 2010]
Canonical amino-acid sequenceUniProt
414 residues, UniProt reviewed canonical sequence.
>P24468|NR2F2
1 MAMVVSTWRD PQDEVPGSQG SQASQAPPVP GPPPGAPHTP QTPGQGGPAS TPAQTAAGGQ
61 GGPGGPGSDK QQQQQHIECV VCGDKSSGKH YGQFTCEGCK SFFKRSVRRN LSYTCRANRN
121 CPIDQHHRNQ CQYCRLKKCL KVGMRREAVQ RGRMPPTQPT HGQFALTNGD PLNCHSYLSG
181 YISLLLRAEP YPTSRFGSQC MQPNNIMGIE NICELAARML FSAVEWARNI PFFPDLQITD
241 QVALLRLTWS ELFVLNAAQC SMPLHVAPLL AAAGLHASPM SADRVVAFMD HIRIFQEQVE
301 KLKALHVDSA EYSCLKAIVL FTSDACGLSD VAHVESLQEK SQCALEEYVR SQYPNQPTRF
361 GKLLLRLPSL RTVSSSVIEQ LFFVRLVGKT PIETLIRDML LSGSSFNWPY MAIQLocalizationUniProt · AlphaFold · HPA
Whether an antibody against NR2F2 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)
- 0.39
- Highest tissue expression
- 224 nTPM
Expression across tissuesHPA
Tissue
- ovary: 224 nTPM
- blood vessel: 145 nTPM
- cervix: 122 nTPM
- seminal vesicle: 119 nTPM
- endometrium: 116 nTPM
- spleen: 100 nTPM
Single-cell type
- peritubular myoid cells: 688 nCPM
- pericytes: 683 nCPM
- lymphatic endothelial cells: 528 nCPM
- leydig cells: 527 nCPM
- endometrial stromal cells: 471 nCPM
- vascular smooth muscle cells: 458 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
- hypothalamus: 101 nTPM
- amygdala: 68 nTPM
- thalamus: 67 nTPM
- choroid plexus: 49 nTPM
- midbrain: 46 nTPM
- cerebral cortex: 41 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about NR2F2.
Disease | AllUniProt
Conditions NR2F2 is implicated in, by any mechanism.
- Congenital heart defects, multiple types, 4 (CHTD4) MIM:615779
- 46,XX sex reversal 5 (SRXX5) MIM:618901
Disease | GeneticClinVar
36 pathogenic / likely-pathogenic of 176 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Congenital heart defects, multiple types, 4
- Inborn genetic diseases
- 46,xx sex reversal 5
- NR2F2 associated disorders
- Asplenia
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)
- 0.22
- gnomAD pLI
- 0.99
- gnomAD missense Z
- 3.6
- DepMap mean gene effect
- 0.07
- 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
- anterior/posterior pattern specification
- blood vessel morphogenesis
- cell differentiation
- female gonad development
- fertilization
- forebrain development
- interneuron migration
- lymphatic endothelial cell fate commitment
- maternal placenta development
- negative regulation of endothelial cell migration
- negative regulation of endothelial cell proliferation
- negative regulation of transcription by RNA polymerase II
- negative regulation of vascular endothelial growth factor signaling pathway
- nervous system development
- placenta blood vessel development
- positive regulation of DNA-templated transcription
- positive regulation of systemic arterial blood pressure
- positive regulation of transcription by RNA polymerase II
- regulation of transcription by RNA polymerase II
- response to estradiol
- skeletal muscle tissue development
- trophoblast giant cell differentiation
- radial pattern formation
Molecular functions
- DNA-binding transcription factor activity
- DNA-binding transcription repressor activity, RNA polymerase II-specific
- nuclear receptor activity
- protein homodimerization activity
- retinoic acid binding
- RNA polymerase II cis-regulatory region sequence-specific DNA binding
- sequence-specific DNA binding
- zinc ion binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Nuclear hormone receptor, ligand-binding domain
- Zinc finger, nuclear hormone receptor-type
- Nuclear hormone receptor
- Zinc finger, NHR/GATA-type
- Nuclear hormone receptor-like domain superfamily
- Nuclear hormone receptor family NR2 subfamily
- Ligand-binding domain of nuclear hormone receptor
- Double treble clef zinc finger, C4 type
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of NR2F2 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 NR2F2 as an antibody target. Whether an autoantibody or antibody against NR2F2 could matter depends on whether native NR2F2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
NR2F2 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 NR2F2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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