| 1997 |
COUP-TFI (NR2F1) represses transcription via direct interaction with corepressors N-CoR and SMRT. The C-terminal 35 amino acids of COUP-TFI constitute a repressor domain required for silencing activity. COUP-TFI and unliganded TRβ share common corepressors, demonstrated by squelching experiments and yeast two-hybrid/GST pull-down assays showing direct binding to N-CoR (aa 921-2453) and SMRT fragments. |
Yeast two-hybrid, GST pull-down, cotransfection repression/squelching assays, deletion mutagenesis |
Molecular endocrinology |
High |
9171235
|
| 1992 |
EAR-3/COUP-TFI binds specifically to regulatory elements BA1, CIIIB, and AIIJ in the ApoB, ApoCIII, and ApoAII gene promoters with Kd 1–3 nM, and represses transcription from these elements in cotransfection experiments in HepG2 cells. EAR-3 can compete with and displace HNF-4 from the same elements to suppress transcription. |
EMSA (dissociation constant measurement), cotransfection reporter assays in HepG2 cells, competition binding assays |
The Journal of biological chemistry |
High |
1639815
|
| 1995 |
EAR-3/COUP-TFI represses Oct-3/4 promoter activity through the RAREoct site in P19 embryonal carcinoma cells in a dose-dependent manner via the C-terminal domain. COUP-TFI binds RAREoct with higher affinity than RAR:RXR heterodimers, allowing it to compete with and displace RAR:RXR from the site, actively silencing Oct-3/4 promoter activity. RA treatment of EC cells upregulates COUP-TFI expression, which inversely correlates with Oct-3/4 repression. |
Cotransfection reporter assays, EMSA competition/binding assays, deletion mutagenesis of C-terminal domain |
Molecular and cellular biology |
High |
7823919
|
| 1999 |
Loss of COUP-TFI in mouse cortex results in absence of cortical layer IV due to failure of thalamocortical projections, and subplate neurons undergo improper differentiation and premature cell death. COUP-TFI is required for subplate neuron differentiation which in turn guides thalamocortical axon innervation. |
Coup-tf1 null mouse knockout, histology, axon tracing |
Neuron |
High |
10624948
|
| 2001 |
COUP-TFI acts as an intrinsic factor for early regionalization of the neocortex, independent of thalamic input. COUP-TFI null mice show altered region-specific expression of cortical marker genes and miswired area-specific thalamocortical connections, indicating COUP-TFI works in concert with Pax6 and Emx2 to specify neocortical identity. |
COUP-TFI null mouse knockout, marker gene expression analysis, axon tracing |
Genes & development |
High |
11511537
|
| 2007 |
Cortex-specific deletion of COUP-TFI in mice causes massive expansion of frontal/motor areas and compression of sensory areas. COUP-TFI acts within its expression domain (highest in parietal/occipital, lowest in frontal cortex) to repress frontal/motor area identities and specify sensory area identities, demonstrating it is required for balancing neocortical arealization. |
Cortex-specific conditional knockout (Cre-lox), molecular marker analysis, axonal projection tracing |
Nature neuroscience |
High |
17828260
|
| 2007 |
COUP-TFI loss-of-function and gain-of-function manipulations show it promotes ventral cortical fate, promotes cell cycle exit and neural differentiation, and regulates the balance of early- and late-born neurons, in part by repressing MAPK/ERK, AKT, and β-catenin signaling in cortical progenitors. |
Loss-of-function and gain-of-function in vivo and in vitro, signaling pathway readouts (pERK, pAKT, β-catenin) |
Cerebral cortex |
Medium |
18165280
|
| 2008 |
COUP-TFI (and COUP-TFII) are required for temporal specification of neural stem/progenitor cells in the CNS, including acquisition of gliogenic competence. Double knockdown of Coup-tfI/II in ESC-derived NSPCs and developing mouse forebrain causes sustained neurogenesis and prolonged generation of early-born neurons, demonstrating these factors function as molecular switches for the neurogenic-to-gliogenic transition. |
Double shRNA knockdown in ESC-derived NSPCs and in vivo mouse forebrain, cell fate marker analysis, gliogenic cytokine responsiveness assays |
Nature neuroscience |
High |
19160499
|
| 2008 |
COUP-TFI forms a transcriptional repressor complex with NCoR, TIF1β/KAP-1, HDAC1, SWI/SNF member Brahma, and DBC1 in HeLa cells. Tandem affinity purification identified these components. COUP-TFI interacts directly with NCoR in a manner different from other nuclear receptors; DBC1 stabilizes the COUP-TFI–NCoR interaction. This complex represses TNFAIP8 transcription and is involved in TNFα signaling. |
Tandem affinity purification (TAP), in vitro binding assays, cotransfection reporter assays, TNFAIP8 promoter analysis |
The Journal of biological chemistry |
High |
19112178
|
| 2006 |
COUP-TFI is required for axonal growth and guidance of forebrain commissures (corpus callosum, hippocampal commissure, anterior commissure). In COUP-TFI null mice, fibers fail to cross the midline. Microarray analysis of COUP-TFI null cortex reveals decreased MAP1B and increased RND2 protein levels, identifying these cytoskeleton regulators as downstream effectors of COUP-TFI in axonal morphogenesis. |
COUP-TFI null mouse knockout, axon tracing, microarray expression profiling, primary hippocampal neuron culture, Western blot |
Development |
High |
17021036
|
| 2010 |
COUP-TFI controls timing of birth and specification of corticospinal motor neurons (CSMN) in somatosensory cortex by repressing a CSMN differentiation program. Loss of COUP-TFI causes premature area-specific generation of neurons with CSMN features that project to subcerebral structures, while genuine CSMN fail to project beyond the pons, resulting in impaired skilled motor function. |
Conditional cortical COUP-TFI knockout, axon tracing, motor behavior assays, molecular marker analysis |
PNAS |
High |
20133588
|
| 2011 |
COUP-TFI is required for specification of CGE-derived cortical interneurons. Conditional loss of COUP-TFI in subventricular precursors and postmitotic cells leads to decreased late-born VIP+ and CR+ bipolar neurons and compensatory increase of early-born PV+ MGE-derived interneurons. COUP-TFI mutants are more resistant to pharmacologically induced seizures in a GABAergic signaling-dependent manner. |
Conditional knockout (subventricular precursor and postmitotic), interneuron subtype marker analysis, pharmacological seizure induction |
The Journal of neuroscience |
High |
21430164
|
| 2011 |
COUP-TFI directly represses Rnd2 (a Rho-GTPase modulator of radial migration) expression at the post-mitotic level along the rostrocaudal axis of the neocortex. In COUP-TFI mutant mice, callosal projection neurons are delayed in reaching the cortical plate and have morphological defects. Restoring correct Rnd2 levels cell-autonomously rescues neuron radial migration and morphological transitions as well as axonal elongation and dendritic arborization defects. |
COUP-TFI conditional knockout, in utero electroporation rescue (Rnd2 shRNA), immunostaining, axon/dendrite morphology analysis |
Development |
High |
21965613
|
| 2000 |
COUP-TFI interacts directly with ERα (estrogen receptor alpha), COUP-TF, and ERRα1 in a ligand-dependent manner in vitro. AHR interacts with COUP-TFI in transfected CV-1 cells. COUP-TFI binds consensus xenobiotic response elements (XRE), and overexpression of COUP-TFI inhibits TCDD-activated CYP1A1 promoter reporter activity, suggesting COUP-TFI regulates AHR action via DNA binding competition and protein-protein interaction. |
In vitro protein-protein interaction assays, transfection in CV-1 cells, EMSA (XRE binding), reporter assay in MCF-7 cells |
Archives of biochemistry and biophysics |
Medium |
10620335
|
| 2002 |
COUP-TFI forms a tight physical complex with human ERα. This complex increases the affinity of ERα for ERK2/p42MAPK, resulting in enhanced phosphorylation of hERα Ser118 and strengthened AF-1 transactivation activity. The cooperation is restricted to cell lines permissive to ERα AF-1 activation. |
Co-immunoprecipitation (complex formation), kinase assay (Ser118 phosphorylation), transfection in multiple cell lines, functional reporter assays |
The EMBO journal |
High |
12093745
|
| 2003 |
EAR3/COUP-TFI represses LHR gene transcription via a mechanism involving cross-talk among EAR3, Sp1/Sp3 bound at the Sp1(I) site, and TFIIB. EAR3 specifically decreases association of TFIIB with the Sp1(I) site and reduces RNA polymerase II recruitment to the LHR promoter. Overexpression of TFIIB counteracts EAR3-mediated inhibition. EAR3's N-terminal and DNA-binding domains are required for Sp1 interaction and inhibitory function. |
Cotransfection reporter assays (SL2 cells), ChIP (RNA pol II recruitment), EMSA/co-IP (TFIIB-Sp1 interaction), deletion mutagenesis |
Molecular and cellular biology |
High |
12972613
|
| 2003 |
COUP-TF1 represses HBV pregenomic RNA and pre-C RNA synthesis >10-fold through nuclear receptor response elements NRREpreC and NRREenhI. HNF4α and COUP-TF1 antagonize each other's effects on HBV gene expression and viral DNA synthesis. A naturally occurring HBV variant that prevents COUP-TF1 binding but retains HNF4α binding shows significantly higher pregenomic RNA and viral DNA synthesis. |
Cotransfection in Huh7 cells, viral RNA quantification, viral DNA synthesis assay, natural variant analysis, deletion analysis |
Journal of virology |
Medium |
12551987
|
| 2004 |
COUP-TFI is expressed in oligodendrocyte lineage cells and is required for oligodendrocyte differentiation and CNS myelination. COUP-TFI null mice show delayed axon myelination and increased dysmyelination. In vitro differentiation assays confirm myelination defects are due to delayed oligodendrocyte differentiation. COUP-TFI acts as an upstream regulator of SCIP/Oct-6/Tst-1, a transcription factor involved in axon myelination. |
COUP-TFI null mouse knockout, in vitro oligodendrocyte differentiation assay, in situ hybridization, transfection analysis |
Developmental biology |
High |
14738874
|
| 2000 |
COUP-TFI inhibits BMP-4 1A promoter activity in fetal rat calvarial osteoblasts. Specific binding of COUP-TFI to response regions in the BMP-4 1A 5'-flanking region was demonstrated, and co-transfection of a COUP-TFI expression plasmid with the BMP-4 1A promoter construct showed COUP-TFI silences BMP-4 transcription. |
EMSA (specific binding to promoter elements), cotransfection reporter assay in primary osteoblasts |
The Journal of biological chemistry |
Medium |
7499338
|
| 2000 |
COUP-TFI binds the Nkx2.5 binding site in the calreticulin gene promoter and suppresses calreticulin transcription during cardiac development. Nkx2.5 activates calreticulin gene expression while COUP-TF1 binding to the same site antagonizes Nkx2.5-mediated activation. |
Cotransfection reporter assays, DNA binding assays, promoter analysis |
The Journal of biological chemistry |
Medium |
11106640
|
| 2000 |
In differentiating P19 cells, COUP-TFI dose-dependently regulates neuronal differentiation and migration. Low COUP-TFI enhances neuron outgrowth; high COUP-TFI impedes neuronal differentiation and elevates E-cadherin mRNA. Dominant-negative COUP-TFI inhibits neurite extension. COUP-TFI favors neuron migration through an integrin-dependent mechanism and upregulates vitronectin mRNA and promoter activity. |
Stable and transient transfection in P19 cells, dominant-negative approach, RGD peptide interference assay, RT-PCR, transient transfection reporter assay (vitronectin promoter) |
Molecular endocrinology |
Medium |
11117523
|
| 2000 |
COUP-TFI (as a transactivator) requires amino acids 184-423 for all three mechanisms of transcriptional activation: binding to gAF1/gAF3 accessory elements, direct DNA binding transactivation, and coactivation through DNA-bound HNF-4. GRIP1 and SRC-1 potentiate COUP-TFI activity and associate with COUP-TFI in vivo via this same region. |
Deletion mutagenesis, cotransfection reporter assays, in vivo co-immunoprecipitation with GRIP1/SRC-1 |
The Journal of biological chemistry |
Medium |
10652338
|
| 2006 |
COUP-TFI controls Notch signaling in cochlear development. COUP-TFI knockout mice show increased hair cell number and misregulation of Notch components including Jag1 and Hes5, consistent with reduced Notch signaling. Inhibition of Notch activity by γ-secretase inhibitor causes greater increase in hair cell differentiation in COUP-TFI(-/-) than wild-type cochlear cultures, indicating hypersensitivity to Notch inactivation in COUP-TFI null cochlea. |
COUP-TFI knockout mouse, in vitro organ culture with γ-secretase inhibitor, Notch target gene expression analysis |
Development |
Medium |
16914494
|
| 2010 |
Genome-wide identification of direct COUP-TFI target genes using integration of microarray data and COUP-TFI ChIP. Fabp7 is a direct COUP-TFI target: COUP-TFI occupies conserved binding sites in the Fabp7 promoter in vivo (ChIP), Fabp7 transcript and protein are reduced in COUP-TFI null tissues, and the Fabp7 promoter shows active chromatin marks (H3K9ac, CBP, SRC-1 enrichment) dependent on COUP-TFI. |
Microarray (COUP-TFI KO vs WT inner ear), computational binding site prediction, ChIP (in vivo and in vitro), Western blot, chromatin state analysis |
PloS one |
High |
20111703
|
| 2012 |
NR2F1 represses MTTP gene expression by binding to a direct repeat 1 (DR1) element in the MTTP promoter, which suppresses synergistic activation by HNF-4α and HNF-1α. This repression is further enhanced by nuclear receptor corepressor 1 (NCoR1). NR2F1 does not alter individual activities of HNF-4α or HNF-1 but specifically abrogates their synergistic cooperation. |
Cotransfection reporter assays, EMSA (DR1 binding), corepressor overexpression |
Journal of lipid research |
Medium |
22357705
|
| 2013 |
PRC2 (specifically Suz12-dependent) is recruited to the NR2F1 promoter upon retinoic acid treatment, transiently increasing H3K27me3 marks and attenuating RA-induced NR2F1 transcription. Functional depletion of Suz12 by shRNA enhances RA-associated NR2F1 transcription, identifying PRC2 as a repressive modulator of NR2F1 expression. |
shRNA depletion of Suz12, RT-PCR, ChIP (H3K27me3, PRC2 occupancy), comparison with Hoxa5 gene |
Nucleic acids research |
Medium |
23666625
|
| 2013 |
COUP-TFI and Sp8 reciprocally repress each other's expression in cortical progenitors. Misexpression of Sp8 represses COUP-TFI, and conditional ablation of Sp8 has the opposite effect. Transgenic misexpression of COUP-TFI downregulates Sp8. Sp8 promotes FGF target molecule expression in an Fgf8-independent manner. |
Binary transgenic misexpression, conditional Sp8 knockout, molecular marker analysis in developing cortex |
Cerebral cortex |
Medium |
23307639
|
| 2013 |
COUP-TFI regulates activity-dependent tyrosine hydroxylase (TH) expression in dopaminergic olfactory bulb interneurons. Odor deprivation downregulates both TH and COUP-TFI in dopaminergic cells. Conditional inactivation of COUP-TFI in the EMX1 lineage reduces TH and ZIF268 expression. Lentiviral COUP-TFI deletion in adult-generated interneurons confirms cell-autonomous control of TH expression through ZIF268 induction. |
Conditional knockout (EMX1-Cre), odor deprivation paradigm, lentiviral cell-autonomous deletion, immunostaining |
Development |
High |
24227652
|
| 2014 |
NR2F1 missense mutations in the zinc-finger DNA-binding domain and the putative ligand-binding domain decrease NR2F1 transcriptional activity as measured by luciferase reporter assay, establishing that NR2F1 DNA-binding and ligand-binding domain integrity is required for transcriptional function. |
Luciferase reporter assay with patient-derived missense mutant constructs |
American journal of human genetics |
Medium |
24462372
|
| 2015 |
NR2F1 drives tumor cell dormancy by inducing global chromatin repression and upregulating SOX9, RARβ, CDK inhibitors, and the pluripotency gene NANOG. NR2F1-dependent quiescence is recapitulated by co-treatment with 5-Aza-C and retinoic acid. In vivo blockade of NR2F1 interrupts growth arrest or survival of dormant DTCs in different organs. |
In vitro dormancy models (HNSCC), in vivo mouse models, epigenetic co-treatment (5-Aza-C + RA), gene knockdown/overexpression, ChIP (chromatin repression analysis), bone marrow DTC analysis from prostate cancer patients |
Nature communications |
High |
25636082
|
| 2017 |
Coup-TF1 and Coup-TF2 (Nr2f1 and Nr2f2) expressed in an arc-shaped MGE progenitor domain promote time-dependent survival of this neuroepithelium and specification of layer V SST+ cortical interneurons. They autonomously repress PV+ fate in MGE progenitors, in part by directly driving Sox6 expression. |
Conditional knockout of Coup-TF1/TF2 in MGE progenitors, interneuron subtype marker analysis, Sox6 expression analysis |
Development |
High |
28694260
|
| 2019 |
In the developing sensory neocortex, Foxg1 binds to an H3K4me1-enriched enhancer site to repress COUP-TFI expression. Ectopic Foxg1 in layer 4 cells transforms local projection neurons to callosal projection neurons; removal of Foxg1 in long-range projection neurons derepresses COUP-TFI and activates a layer 4 neuron-specific program. Early growth response genes (Egr) repress Foxg1 in layer 4 precursors via TGF-β signaling. |
ChIP (H3K4me1 enhancer), in utero electroporation (gain/loss of function), conditional knockout, layer-specific marker analysis |
Nature communications |
High |
31395862
|
| 2018 |
COUP-TFI/NR2F1 is necessary and sufficient to promote neurogenesis by suppressing astrogliogenesis in adult hippocampal neural stem cells. Inducible COUP-TFI knockout reduces neurogenesis and increases astrocyte production without depleting the NSC pool. Forced COUP-TFI expression decreases astrogliogenesis and rescues the neuro-astrogliogenic imbalance under neuroinflammation. |
Inducible conditional knockout, retroviral loss-of-function, genetic fate mapping, gain-of-function overexpression, neuroinflammation model |
Cell reports |
High |
29996095
|
| 2019 |
NR2F1 promotes CXCL12 and CXCR4 expression in salivary adenoid cystic carcinoma cells and activates CXCL12/CXCR4 pathway. ChIP assays demonstrate direct NR2F1 binding at the CXCL12/CXCR4 loci. Overexpression of CXCL12 partially rescues proliferation, migration, and invasion activities suppressed by NR2F1 silencing. |
NR2F1 overexpression/siRNA knockdown, ChIP (CXCL12/CXCR4 promoters), proliferation/migration/invasion assays, rescue experiments |
BMC cancer |
Medium |
31357956
|
| 2020 |
NR2F1 regionally controls long-term self-renewal of neural progenitor cells via modulation of cell cycle genes and Pax6. In BBSOAS patients with NR2F1 haploinsufficiency, polymicrogyria-like brain malformations occur in parietal/occipital cortex. In cerebral organoids, reduced NR2F1 levels affect neurogenesis and PAX6 expression. |
BBSOAS mouse model (Nr2f1 haploinsufficient), patient brain MRI, cerebral organoids (NR2F1 knockdown), cell cycle gene expression analysis |
The EMBO journal |
High |
32484994
|
| 2020 |
NR2F1 expression is positively regulated by p38α signaling and repressed by HER2 and WNT4 pathways in early-stage breast cancer cells. Loss of NR2F1 function increases in vivo dissemination accompanied by decreased E-cadherin, activated WNT-dependent β-catenin signaling, disorganized laminin 5, and increased EMT genes (TWIST1, ZEB1, PRRX1), promoting a hybrid luminal/basal phenotype. |
High-resolution intravital imaging, NR2F1 loss-of-function, E-cadherin/β-catenin/laminin immunostaining, signaling pathway inhibitors (p38α, HER2, WNT4), gene expression analysis |
Cancer research |
Medium |
35471456
|
| 2021 |
A specific small-molecule agonist (DIM-C-Pyr-4 derivative) of NR2F1 activates dormancy programs in malignant cells via a self-regulated increase in NR2F1 mRNA/protein and downstream transcription. This leads to growth arrest, inhibition of mTOR signaling, metastasis suppression, and induction of a neural crest lineage program. The effect is lost when NR2F1 is knocked out by CRISPR-Cas9. |
Small-molecule agonist treatment, CRISPR-Cas9 NR2F1 knockout (loss of function confirmation), RNA-seq, 3D culture assay, patient-derived organoids, in vivo mouse metastasis model, immunofluorescence (NR2F1hi/p27hi/Ki67lo phenotype) |
The Journal of experimental medicine |
High |
34812843
|
| 2021 |
LRRK2-G2019S mutation in Parkinson's disease decreases NR2F1 expression in neuroepithelial stem cells, neurons, and midbrain organoids. NR2F1-deficient mouse embryos show accelerated dopaminergic differentiation in vivo, suggesting NR2F1 normally restrains cell-cycle exit and differentiation timing in dopaminergic neurogenesis. |
Patient-specific NESCs (iPSC-derived), high-throughput image analysis, single-cell RNA sequencing, NR2F1-deficient mouse embryos, midbrain organoids |
Cell reports |
Medium |
34686322
|
| 2022 |
METTL3 methylates NR2F1 mRNA in an m6A-dependent manner to regulate NR2F1 expression in retinal pigment epithelium cells. NR2F1 deficiency reverses the decreased Occludin expression and increased IL-6 secretion observed in METTL3-defective RPE cells, placing NR2F1 downstream of m6A modification by METTL3 in RPE inflammation regulation. |
MeRIP-sequencing (m6A mapping), RNA-seq, METTL3 silencing/NR2F1 silencing, Western blot (Occludin), ELISA (IL-6), rescue experiments |
Frontiers in immunology |
Medium |
35936005
|
| 2023 |
SETD2 inactivation reduces NR2F1 transcription by impairing H3K36me3 deposition and chromatin accessibility at the NR2F1 locus. Reduced NR2F1 activates the STAT1 signaling pathway to promote chemokines, PD-1 expression, and antigen presentation. ChIP-seq and ATAC-seq confirm the SETD2→H3K36me3→NR2F1 chromatin regulatory axis. |
ATAC-seq, ChIP-seq (H3K36me3), RNA-seq, single-cell RNA-seq, Setd2 knockout syngeneic mouse models, flow cytometry |
Journal for immunotherapy of cancer |
High |
38056895
|
| 2007 |
COUP-TFI activation of the vitronectin gene in P19 cells is accompanied by recruitment of thymine DNA glycosylase (TDG) and p68 RNA helicase. DNA methyltransferases Dnmt3a and Dnmt3b are loaded onto the activated vitronectin gene, with strand-biased decrease in CpG methylation. Dnmt3a co-immunoprecipitates with COUP-TFI and TDG in vivo; cotransfection shows Dnmt3a/b enhances COUP-TFI-mediated activation of a methylated reporter gene. |
ChIP (TDG, p68, Dnmt3a occupancy), bisulfite sequencing (CpG methylation), co-immunoprecipitation (Dnmt3a–COUP-TFI–TDG), cotransfection reporter assay |
Molecular endocrinology |
Medium |
17579209
|
| 2009 |
COUP-TFI binds retinoic acid-responsive elements (RAREs) in the ceramide kinase (CERK) promoter and represses CERK transcription during ATRA-induced differentiation of SH-SY5Y neuroblastoma cells. EMSA shows ATRA-induced binding of COUP-TFI, RARα, and RXRα to the RARE. ChIP confirms recruitment of COUP-TFI and corepressors to this region. siRNA knockdown of COUP-TFI relieves CERK repression. |
EMSA, DNA pull-down, ChIP (COUP-TFI and corepressor recruitment), siRNA knockdown, promoter truncation/mutation assays |
Journal of neurochemistry |
Medium |
19903244
|
| 2017 |
COUP-TFI is required for proper hippocampal development along the septo-temporal longitudinal axis. Loss of cortical COUP-TFI results in dysmorphic hippocampus with altered shape, volume, and connectivity, particularly in dorsal and intermediate regions. Topographic entorhinal cortex inputs are strongly impaired in the dorsal hippocampus. These structural changes are associated with selective spatial learning and memory impairment. |
Cortical COUP-TFI conditional knockout, hippocampal volumetry/shape analysis, axon tracing, spatial memory behavioral testing (Morris water maze or equivalent) |
Cerebral cortex |
High |
26813976
|
| 2019 |
COUP-TFI is required in dentate gyrus progenitors for modulating Cxcr4 receptor expression during granule cell neurogenesis and migration. Loss of COUP-TFI in progenitors leads to decreased granule cell proliferation, precocious differentiation, increased apoptosis, and high Cxcr4 expression with aberrant migration. High COUP-TFI expression downregulates Cxcr4. Increased Cxcr4 expression in wild-type cells phenocopies COUP-TFI loss-of-function migration defects. |
Conditional knockout (progenitor vs. postmitotic), gain-of-function Cxcr4 overexpression, immunostaining, proliferation and migration analysis |
Development |
High |
28506990
|