Affinage

Showing NR2F2 — COUP-TFII is a alias.

NR2F2

COUP transcription factor 2 · UniProt P24468

Length
414 aa
Mass
45.6 kDa
Annotated
2026-06-10
100 papers in source corpus 51 papers cited in narrative 52 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

NR2F2 (COUP-TFII) is an orphan nuclear receptor that acts as a context-dependent transcriptional regulator governing cell-fate decisions across vascular, cardiac, reproductive, neural, metabolic, and mesenchymal lineages (PMID:15875024, PMID:23725765, PMID:21873211, PMID:18818749). Its ligand-binding domain adopts an autorepressed conformation in which helix α10 occupies the ligand pocket and the AF-2 helix folds into the cofactor groove; retinoic acid relieves this state to permit coactivator recruitment, and mutations disrupting cofactor binding, dimerization, or ligand binding abolish activity (PMID:18798693). NR2F2 can bind DNA directly at DR-type elements (e.g. the Star DR1-like and INSL3 DR0-like promoter sites) or operate by tethering to other transcription factors and by competitive displacement, as when it outcompetes RAR:RXR at the Oct-3/4 RAREoct site (PMID:24899578, PMID:24780841, PMID:7823919). In the vasculature it establishes venous identity by binding HEY1/HEY2 promoters as a homodimer to repress Notch-driven arterial differentiation, while heterodimerization with PROX1 abolishes this repression and instead activates lymphatic endothelial genes (VEGFR-3, FGFR-3, neuropilin-1) — a dimer-state switch that partitions venous versus lymphatic fate (PMID:15875024, PMID:18815287, PMID:23345397). Its abundance and activity are tuned at multiple levels: BRG1 remodels its venous promoter, Tie2/Akt signaling stabilizes the protein against proteasomal turnover, the Fbxo21 E3 ligase targets it for degradation, and miR-302/miR-101/miR-27a repress its expression (PMID:23406903, PMID:28005008, PMID:33531987, PMID:23136034, PMID:27108958). Through this regulatory logic NR2F2 directs atrial versus ventricular cardiomyocyte identity, adipogenic versus osteo-/myogenic mesenchymal fate, Leydig cell differentiation and steroidogenesis, and GABAergic neuron migration via neuropilin induction (PMID:23725765, PMID:21873211, PMID:18818749, PMID:26305926). Dysregulation drives disease: cardiac overexpression causes heart failure by repressing the PGC-1/mitochondrial network, fibroblast COUP-TFII enhances glycolysis and represses PGC1α to drive organ fibrosis, and in cancer it antagonizes SMAD4-dependent TGF-β checkpoints, promotes EMT and metastasis, and couples KRAS/MEK signaling to LDHA-driven glycolysis and mTORC1 activation (PMID:26356605, PMID:34031962, PMID:23201680, PMID:25032732, PMID:30988000).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1995 Medium

    Established the first molecular mechanism of COUP-TFII repression: it silences a target promoter by outcompeting an activating nuclear-receptor heterodimer rather than by a passive mechanism.

    Evidence Promoter-reporter assays, EMSA competition, and domain deletion in embryonal carcinoma cells showing displacement of RAR:RXR from the Oct-3/4 RAREoct site

    PMID:7823919

    Open questions at the time
    • Did not resolve whether displacement operates at endogenous loci genome-wide
    • C-terminal silencing domain partners not identified
  2. 1997 Medium

    Mapped the repression machinery, distinguishing active repression from transrepression and implicating shared coactivator squelching with liver-enriched factors.

    Evidence GAL4-fusion domain deletion series and co-transfection with HNF-3/C/EBP/HNF-4 transactivators

    PMID:9271371 PMID:9395397

    Open questions at the time
    • Specific coactivators competed for were inferred, not biochemically isolated
    • The Shh-responsive transcription factor activated by dephosphorylation was not identified
  3. 1999 High

    Defined COUP-TFII as essential for cardiovascular morphogenesis and identified Angiopoietin-1 as a downstream effector linking it to mesenchymal-endothelial signaling.

    Evidence Targeted gene deletion in mice with in situ analysis of Ang-1

    PMID:10215630

    Open questions at the time
    • Direct promoter binding to Ang-1 not shown in this study
    • Did not separate angiogenic from cardiac roles
  4. 2005 High

    Placed COUP-TFII at the top of venous identity by showing it represses Notch signaling to prevent arterial fate, resolving how veins are molecularly specified.

    Evidence Endothelial conditional knockout and transgenic overexpression with arterial/venous marker analysis in mice

    PMID:15875024

    Open questions at the time
    • Direct Notch-target promoter binding not yet demonstrated
    • Did not address lymphatic fate
  5. 2008 High

    Provided the structural basis for ligand-dependent regulation and defined the PROX1 partnership that switches COUP-TFII output toward lymphatic identity.

    Evidence 1.48 Å crystal structure with mutagenesis and coactivator assays; reciprocal Co-IP and target-gene analysis for the COUP-TFII/Prox1 complex; stage-specific Leydig knockout with testosterone rescue

    PMID:18798693 PMID:18815287 PMID:18818749

    Open questions at the time
    • Endogenous physiological ligand remains unidentified
    • Stoichiometry and DNA-binding mode of the COUP-TFII/Prox1 complex not structurally resolved
  6. 2013 High

    Unified vascular biology into a dimer-state model: homodimers repress HEY1/HEY2 to block arterial fate while NR2F2/PROX1 heterodimers relieve this and drive lymphatic genes; concurrently established direct atrial-identity target binding and an upstream BRG1 input.

    Evidence ChIP and promoter binding distinguishing homodimer vs heterodimer activity in ECs; cardiomyocyte conditional knockout with ChIP and electrophysiology; endothelial Brg1 knockout with ChIP on the COUP-TFII promoter

    PMID:23345397 PMID:23406903 PMID:23725765

    Open questions at the time
    • How dimer choice is biochemically controlled in vivo not defined
    • BRG1 study correlative for chromatin remodeling causality
  7. 2010 High

    Demonstrated COUP-TFII bidirectionally tunes the angiogenic program — activating Angiopoietin-1 in pericytes while repressing VEGFR-1 in endothelium — and defined a mutual repression loop with OCT4 governing pluripotency exit.

    Evidence Conditional knockouts in tumor and RIP-Tag models with Ang-1 rescue and VEGFR-1 repression assays; reporter and knockdown experiments mapping the OCT4/miR-302/NR2F2 loop in hESCs

    PMID:20133706 PMID:20978203 PMID:21151097

    Open questions at the time
    • Cell-type basis for activation vs repression of angiogenic targets not mechanistically explained
    • Direct OCT4 promoter occupancy partly inferred
  8. 2012 High

    Generalized COUP-TFII as a master fate selector by showing direct, lineage-specific target regulation in adipose, mesenchymal, renal, neural, and proliferative contexts.

    Evidence ChIP-validated direct targets (Wnt10b, Eya1/Wt1, Nrp1/Nrp2, E2F1 via Sp1 tethering) across knockout and knockdown systems; SMAD4 antagonism by genetic epistasis in PTEN-null prostate tumors

    PMID:19117548 PMID:21873211 PMID:22492355 PMID:22669823 PMID:22734039 PMID:23201680

    Open questions at the time
    • Whether a single biochemical mode explains both DNA-direct and tethered regulation unresolved
    • Lineage specificity of cofactor selection not defined
  9. 2014 High

    Resolved direct DNA-binding mechanisms at steroidogenic promoters and showed cooperation with SF1, while extending the repertoire to EMT and inflammatory targets.

    Evidence ChIP, EMSA, and DR-element mutagenesis at Star and INSL3 promoters with SF1 cotransfection; ChIP and reporter assays on Snail1, COX-2, and endometrial ChIP-seq

    PMID:24176914 PMID:24423359 PMID:24780841 PMID:24899578 PMID:25032732

    Open questions at the time
    • Structural basis of the SF1 interaction not determined
    • Genome-wide binding only mapped in select cell types
  10. 2016 Medium

    Established post-translational control of COUP-TFII abundance and connected it to oncogenic metabolic rewiring and inflammatory signaling.

    Evidence Tie2/Akt stabilization with proteasome-inhibitor rescue; ChIP/luciferase for the miR-21/Smad7 axis; miR-101/27a regulation of the FOXM1/CENPF cascade; Co-IP and EMSA showing NFκB inhibition

    PMID:24141032 PMID:27108958 PMID:28005008 PMID:28192117

    Open questions at the time
    • The stabilizing E3/deubiquitinase machinery downstream of Akt not identified here
    • NFκB interaction shown by single-lab Co-IP without reciprocal in vivo validation
  11. 2019 Medium

    Integrated COUP-TFII into KRAS-driven glycolysis and cofactor networks with pioneer factors, defining actionable mechanisms.

    Evidence Genetic/pharmacological dissection of KRAS→COUP-TFII→LDHA→lactate→mTORC1; ChIP-seq/ATAC-seq showing NR2F2 cofactor activity with FOXA1/GATA3 at ERα sites

    PMID:30988000 PMID:31588232

    Open questions at the time
    • Direct LDHA promoter occupancy by COUP-TFII not fully resolved
    • FOXA1/GATA3 cooperativity from single-lab genomic dataset
  12. 2020 High

    Defined COUP-TFII as a druggable driver and disease node in heart failure, fibrosis, and Parkinson's via mitochondrial/metabolic gene repression.

    Evidence Small-molecule LBD binder disrupting FOXA1 interaction with in vivo antitumor efficacy; cardiac and fibroblast knockout/overexpression with ChIP on PGC1α; DA-neuron gain/loss-of-function repressing ALDH in MitoPark mice

    PMID:26356605 PMID:32494682 PMID:32579581 PMID:34031962

    Open questions at the time
    • Whether inhibitor selectivity extends beyond FOXA1-dependent complexes unknown
    • Epigenetic mechanism of ALDH repression only partially characterized
  13. 2023 Medium

    Revealed isoform-level and species-specific regulation expanding the mechanistic model: a DBD-lacking isoform modulates full-length activity, and a hinge-region/Fog2 interaction controls blood pressure.

    Evidence DNA-methylation-regulated alternative-TSS isoform with EMT/NCC functional assays in melanoma; zinc-finger-nuclease hinge-deletion rat with Co-IP and blood-pressure phenotyping

    PMID:25687237 PMID:37015919

    Open questions at the time
    • Mechanism by which Iso2 modulates full-length NR2F2 not biochemically defined
    • Fog2 interaction effect on transcriptional targets not mapped

Open questions

Synthesis pass · forward-looking unresolved questions
  • The endogenous physiological ligand and the rules that select between DNA-direct binding, factor tethering, homodimer repression, and heterodimer activation in a given cell type remain undefined.
  • No native ligand identified despite retinoic-acid responsiveness
  • No unifying model for dimer-partner and cofactor selection across lineages
  • Structural basis of most protein-protein tethering interactions unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 7 GO:0003677 DNA binding 5 GO:0098772 molecular function regulator activity 5
Localization
GO:0005634 nucleus 4
Pathway
R-HSA-1643685 Disease 6 R-HSA-1266738 Developmental Biology 5 R-HSA-74160 Gene expression (Transcription) 5 R-HSA-162582 Signal Transduction 4 R-HSA-1430728 Metabolism 3
Partners
FOG2FOXA1GATA3GRHNF4PROX1RELBSF1
Complex memberships
NR2F2/PROX1 lymphatic co-regulator complex

Evidence

Reading pass · 52 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 COUP-TFII (NR2F2) is specifically expressed in venous but not arterial endothelium; endothelial-specific ablation enables veins to acquire arterial characteristics including NP-1 and Notch signaling molecule expression, while ectopic expression causes vein-artery fusion. COUP-TFII represses Notch signaling to maintain vein identity. Conditional knockout and transgenic overexpression in mouse endothelial cells; arterial/venous marker analysis Nature High 15875024
1999 COUP-TFII is required for angiogenesis and heart development; null mice fail to remodel the primitive capillary plexus, and atria/sinus venosus do not develop past the primitive tube stage. Angiopoietin-1 expression is down-regulated in COUP-TFII mutant hearts, suggesting COUP-TFII controls mesenchymal-endothelial signaling through Angiopoietin-1. Targeted gene deletion in mice; in situ hybridization and expression analysis of Angiopoietin-1 Genes & Development High 10215630
2008 Crystal structure of human COUP-TFII ligand-binding domain at 1.48 Å reveals an autorepressed conformation where helix α10 is bent into the ligand-binding pocket and the AF-2 helix is folded into the cofactor binding site, preventing coactivator recruitment. Retinoic acids can promote COUP-TFII to recruit coactivators and activate transcription by releasing the receptor from this autorepressed conformation. Mutations disrupting cofactor binding, dimerization, or ligand binding substantially reduce transcriptional activity. X-ray crystallography (1.48 Å); cell-based transcription assays; site-directed mutagenesis; coactivator recruitment assays PLoS Biology High 18798693
2008 COUP-TFII physically interacts with Prox1 to form a stable complex in lymphatic endothelial cells (LECs) and multiple other cell types. This COUP-TFII/Prox1 complex functions as a co-regulator to control lineage-specific genes including VEGFR-3, FGFR-3, and neuropilin-1, and is required along with Prox1 to maintain LEC phenotype. Co-immunoprecipitation; stable complex formation assays; gene expression analysis with knockdown Blood High 18815287
2013 COUP-TFII homodimers inhibit arterial differentiation in venous ECs through direct binding to promoter regions of Notch target genes HEY1 and HEY2, whereas NR2F2/PROX1 heterodimers lack this inhibitory effect on HEY1/2, resulting in non-canonical HEY1/2 expression in LECs. NR2F2/PROX1 heterodimers actively induce LEC-specific gene expression. Chromatin immunoprecipitation; promoter binding assays; gain- and loss-of-function in endothelial cells; gene expression profiling Journal of Cell Science High 23345397
2012 COUP-TFII inhibits SMAD4-dependent transcription to override the TGF-β-dependent growth checkpoint in PTEN-null prostate tumors. Conditional overexpression of COUP-TFII in mouse prostate cooperates with PTEN deletion to drive metastatic progression; conditional loss of SMAD4 diminishes the inhibitory effects of COUP-TFII ablation, establishing functional counteraction between COUP-TFII and SMAD4. Genetically engineered mouse models (conditional overexpression and knockout); epistasis analysis of COUP-TFII and SMAD4 double mutants; transcriptional reporter assays Nature High 23201680
2007 Stromal COUP-TFII mediates progesterone control of uterine implantation by suppressing epithelial estrogen receptor (ERα) activity. Conditional knockout of uterine COUP-TFII leads to implantation failure and impaired decidualization; BMP2 lies downstream of COUP-TFII in a pathway regulated by the progesterone-Indian hedgehog-Patched-COUP-TFII-BMP2 axis. Conditional COUP-TFII knockout mouse; ERα antagonist rescue experiments; pathway analysis in vivo PLoS Genetics High 17590085
2010 Stromal COUP-TFII suppresses ERα activity in the uterine luminal epithelium during the periimplantation period; pharmacological inhibition of ERα with ICI 182,780 rescues embryo attachment and decidualization (including Wnt4 and BMP2 expression) in COUP-TFII knockout uteri, demonstrating that COUP-TFII regulates implantation through controlling ERα activity. Conditional knockout mouse; ERα antagonist (ICI 182,780) rescue; gene expression analysis of ERα target genes Molecular Endocrinology High 20219888
1997 A Sonic hedgehog (Shh) response element in the COUP-TFII promoter binds a factor distinct from Gli. Shh-N signaling can be mimicked by protein phosphatase treatment to activate this binding activity, and Shh-N-induced activation of COUP-TFII is blocked by phosphatase inhibitors, indicating that Shh-N signaling activates COUP-TFII expression through dephosphorylation of a target transcription factor. Promoter binding assays; pharmacological phosphatase inhibitor experiments; Shh-N stimulation in P19 cells Science Medium 9395397
2013 Cardiomyocyte-specific COUP-TFII ablation produces ventricularized atria with ventricle-like action potentials, larger cardiomyocyte size, and T-tubule development. ChIP assays identify Tbx5, Hey2, Irx4, MLC2v, MLC2a, and MLC1a as direct COUP-TFII target genes in atria, demonstrating that COUP-TFII directly binds and regulates atrial identity genes. Cardiomyocyte-specific conditional knockout; electrophysiology; chromatin immunoprecipitation with E13.5 atrial tissue; genome-wide gene expression profiling Developmental Cell High 23725765
2010 COUP-TFII in pericytes directly regulates transcription of Angiopoietin-1 to enhance tumor neoangiogenesis; provision of exogenous Angiopoietin-1 partially rescues angiogenic defects in COUP-TFII-deficient mice, demonstrating COUP-TFII controls Angiopoietin-1/Tie2 signaling. Conditional adult COUP-TFII knockout; xenograft tumor models; Angiopoietin-1 rescue experiment; transcriptional regulation assays PNAS High 20133706
2010 COUP-TFII suppresses VEGFR-1 transcription in endothelial cells to regulate VEGF/VEGFR-2 signaling balance during tumor angiogenesis; COUP-TFII plays a cell-autonomous role in endothelial cell proliferation and migration. Conditional COUP-TFII knockout in tumor microenvironment; RIP-Tag pancreatic islet tumor model; transcriptional repression assays for VEGFR-1 Cancer Research Medium 20978203
2009 COUP-TFII plays a pivotal role in white adipocyte development; COUP-TFII heterozygous mice have less white adipose tissue and decreased expression of key WAT regulators. ChIP analysis reveals Wnt10b is a direct transcriptional target of COUP-TFII, and knockdown of COUP-TFII in 3T3-L1 cells increases Wnt10b expression. Heterozygous knockout mice; 3T3-L1 knockdown; chromatin immunoprecipitation; gene expression analysis Cell Metabolism High 19117548
2011 COUP-TFII inactivation in mesenchymal progenitors shifts lineage fate toward osteoblast and myoblast development while impairing adipogenic and chondrogenic programs. COUP-TFII directs mesenchymal progenitor plasticity through combined modulation of Wnt signaling, Runx2 activity, and PPARγ and Sox9 expression. Conditional knockout in mesenchymal progenitors; in vivo bone density, muscle mass, and fat/cartilage quantification; pathway analysis PNAS Medium 21873211
2012 COUP-TFII directly regulates E2F1 transcription by tethering to Sp1 binding sites in the E2F1 promoter (demonstrated by ChIP) to modulate cell proliferation. COUP-TFII also directly regulates Foxc1, Np-1, and Hey2 (Notch pathway genes) as shown by ChIP in HUVECs. Microarray in COUP-TFII-depleted HUVECs; chromatin immunoprecipitation; gene expression analysis Molecular Endocrinology Medium 22734039
2013 BRG1 chromatin-remodeling enzyme promotes COUP-TFII expression in venous endothelial cells by binding conserved regulatory elements in the COUP-TFII promoter and remodeling chromatin accessibility; conditional deletion of Brg1 from vascular endothelium downregulates COUP-TFII and causes aberrant arterial marker expression on veins. Conditional endothelial Brg1 knockout; chromatin accessibility assays; ChIP for BRG1 binding to COUP-TFII promoter Development Medium 23406903
2016 Tie2 signaling maintains COUP-TFII protein levels in venous endothelial cells via Akt-mediated stabilization; Ang-1 stimulation increases COUP-TFII protein, while Tie2 knockdown or PI3K/Akt pathway blockade reduces COUP-TFII levels, an effect reversed by proteasome inhibition. Tie2/Tek conditional knockout mice; Ang-1 stimulation assays; Tie2 knockdown in cultured ECs; PI3K/Akt inhibition; proteasome inhibitor rescue eLife Medium 28005008
2008 COUP-TFII is required for Leydig cell differentiation; ablation prior to puberty arrests Leydig cell differentiation at the progenitor stage, causing testosterone deficiency and spermatogenetic arrest. Testosterone administration rescues most but not all defects, while Leydig cell maturation failure persists, establishing COUP-TFII as intrinsically required for Leydig cell differentiation but not maintenance. Tamoxifen-inducible conditional knockout at different developmental stages; testosterone rescue experiment; histological analysis of Leydig cell differentiation PLoS ONE High 18818749
2014 COUP-TFII (NR2F2) directly activates Star (steroidogenic acute regulatory protein) gene transcription in Leydig cells by binding to a DR1-like element between -131 and -95 bp of the Star promoter; mutation of the DR1-like element that prevents COUP-TFII binding blunts promoter activation. COUP-TFII also cooperates with SF1 via protein-protein interactions to further enhance INSL3 and Star transcription. siRNA knockdown in MA-10/MLTC-1 cells; promoter deletion analysis; ChIP; electrophoretic mobility shift assay; site-directed mutagenesis; cotransfection with SF1 Biology of Reproduction High 24899578
2014 COUP-TFII directly binds a DR0-like element in the INSL3 promoter (-186 to -79 bp) to activate Insl3 transcription in Leydig cells; mutation of the DR0-like element prevents COUP-TFII binding. COUP-TFII also acts through protein-protein interactions with SF1 bound at the Insl3 promoter to further activate transcription. siRNA knockdown; promoter deletion assays; ChIP; DNA precipitation assay; DR0-like element mutagenesis; cotransfection with SF1 Journal of Molecular Endocrinology High 24780841
2015 Increased COUP-TFII in adult cardiomyocytes causes heart failure by repressing genes critical for mitochondrial electron transport chain activity, oxidative stress detoxification, and mitochondrial dynamics, resulting in increased ROS and reduced oxygen consumption. COUP-TFII also suppresses the PGC-1 network and decreases glucose and lipid utilization gene expression. COUP-TFII haploinsufficiency attenuates dilated cardiomyopathy in a calcineurin transgenic model. Cardiac-specific COUP-TFII overexpression transgenic mice; cardiac-specific heterozygous knockout; mitochondrial respiration assays; ROS measurement; gene expression profiling Nature Communications High 26356605
2021 COUP-TFII enhances glycolysis and suppresses fatty acid oxidation in myofibroblasts to drive kidney fibrosis; COUP-TFII binds the PGC1α promoter (ChIP-qPCR) and reduces PGC1α expression, thereby suppressing mitochondrial metabolism. Overexpression of COUP-TFII induces αSMA and collagen 1 production; knockout decreases glycolysis and collagen 1 levels. Conditional knockout in mice; fibroblast overexpression; ChIP-qPCR for PGC1α promoter; unbiased proteomics; glycolysis and FAO metabolic assays EMBO Reports High 34031962
2016 COUP-TFII regulates satellite cell function in skeletal muscle; ectopic COUP-TFII expression in satellite cells causes Duchenne-like dystrophy through deficient SC proliferation and impaired myoblast fusion. Mechanistically, COUP-TFII represses expression of Npnt, Itgb1D, and Cav3 (genes important for cell-cell fusion) and reduces activation of focal adhesion kinase (FAK). Satellite cell-specific COUP-TFII overexpression transgenic mice; mdx dystrophic model; satellite cell functional assays; gene expression analysis; FAK activation assays Journal of Clinical Investigation Medium 27617862
2017 COUP-TFII represses myoblast fusion during skeletal muscle development by transcriptionally repressing Npnt, Itgb1D, and Cav3, and reducing focal adhesion kinase (FAK) activation; maintaining COUP-TFII expression in myogenic precursors (via ectopic expression) causes inefficient skeletal muscle development in mice. Myogenic precursor-specific COUP-TFII overexpression mouse model; myoblast fusion assays; FAK activation measurement; gene expression analysis Scientific Reports Medium 28600496
2012 COUP-TFII is required for metanephric mesenchyme specification; deletion at E7.5 results in absence of Eya1, Six2, Pax2, and Gdnf in the metanephric mesenchyme. COUP-TFII directly regulates Eya1 and Wt1 expression in the metanephric mesenchyme. Conditional knockout at E7.5; ChIP; gene expression analysis of developmental regulators Development Medium 22669823
2012 COUP-TFII controls amygdala development by directly regulating Nrp1 and Nrp2 (semaphorin receptors controlling neuronal migration) in CGE-derived cells; ChIP assays in telencephalon confirm Nrp1 and Nrp2 as direct COUP-TFII targets, and CGE-specific conditional knockout causes failure of Pax6+ cell migration into the BMA nucleus. Rx-Cre conditional knockout mice; in vivo ChIP in telencephalon for Nrp1/Nrp2 promoters; cell migration analysis Development Medium 22492355
2008 COUP-TFII is preferentially expressed in caudal ganglionic eminence (CGE) neurons; transplantation of COUP-TFII-expressing MGE cells into CGE redirects their migration caudally, and knockdown of COUP-TFII inhibits caudal migration of CGE cells, demonstrating COUP-TFII is both necessary and sufficient for CGE-specific caudal migratory behavior. Transcriptome comparison of CGE/MGE/LGE; transplantation experiments; siRNA knockdown; migration assays Journal of Neuroscience High 19074032
2015 COUP-TFII-induced expression of Neuropilin-2 (Nrp2) controls the destination of POa-derived GABAergic neurons; suppression of COUP-TFII/Nrp2 redirects cells to the neocortex, while overexpression causes cells to end up in the medial amygdala, establishing COUP-TFII/Nrp2 as a molecular switch for migration pathway selection. In utero electroporation for gain- and loss-of-function; live cell migration tracking; Nrp2 expression analysis PNAS Medium 26305926
2010 OCT4 and OCT4-induced miR-302 directly repress NR2F2 transcription and translation in undifferentiated hESCs; conversely, NR2F2 directly inhibits OCT4 during differentiation, forming a mutual repression loop. NR2F2 is among the earliest neural markers detected during hESC differentiation. Reporter assays; siRNA knockdown; miR-302 overexpression; chromatin-based transcription analysis in hESCs EMBO Journal Medium 21151097
2013 miR-302 directly targets NR2F2 mRNA (confirmed by luciferase reporter assay); NR2F2 directly inhibits OCT4 promoter activity. shRNA knockdown of NR2F2 mimics miR-302 overexpression by enhancing iPSC reprogramming efficiency. Luciferase reporter assay with NR2F2 3'UTR; OCT4 promoter activity assay; shRNA knockdown; reprogramming efficiency quantification Stem Cells Medium 23136034
1995 ARP-1/COUP-TFII represses Oct-3/4 promoter activity through the RAREoct site in embryonal carcinoma cells in a dose-dependent manner; the C-terminal domain harbors the silencing region. COUP-TFII competes with and displaces RAR:RXR heterodimers from the RAREoct site due to higher binding affinity, thereby silencing Oct-3/4. Promoter-reporter assays; electrophoretic mobility shift assay (EMSA) for competitive binding; domain deletion analysis; P19 EC cell differentiation model Molecular and Cellular Biology Medium 7823919
1997 The C-terminal domain of ARP-1/COUP-TFII (residues 210-414, encompassing helices 3-12) confers active repressor activity when fused to a heterologous DBD. The domains required for transrepression include the DBD and residues 193-399. Transrepression (not active repression) is the predominant mechanism, likely involving interaction with coactivator proteins used by liver-enriched transactivators (HNF-3, C/EBP, HNF-4) but not Sp1 or ATF. GAL4-fusion domain deletion analysis; transcription assays; Flu-tagged mutant series; co-transfection with liver-enriched and ubiquitous transactivators Molecular and Cellular Biology Medium 9271371
2000 COUP-TFII synergistically activates CYP7A1 (cholesterol 7α-hydroxylase) transcription together with HNF4; in vitro-translated COUP-TFII binds DR0 and DR4 elements in the CYP7A1 promoter. The synergistic effect of HNF4 and COUP-TFII results from protein-protein interactions facilitated by juxtaposition of their binding elements rather than absolute requirement for the COUP-TFII binding sites. Cotransfection reporter assays; EMSA with in vitro-translated COUP-TFII; promoter mutagenesis Journal of Lipid Research Medium 10627496
2004 Glucocorticoid receptor (GR) physically interacts with COUP-TFII; GR stimulates COUP-TFII-induced transactivation via its AF-1 domain, while COUP-TFII represses GR-governed transcriptional activity by tethering corepressors SMRT and NCoR via its C-terminal domain. Co-immunoprecipitation; domain mapping; transcriptional assays with AF-1 mutants; corepressor recruitment assays Annals of the New York Academy of Sciences Medium 15265774
2016 COUP-TFII directly binds the miR-21 promoter (demonstrated by ChIP and luciferase assay) to transcriptionally activate miR-21 expression in CRC cells; miR-21 then targets Smad7, allowing COUP-TFII to promote TGF-β-induced EMT indirectly through this NR2F2→miR-21→Smad7 axis. ChIP; luciferase reporter assay; siRNA knockdown; EMT marker analysis Biochemical and Biophysical Research Communications Medium 28192117
2016 COUP-TFII directly binds the COX-2 promoter to inhibit its transcription (demonstrated by ChIP and reporter assays); proinflammatory cytokines (IL-1β, TNF-α, TGF-β1) reduce COUP-TFII expression via microRNA-302a (which targets COUP-TFII 3'UTR), leading to de-repression of COX-2 in endometriosis. ChIP; luciferase reporter assay; miR-302a overexpression; COUP-TFII knockout mouse endometriosis transplantation model; primary human endometrial stromal cells Journal of Clinical Endocrinology and Metabolism Medium 24423359
2018 COUP-TFII binds the ANG (angiogenin) promoter to suppress its transcription (demonstrated by ChIP and promoter activity assays); hypoxia reduces COUP-TFII levels leading to de-repression of ANG and enhanced angiogenesis in endometriosis. ChIP; luciferase promoter activity assay; siRNA knockdown and overexpression; HUVEC tube formation assay Human Reproduction Medium 29982401
2014 COUP-TFII directly targets the Snail1 promoter to regulate Snail1 transcription and expression in colorectal cancer cells; COUP-TFII together with Snail1 inhibits E-cadherin, ZO-1, and β-catenin expression to promote cell migration and metastasis. ChIP; promoter reporter assay; COUP-TFII overexpression/knockdown; tamoxifen-inducible knockout mice; cell migration and invasion assays British Journal of Cancer Medium 25032732
2019 KRAS/MEK signaling upregulates COUP-TFII, which increases LDHA (lactate dehydrogenase A) expression leading to lactate production; lactate then inhibits TSC2-Rheb interaction to activate mTORC1, connecting KRAS signaling to glycolysis and mTORC1 activation via COUP-TFII. COUP-TFII overexpression and knockdown; LDHA expression analysis; TSC2-Rheb interaction assays; mTORC1 activity measurements; MEK inhibition EMBO Reports Medium 30988000
2020 A small-molecule COUP-TFII inhibitor (identified by high-throughput screening) directly binds the COUP-TFII ligand-binding domain and disrupts COUP-TFII interaction with FOXA1 and other transcription regulators, thereby repressing COUP-TFII transcriptional activity on target genes and exerting antitumor effects in prostate cancer models. High-throughput screening; ligand-binding domain binding assay; Co-IP for FOXA1-COUP-TFII interaction disruption; target gene expression; xenograft and patient-derived xenograft mouse models Science Advances High 32494682
2019 NR2F2 functions as a co-factor with pioneer factors FOXA1 and GATA3 to promote ERα-dependent transcription in breast cancer; NR2F2 binds to most ERα binding sites independently of estrogen. Perturbation of NR2F2 decreases ERα DNA binding, chromatin accessibility, and estrogen-dependent cell growth. ChIP-seq (40 transcription factors in ENCODE); ATAC-seq; RNA-seq; NR2F2 perturbation experiments; ERα binding analysis Theranostics Medium 31588232
2015 COUP-TFII haploinsufficiency is regulated by insulin and glucose: insulin represses COUP-TFII in pancreatic β-cells through Foxo1 signaling, and high glucose represses COUP-TFII in hepatocytes through both Foxo1 and ChREBP. Ex vivo, COUP-TFII reduces insulin production and secretion; pancreatic COUP-TFII expression is activated by TCF7L2 (Wnt signaling), creating a feedback loop. Pancreatic-specific conditional knockout mice; Foxo1 signaling inhibition; ChREBP knockdown in hepatocytes; islet isolation ex vivo experiments; TCF7L2 reporter assays Molecular and Cellular Biology Medium 18765640
2012 COUP-TFII induces β-catenin gene expression and its target genes (cyclin D1, axin 2) in pancreatic β-cells; GLP-1 activation of the β-catenin pathway is impaired in COUP-TFII-deficient islets. COUP-TFII expression is activated by TCF7L2 in human islets and rat β-cells, forming a feedback loop. COUP-TFII is required for GLP-1-mediated β-catenin signaling and neonatal β-cell mass determination. Pancreatic conditional knockout (pdx1-Cre); islet isolation; gain- and loss-of-function in cultured β-cells; GLP-1 stimulation assays; gene expression analysis PLoS ONE Medium 22292058
2016 miR-101 and miR-27a negatively regulate COUP-TFII expression; loss of miR-101 increases COUP-TFII, which in turn activates FOXM1 and CENPF expression to promote prostate cancer metastasis. COUP-TFII is a critical intermediate in the miRNA→COUP-TFII→FOXM1→CENPF metastatic cascade and also contributes to enzalutamide resistance. miRNA overexpression and inhibition; COUP-TFII knockdown/overexpression; downstream FOXM1/CENPF expression analysis; clinical PCa dataset correlation Nature Communications Medium 27108958
2015 A 5 amino acid deletion in the hinge region of NR2F2 (from zinc-finger nuclease gene editing) reduces interaction between wild-type NR2F2 and Fog2 (Friend of Gata2); the mutant NR2F2 protein has greater interaction with Fog2, and Nr2f2-mutant rats have significantly lower systolic and diastolic blood pressure, establishing the hinge region-Fog2 interaction as critical for blood pressure regulation. Zinc-finger nuclease-generated Nr2f2 mutant rat; protein-protein interaction assays (co-IP); blood pressure measurement Nature Communications Medium 25687237
2010 NR2F2 directly activates TFAP2A (AP-2α) promoter activity to promote human villous cytotrophoblast differentiation to syncytiotrophoblast; siRNA silencing of NR2F2 blocks induction of TFAP2A mRNA and STB marker genes (hPL, PSG1, CRH). NR2F2-mediated TFAP2A induction is potentiated by RAR-α and RXR-α. TFAP2A promoter reporter assays; siRNA knockdown in primary CTB cells and JEG-3 cells; cotransfection with RARA and RXRA PLoS ONE Medium 20195529
2021 COUP-TFII overexpression in fibroblasts induces αSMA and collagen 1 production; COUP-TFII binds the PGC1α promoter (by ChIP-qPCR) and represses PGC1α expression to suppress fatty acid oxidation and enhance glycolysis, driving myofibroblast activation and organ fibrosis. Knockout of COUP-TFII in mice attenuates injury-induced kidney fibrosis. Conditional fibroblast-specific knockout mice; unbiased proteomics; ChIP-qPCR; glycolysis/FAO metabolic assays; αSMA and collagen 1 quantification EMBO Reports High 34031962
2023 An alternative NR2F2 isoform (NR2F2-Iso2), transcribed from an alternative TSS and lacking the N-terminal DNA-binding domain, is regulated by DNA methylation during melanocyte differentiation. NR2F2-Iso2 re-expression during metastatic melanoma progression drives EMT and neural crest cell-like features by modulating the activity of full-length NR2F2 (Iso1) on EMT- and NCC-associated target genes. DNA methylation profiling; alternative TSS identification; functional gain- and loss-of-function; EMT and NCC target gene expression analysis Nature Communications Medium 37015919
2021 Fbxo21 (an F-box E3 ubiquitin ligase) ubiquitinates NR2F2 protein and targets it for proteasomal degradation in gastric cancer cells; Fbxo21 expression is negatively correlated with NR2F2 protein levels, and NR2F2 re-expression rescues EMT inhibition caused by Fbxo21 overexpression. Co-immunoprecipitation; ubiquitination assay; proteasome inhibitor treatment; gain- and loss-of-function; EMT marker analysis Journal of Cancer Medium 33531987
2020 Elevated COUP-TFII in dopaminergic (DA) neurons represses cytosolic aldehyde dehydrogenase gene expression (epigenetic mechanism), leading to DOPAL accumulation, enhanced oxidative stress, and mitochondrial dysfunction with reduced cristae. Overexpression of COUP-TFII in DA neurons accelerates PD progression in MitoPark mice; underexpression of COUP-TFII slows motor deterioration. DA neuron-specific COUP-TFII overexpression and underexpression in mice; MitoPark PD model; mitochondrial morphology (EM); aldehyde dehydrogenase gene expression; epigenetic analysis PLoS Genetics Medium 32579581
2014 COUP-TFII regulates gene expression in human endometrial stromal cells involved in cell adhesion, angiogenesis, and inflammation, including inflammatory cytokines; ChIP-seq identifies direct COUP-TFII binding sites across the endometrial stromal transcriptome. siRNA knockdown in primary human endometrial stromal cells; microarray; ChIP followed by deep sequencing (ChIP-seq) Molecular Endocrinology Medium 24176914
2013 NR2F2 (COUP-TFII) inhibits NFκB activation in breast cancer cells; COUP-TFII co-immunoprecipitates with NFκB subunits RelB and NFκB1 in MCF-7 cells; COUP-TFII inhibits NFκB-DNA binding in vitro and impairs coactivator-induced NFκB transactivation. Co-immunoprecipitation; EMSA for NFκB-DNA binding; NFκB reporter assays; COUP-TFII overexpression in LCC9 cells Molecular and Cellular Endocrinology Medium 24141032

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Suppression of Notch signalling by the COUP-TFII transcription factor regulates vein identity. Nature 522 15875024
1999 The orphan nuclear receptor COUP-TFII is required for angiogenesis and heart development. Genes & development 437 10215630
2007 COUP-TFII mediates progesterone regulation of uterine implantation by controlling ER activity. PLoS genetics 178 17590085
2008 Identification of COUP-TFII orphan nuclear receptor as a retinoic acid-activated receptor. PLoS biology 172 18798693
2010 A regulatory circuitry comprised of miR-302 and the transcription factors OCT4 and NR2F2 regulates human embryonic stem cell differentiation. The EMBO journal 161 21151097
2012 COUP-TFII inhibits TGF-β-induced growth barrier to promote prostate tumorigenesis. Nature 158 23201680
2014 Rare variants in NR2F2 cause congenital heart defects in humans. American journal of human genetics 139 24702954
1995 A dynamic balance between ARP-1/COUP-TFII, EAR-3/COUP-TFI, and retinoic acid receptor:retinoid X receptor heterodimers regulates Oct-3/4 expression in embryonal carcinoma cells. Molecular and cellular biology 138 7823919
2008 Prox1 physically and functionally interacts with COUP-TFII to specify lymphatic endothelial cell fate. Blood 136 18815287
1997 Mediation of Sonic hedgehog-induced expression of COUP-TFII by a protein phosphatase. Science (New York, N.Y.) 130 9395397
2008 COUP-TFII is preferentially expressed in the caudal ganglionic eminence and is involved in the caudal migratory stream. The Journal of neuroscience : the official journal of the Society for Neuroscience 125 19074032
2009 The nuclear orphan receptor COUP-TFII plays an essential role in adipogenesis, glucose homeostasis, and energy metabolism. Cell metabolism 119 19117548
2013 Atrial identity is determined by a COUP-TFII regulatory network. Developmental cell 114 23725765
2013 MicroRNA-302 increases reprogramming efficiency via repression of NR2F2. Stem cells (Dayton, Ohio) 111 23136034
2000 HNF4 and COUP-TFII interact to modulate transcription of the cholesterol 7alpha-hydroxylase gene (CYP7A1). Journal of lipid research 110 10627496
2005 COUP-TFII is essential for radial and anteroposterior patterning of the stomach. Development (Cambridge, England) 108 15829524
2010 COUP-TFII regulates tumor growth and metastasis by modulating tumor angiogenesis. Proceedings of the National Academy of Sciences of the United States of America 102 20133706
2016 Dysregulation of miRNAs-COUP-TFII-FOXM1-CENPF axis contributes to the metastasis of prostate cancer. Nature communications 98 27108958
2008 Essential roles of COUP-TFII in Leydig cell differentiation and male fertility. PloS one 97 18818749
2010 Expression of COUP-TFII nuclear receptor in restricted GABAergic neuronal populations in the adult rat hippocampus. The Journal of neuroscience : the official journal of the Society for Neuroscience 94 20130170
2014 MicroRNA-194 reciprocally stimulates osteogenesis and inhibits adipogenesis via regulating COUP-TFII expression. Cell death & disease 90 25412310
2018 Loss of Function of the Nuclear Receptor NR2F2, Encoding COUP-TF2, Causes Testis Development and Cardiac Defects in 46,XX Children. American journal of human genetics 71 29478779
1996 Positive regulation of the vHNF1 promoter by the orphan receptors COUP-TF1/Ear3 and COUP-TFII/Arp1. Molecular and cellular biology 71 8622679
2012 COUP-TFII is a major regulator of cell cycle and Notch signaling pathways. Molecular endocrinology (Baltimore, Md.) 70 22734039
2007 Deletion of the orphan nuclear receptor COUP-TFII in uterus leads to placental deficiency. Proceedings of the National Academy of Sciences of the United States of America 70 17404209
2013 COUP-TFII orchestrates venous and lymphatic endothelial identity by homo- or hetero-dimerisation with PROX1. Journal of cell science 68 23345397
2010 Suppression of ERalpha activity by COUP-TFII is essential for successful implantation and decidualization. Molecular endocrinology (Baltimore, Md.) 68 20219888
2018 LncRNA NR2F2-AS1 promotes tumourigenesis through modulating BMI1 expression by targeting miR-320b in non-small cell lung cancer. Journal of cellular and molecular medicine 65 30592135
2004 The nuclear orphan receptor COUP-TFII is required for limb and skeletal muscle development. Molecular and cellular biology 63 15572686
2016 Angiopoietin receptor Tie2 is required for vein specification and maintenance via regulating COUP-TFII. eLife 62 28005008
2019 COUP-TFII in Health and Disease. Cells 60 31906104
2011 Nuclear receptor chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) modulates mesenchymal cell commitment and differentiation. Proceedings of the National Academy of Sciences of the United States of America 60 21873211
2015 Increased COUP-TFII expression in adult hearts induces mitochondrial dysfunction resulting in heart failure. Nature communications 59 26356605
2013 BRG1 promotes COUP-TFII expression and venous specification during embryonic vascular development. Development (Cambridge, England) 59 23406903
2012 COUP-TFII controls amygdala patterning by regulating neuropilin expression. Development (Cambridge, England) 57 22492355
2010 Nuclear receptor COUP-TFII controls pancreatic islet tumor angiogenesis by regulating vascular endothelial growth factor/vascular endothelial growth factor receptor-2 signaling. Cancer research 57 20978203
2017 NR2F2 inhibits Smad7 expression and promotes TGF-β-dependent epithelial-mesenchymal transition of CRC via transactivation of miR-21. Biochemical and biophysical research communications 51 28192117
2017 The Transcription Factors COUP-TFI and COUP-TFII have Distinct Roles in Arealisation and GABAergic Interneuron Specification in the Early Human Fetal Telencephalon. Cerebral cortex (New York, N.Y. : 1991) 51 28922831
2014 The nuclear receptor NR2F2 activates star expression and steroidogenesis in mouse MA-10 and MLTC-1 Leydig cells. Biology of reproduction 51 24899578
2017 Coup-TF1 and Coup-TF2 control subtype and laminar identity of MGE-derived neocortical interneurons. Development (Cambridge, England) 50 28694260
2015 miR-30-HNF4γ and miR-194-NR2F2 regulatory networks contribute to the upregulation of metaplasia markers in the stomach. Gut 50 25800782
1997 Functional domains of the human orphan receptor ARP-1/COUP-TFII involved in active repression and transrepression. Molecular and cellular biology 50 9271371
2016 miR-27b inhibits gastric cancer metastasis by targeting NR2F2. Protein & cell 47 27844448
2015 Venous Endothelial Marker COUP-TFII Regulates the Distinct Pathologic Potentials of Adult Arteries and Veins. Scientific reports 45 26537113
2013 COUP-TFII regulates human endometrial stromal genes involved in inflammation. Molecular endocrinology (Baltimore, Md.) 45 24176914
2017 A COUP-TFII Human Embryonic Stem Cell Reporter Line to Identify and Select Atrial Cardiomyocytes. Stem cell reports 43 29173897
1996 Developmental expression and differential regulation by retinoic acid of Xenopus COUP-TF-A and COUP-TF-B. Mechanisms of development 43 8652410
2015 MicroRNA-302a stimulates osteoblastic differentiation by repressing COUP-TFII expression. Journal of cellular physiology 42 25215426
2011 Transcription factor COUP-TFII is indispensable for venous and lymphatic development in zebrafish and Xenopus laevis. Biochemical and biophysical research communications 41 21641336
2014 Suppression of COUP-TFII by proinflammatory cytokines contributes to the pathogenesis of endometriosis. The Journal of clinical endocrinology and metabolism 40 24423359
2013 Sonic hedgehog (Shh) regulates the expression of angiogenic growth factors in oxygen-glucose-deprived astrocytes by mediating the nuclear receptor NR2F2. Molecular neurobiology 40 23378030
2013 Expression and functional pathway analysis of nuclear receptor NR2F2 in ovarian cancer. The Journal of clinical endocrinology and metabolism 40 23690307
2012 Multiple roles of COUP-TFII in cancer initiation and progression. Journal of molecular endocrinology 40 22966133
2012 COUP-TFII is essential for metanephric mesenchyme formation and kidney precursor cell survival. Development (Cambridge, England) 39 22669823
2002 Expression of COUP-TFII in metabolic tissues during development. Mechanisms of development 39 12385758
2016 MicroRNA-382 inhibits prostate cancer cell proliferation and metastasis through targeting COUP-TFII. Oncology reports 38 27748848
2014 The role of the orphan nuclear receptor COUP-TFII in tumorigenesis. Acta pharmacologica Sinica 38 25283503
2011 COUP-TFII expressing interneurons in human fetal forebrain. Cerebral cortex (New York, N.Y. : 1991) 38 22178710
2021 NR2F2 controls malignant squamous cell carcinoma state by promoting stemness and invasion and repressing differentiation. Nature cancer 37 35122061
2016 MiR-382 inhibits cell growth and invasion by targeting NR2F2 in colorectal cancer. Molecular carcinogenesis 37 26800338
2015 The COUP-TFII/Neuropilin-2 is a molecular switch steering diencephalon-derived GABAergic neurons in the developing mouse brain. Proceedings of the National Academy of Sciences of the United States of America 37 26305926
2014 The INSL3 gene is a direct target for the orphan nuclear receptor, COUP-TFII, in Leydig cells. Journal of molecular endocrinology 36 24780841
2008 The transcription factor COUP-TFII is negatively regulated by insulin and glucose via Foxo1- and ChREBP-controlled pathways. Molecular and cellular biology 36 18765640
2016 De novo frameshift mutation in COUP-TFII (NR2F2) in human congenital diaphragmatic hernia. American journal of medical genetics. Part A 34 27363585
2022 Nr2f2 Overexpression Aggravates Ferroptosis and Mitochondrial Dysfunction by Regulating the PGC-1α Signaling in Diabetes-Induced Heart Failure Mice. Mediators of inflammation 33 36081650
2013 COUP-TFII in pancreatic adenocarcinoma: clinical implication for patient survival and tumor progression. International journal of cancer 33 24122412
2019 Oncogenic KRAS signaling activates mTORC1 through COUP-TFII-mediated lactate production. EMBO reports 32 30988000
2019 Cooperativity of co-factor NR2F2 with Pioneer Factors GATA3, FOXA1 in promoting ERα function. Theranostics 32 31588232
2014 COUP-TFII regulates metastasis of colorectal adenocarcinoma cells by modulating Snail1. British journal of cancer 32 25032732
2010 Involvement of transcription factor NR2F2 in human trophoblast differentiation. PloS one 32 20195529
2021 Orphan nuclear receptor COUP-TFII enhances myofibroblast glycolysis leading to kidney fibrosis. EMBO reports 30 34031962
2020 Small-molecule inhibitor targeting orphan nuclear receptor COUP-TFII for prostate cancer treatment. Science advances 30 32494682
2020 NR2F2 plays a major role in insulin-induced epithelial-mesenchymal transition in breast cancer cells. BMC cancer 30 32631390
2017 A novel NR2F2 loss-of-function mutation predisposes to congenital heart defect. European journal of medical genetics 30 29222010
2014 The critical roles of COUP-TFII in tumor progression and metastasis. Cell & bioscience 30 25328664
2004 Interaction of the glucocorticoid receptor and the chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII): implications for the actions of glucocorticoids on glucose, lipoprotein, and xenobiotic metabolism. Annals of the New York Academy of Sciences 30 15265774
2001 COUP-TFI and COUP-TFII regulate expression of the NHE through a nuclear hormone responsive element with enhancer activity. European journal of biochemistry 26 11168401
2014 High NR2F2 transcript level is associated with increased survival and its expression inhibits TGF-β-dependent epithelial-mesenchymal transition in breast cancer. Breast cancer research and treatment 25 25129343
2016 NR2F2 regulates chondrogenesis of human mesenchymal stem cells in bioprinted cartilage. Biotechnology and bioengineering 24 27345768
2016 COUP-TFII regulates satellite cell function and muscular dystrophy. The Journal of clinical investigation 24 27617862
2015 Transcription factors COUP-TFI and COUP-TFII are required for the production of granule cells in the mouse olfactory bulb. Development (Cambridge, England) 24 25922524
2017 Dysregulation of nuclear receptor COUP-TFII impairs skeletal muscle development. Scientific reports 23 28600496
2012 COUP-TFII controls mouse pancreatic β-cell mass through GLP-1-β-catenin signaling pathways. PloS one 23 22292058
2018 COUP-TFII revisited: Its role in metabolic gene regulation. Steroids 22 30481528
2016 The orphan nuclear receptor COUP-TFII coordinates hypoxia-independent proangiogenic responses in hepatic stellate cells. Journal of hepatology 22 27866920
2021 Fbxo21 regulates the epithelial-to-mesenchymal transition through ubiquitination of Nr2f2 in gastric cancer. Journal of Cancer 21 33531987
2019 NR2F2 loss‑of‑function mutation is responsible for congenital bicuspid aortic valve. International journal of molecular medicine 21 30720060
2005 Dynamic expression of COUP-TFI and COUP-TFII during development and functional maturation of the mouse inner ear. Gene expression patterns : GEP 21 15907456
2023 An epigenetic switch controls an alternative NR2F2 isoform that unleashes a metastatic program in melanoma. Nature communications 20 37015919
2018 Suppression of COUP-TFII upregulates angiogenin and promotes angiogenesis in endometriosis. Human reproduction (Oxford, England) 20 29982401
2013 Aberrant expression and regulation of NR2F2 and CTNNB1 in uterine fibroids. Reproduction (Cambridge, England) 20 23704310
2013 COUP-TFII inhibits NFkappaB activation in endocrine-resistant breast cancer cells. Molecular and cellular endocrinology 20 24141032
2015 Choose your destiny: Make a cell fate decision with COUP-TFII. The Journal of steroid biochemistry and molecular biology 19 26658017
2020 LncRNA NR2F2-AS1 Silencing Induces Cell Cycle Arrest in G0/G1 Phase via Downregulating Cyclin D1 in Colorectal Cancer. Cancer management and research 18 32210626
2020 NR2F2-AS1 accelerates cell proliferation through regulating miR-4429/MBD1 axis in cervical cancer. Bioscience reports 18 32469064
2020 Elevated COUP-TFII expression in dopaminergic neurons accelerates the progression of Parkinson's disease through mitochondrial dysfunction. PLoS genetics 18 32579581
2015 Mutation within the hinge region of the transcription factor Nr2f2 attenuates salt-sensitive hypertension. Nature communications 18 25687237
2023 Heterozygous rare variants in NR2F2 cause a recognizable multiple congenital anomaly syndrome with developmental delays. European journal of human genetics : EJHG 17 37500725
2017 Inactivation of the Nuclear Orphan Receptor COUP-TFII by Small Chemicals. ACS chemical biology 17 28059499
2016 Knockdown of COUP-TFII inhibits cell proliferation and induces apoptosis through upregulating BRCA1 in renal cell carcinoma cells. International journal of cancer 17 27193872

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