| 1987 |
OTF-1 (POU2F1) was purified from HeLa nuclear extracts and shown to directly stimulate transcription of the human histone H2b gene in a reconstituted in vitro system, dependent on an intact octamer element and the TATA motif but not other H2b promoter elements. Activity was absent in G2-synchronized cells, establishing cell-cycle-dependent regulation. |
DNA affinity chromatography purification, SDS-PAGE renaturation, reconstituted in vitro transcription assay |
Cell |
High |
3677172
|
| 1988 |
OTF-1 (POU2F1) is physically and functionally identical to the adenovirus DNA replication factor NF-III: identical SDS-PAGE mobility, same binding site and affinity at the adenovirus origin, ability to substitute for NF-III in activating adenovirus DNA replication in vitro, and NF-III can substitute for OTF-1 in H2b transcription, demonstrating a dual role in transcription and DNA replication. |
SDS-PAGE, DNA-binding assays, in vitro adenovirus DNA replication assay, in vitro transcription complementation assay |
Science |
High |
3413485
|
| 1988 |
OTF-1 (POU2F1) binds the TAATGARAT sequence in HSV immediate-early gene promoters. The herpes simplex virus trans-activator Vmw65 (VP16) induces formation of an additional, more-retarded complex containing OTF-1, and at least one additional cellular factor (distinct from OTF-1) is required for this complex formation. |
Affinity purification, electrophoretic mobility shift assay (EMSA), complementation with OTF-1-depleted nuclear extracts |
Proceedings of the National Academy of Sciences of the United States of America |
High |
2842768
|
| 1990 |
OTF-1 (POU2F1) and Sp1 physically interact and show cooperative binding to DNA: Sp1 binding sites stimulate transcription more strongly when paired with low-affinity OTF-1 sites than high-affinity ones, and this functional cooperation is mirrored by cooperative protein–DNA complex formation in vitro. |
Synthetic enhancer constructs, in vitro transcription assays, EMSA cooperative binding |
Proceedings of the National Academy of Sciences of the United States of America |
High |
2191301
|
| 1990 |
Purified OTF-1 (POU2F1) and OTF-2 show indistinguishable DNA-binding affinity and contacts on H2b and immunoglobulin promoters and equivalent intrinsic capacity to activate transcription from either promoter in OTF-depleted extracts. Full immunoglobulin gene transcription additionally requires a B-cell-specific component that interacts with OTFs. |
High-resolution DNase I footprinting, EMSA competition, reconstituted in vitro transcription with OTF-depleted HeLa and B-cell extracts |
Molecular and cellular biology |
High |
2123291
|
| 1991 |
The MMTV promoter contains two degenerate octamer motifs upstream of the TATA box that bind OTF-1 (POU2F1). In vitro, mutation of these octamer motifs abolishes the stimulatory effect of purified progesterone receptor on transcription without affecting basal transcription. Progesterone and glucocorticoid receptors bound to the HRE facilitate binding of OTF-1 to these sites, revealing OTF-1 as a mediator of hormonal induction through cooperative DNA binding with hormone receptors. |
DNA binding assays, in vitro transcription with purified progesterone receptor, transfection with promoter mutants |
Cell |
High |
1846780
|
| 1991 |
OTF-1 (POU2F1) binds two distinct sites in the Aγ-globin gene promoter: site II (octamer-related) and site I (purine-rich, -291 to -267) with equal affinity despite site I having no obvious octamer similarity, as shown by immunological identity and methylation interference footprinting. |
Immunological identity assay, EMSA, methylation interference footprinting |
Biochemistry |
Medium |
2007132
|
| 1992 |
The glucocorticoid receptor (GR) negatively regulates OTF-1 (POU2F1) function in a hormone-dependent manner by directly associating with OTF-1 in solution, independent of DNA binding, resulting in repression of OTF-1 DNA-binding activity. The homeodomain subdomain of OTF-1 that interacts with VP16 is also critical for GR interaction. |
In vivo reporter assays, nuclear extract DNA-binding assay, in vitro incubation with purified GR, chemical cross-linking and immunoprecipitation |
Molecular and cellular biology |
High |
1406672
|
| 1998 |
OTF-1 (POU2F1) can bind its cognate site on the MMTV promoter assembled into an H3/H4 tetramer particle but cannot access the same site on a full histone octamer particle. SWI/SNF complex remodels the octamer particle to a tetramer-like state in an ATP-dependent manner, enabling OTF-1 binding. |
Chromatin reconstitution with recombinant histones, site-directed hydroxyl radical mapping, factor-binding assays on nucleosomal templates, SWI/SNF remodeling assay |
Journal of molecular biology |
High |
9614938
|
| 2006 |
Oct-1 (Pou2f1) acts as a co-factor for Sox2 during mouse lens and nasal placode induction. Genetic combination of Sox2 and Pou2f1 hypomorphic alleles causes impaired lens placode induction and complete failure of nasal placode induction. Oct-1 and Sox2 cooperatively bind composite Sox/Octamer sites in the Pax6 lens ectoderm enhancer to drive transactivation, and these same sites are required for enhancer activity in transgenic mice. |
Genetic epistasis (compound heterozygous mouse mutants), in vitro transactivation assay, transgenic enhancer analysis in mice |
Developmental biology |
High |
17140559
|
| 2013 |
Oct1/Pou2f1 is modified by O-linked β-N-acetylglucosamine (O-GlcNAc) at positions T255 and S728. Under anchorage-independent overgrowth conditions, O-GlcNAcylation correlates with 3-fold increased Oct1 binding to the Gadd45a promoter, transcriptional repression of Gadd45a, reduced association with lamin B1, and reduced nuclear periphery puncta. The O-GlcNAc sites are required for both Gadd45a repression under overgrowth and Gadd45a activation upon acute starvation, and for anchorage-independent survival. Specific ubiquitination sites on Oct1 were also identified. |
O-GlcNAc site mapping, ChIP assay, site-directed mutagenesis of modification sites, FRAP/localization imaging, functional reporter assays |
FASEB journal |
High |
23580612
|
| 2015 |
In gastric cancer cells, the ACK1 kinase phosphorylates AKT at Thr308 and Ser473, activating the AKT pathway which up-regulates POU2F1, which in turn directly binds the ECD promoter to drive ECD transcription. ECD silencing blocks ACK1-induced EMT, migration, and invasion, placing POU2F1 as a transcriptional effector downstream of ACK1/AKT in this signalling axis. |
SILAC proteomics, promoter binding assay, knockdown/overexpression functional assays, in vivo metastasis model, phosphorylation analysis |
The Journal of pathology |
Medium |
25678401
|
| 2017 |
POU2F1 directly binds the CTHRC1 promoter and activates its transcription; HPV E6/E7 proteins regulate CTHRC1 expression via an E6/E7-p53-POU2F1 axis in cervical cancer, and CTHRC1 promotes invasion by activating the Wnt/PCP signaling pathway. |
Promoter binding/reporter assays, gain/loss-of-function, in vitro invasion assay, in vivo metastasis model |
Scientific reports |
Medium |
28303973
|
| 2017 |
POU2F1 is regulated upstream by the AKT pathway in hepatocellular carcinoma cells, and POU2F1 overexpression reverses the inhibition of malignant phenotypes (proliferation, EMT, migration, invasion) caused by AKT knockdown, positioning POU2F1 as a key downstream effector of AKT. POU2F1 induces transcription of EMT genes Twist1, Snai1, Snai2, and ZEB1. |
Knockdown/overexpression epistasis, Western blotting, in vitro functional assays |
Oncotarget |
Medium |
28489585
|
| 2017 |
POU2F1 directly binds the promoters of fibrosis repressors IL1R2, CD69, and TGIF2 (shown by ChIP) in cardiac fibroblasts and represses their expression. Pathological substrate stiffness upregulates POU2F1, which promotes cardiac fibroblast differentiation into myofibroblasts; POU2F1 knockdown upregulates these repressors and attenuates differentiation. |
ChIP assay, knockdown/overexpression on polyacrylamide hydrogels and in mouse MI tissue, immunofluorescence, Western blotting |
Science China. Life sciences |
Medium |
32617828
|
| 2017 |
POU2F1 is methylation-sensitive in its DNA binding at the HSP70 promoter: hypermethylation of a distal HSP70 promoter region reduces POU2F1 binding and reduces recruitment of the NuRD chromatin-remodeling complex, resulting in higher histone H3 acetylation at the HSP70 promoter. |
In vitro methylation-transcription assay, in vivo MeDIP, chromatin immunoprecipitation (POU2F1 and NuRD complex), histone acetylation analysis |
Journal of neurochemistry |
Medium |
28278364
|
| 2019 |
Oct1/Pou2f1 deletion in mouse colon blocks recovery from dextran sodium sulfate-induced damage and impairs organoid passaging, but preserves homeostasis. In a carcinogen-induced colon cancer model, Oct1 loss severely restricts tumorigenicity, while in an Apc-LOH model, Oct1 loss progressively increases tumor burden. Oct1 ChIP-seq identifies direct target genes associated with mitotic stability, metabolism, and stress response. |
Conditional gene deletion in mouse colon, organoid assays, DSS treatment model, chemical carcinogenesis model, Apc-LOH model, ChIP-seq |
PLoS genetics |
High |
31059499
|
| 2020 |
In developing mouse retina, Pou2f1 induces Pou2f2 expression; Pou2f2 then binds a POU motif in the Nrl (rod-inducing factor) promoter to repress its expression, thereby controlling the temporal window of cone photoreceptor production. Forced sustained Pou2f1/2 expression expands cone production; conditional inactivation of Pou2f2 increases Nrl and reduces cones. Pou2f1 is part of a cross-regulatory cascade with temporal factors Ikzf1 and Casz1. |
Retroviral misexpression, conditional knockout, promoter binding assay (POU motif in Nrl promoter), genetic epistasis |
Development |
High |
32878923
|
| 2021 |
POU2F1 directly binds the promoter of TTC3-AS1 (by ChIP and DNA-affinity precipitation) and activates its transcription in gastric cancer cells. TTC3-AS1 knockdown neutralizes the pro-tumor effects of POU2F1 overexpression in vitro and in mouse GC models, placing TTC3-AS1 downstream of POU2F1. |
ChIP assay, DNA-affinity precipitation, luciferase reporter assay, knockdown/overexpression, in vivo mouse model |
Journal of oncology |
Medium |
34257651
|
| 2021 |
POU2F1 directly binds and suppresses the NPR3 promoter (primarily at the -900 to -800 bp region), as shown by dual-luciferase reporter and site-directed mutagenesis assays. POU2F1 over-expression enhances cell proliferation and activates the PI3K/AKT pathway, effects reversed by NPR3 overexpression. |
Dual-luciferase reporter assay, site-directed mutagenesis, knockdown/overexpression, in vivo xenograft |
Cellular signalling |
Medium |
34229087
|
| 2021 |
POU2F1 autoregulates its own gene through two mechanisms: it acts via negative feedback on the ubiquitous (U) promoter through low-affinity binding sites, and via positive feedback on the tissue-specific (L) promoter through high-affinity canonical Oct sites. Knockdown activates the U promoter and downregulates the L promoter; overexpression has opposite effects. Binding confirmed by ChIP and EMSA. |
ChIP, EMSA, promoter reporter assay, knockdown/overexpression in Namalwa cells |
Molekuliarnaia biologiia |
Medium |
34837701
|
| 2021 |
POU2F1 activates transcription of CRK, which in turn promotes PD-L1 expression in lung cancer cells. POU2F1 overexpression increases PD-L1 surface expression; knockdown of POU2F1 reduces PD-L1 and enhances anti-PD-1 efficacy in a mouse tumor model. |
Luciferase reporter assay (CRK promoter), overexpression/knockdown, flow cytometry, immunofluorescence, in vivo mouse tumor model with anti-PD-1 |
American journal of translational research |
Medium |
33594317
|
| 2022 |
POU2F1 directly binds the ALDOA promoter (by ChIP and luciferase assay) to enhance ALDOA expression, thereby promoting aerobic glycolysis, the pentose phosphate pathway, and oxaliplatin resistance in colon cancer cells. |
ChIP assay, dual-luciferase reporter assay, knockdown/overexpression functional assays, metabolic flux measurements |
Oncogene |
Medium |
34997215
|
| 2022 |
C/EBPβ is a transcriptional activator of POU2F1, as confirmed by dual-luciferase reporter assay. Exercise training activates AMPK, which suppresses C/EBPβ, thereby reducing POU2F1 expression and attenuating Ang II-induced cardiac fibrosis in vivo. POU2F1 overexpression in vivo nullifies the cardioprotective effect of exercise. |
Dual-luciferase reporter assay, in vivo adeno-associated virus overexpression, AMPK agonist/inhibitor pharmacology, RNA sequencing |
Journal of sport and health science |
Medium |
36374849
|
| 2023 |
In spinal dorsal horn neurons, POU2F1 binds to the DNMT3a promoter and activates its transcription; oxaliplatin treatment upregulates POU2F1, leading to increased DNMT3a expression, hypermethylation of the Lrfn4 promoter, and decreased LRFN4 expression, which mediates mechanical allodynia and cold hyperalgesia. Intrathecal POU2F1 siRNA prevents DNMT3a upregulation and LRFN4 downregulation. |
ChIP assay (POU2F1 on DNMT3a promoter), MeDIP, qPCR, siRNA knockdown in vivo, behavioral pain assays |
Neurochemical research |
Medium |
37592110
|
| 2024 |
TRIM21 E3 ubiquitin ligase directly interacts with POU2F1 and induces K48-linked ubiquitination at K272 of POU2F1, leading to its proteasomal degradation. DADS treatment promotes this K272 ubiquitination by upregulating TRIM21 via attenuation of PI3K/AKT signaling. Reduced POU2F1 impairs PPP flux and PRPP production, enhancing DNA damage and apoptosis in CRC cells. |
Co-immunoprecipitation, ubiquitination site mapping, K272 mutagenesis, TRIM21 knockdown/overexpression, PI3K signaling manipulation, in vivo tumor model |
International journal of biological sciences |
High |
38385081
|
| 2019 |
POU2F1 protein directly binds the -713 to -703 bp region of the Slc7a11 promoter to inhibit its transcriptional activity, as shown by dual-luciferase reporter and site-directed mutagenesis assays in rabbit melanocytes. |
Dual-luciferase reporter assay, site-directed mutagenesis, rabbit melanocyte culture, knockdown/overexpression |
International journal of molecular sciences |
Medium |
31137576
|
| 2014 |
POU2F1 consensus binding sites within the 5' DNA of HOXD10 and HOXD11 are required for optimal promoter activity (by luciferase reporter), and POU2F1 knockdown significantly reduces HOXD10 and HOXD11 expression and inhibits HNSCC cell proliferation. |
Luciferase reporter assay with mutant POU2F1 binding sites, siRNA knockdown, proliferation and invasion assays |
Oncotarget |
Medium |
25301728
|
| 2020 |
In gastric cancer, POU2F1 directly binds to POU2F1 binding sites within both the miR-4490 promoter (repressing miR-4490 transcription) and the USP22 promoter (activating USP22 transcription), as confirmed by ChIP and dual-luciferase reporter assays. POU2F1 promotes GC proliferation and EMT-induced metastasis through this axis. |
ChIP assay, dual-luciferase reporter assay, ISH, IHC, flow cytometry, in vitro/in vivo functional assays |
Cellular oncology |
Medium |
32857323
|
| 2021 |
POU2F1 binds the FAM201A promoter and transcriptionally activates it, forming a positive feedback loop with miR-146a-5p: FAM201A sponges miR-146a-5p to upregulate POU2F1, and POU2F1 in turn drives FAM201A transcription. Confirmed by ChIP and luciferase reporter assay in chondrocytes. |
ChIP assay, luciferase reporter assay, miRNA sponge assay, IL-1β chondrocyte injury model |
Molecular medicine reports |
Medium |
34796909
|
| 2022 |
POU2F1 directly binds and activates the promoter of TTC3-AS1 in gastric cancer (confirmed by ChIP and DNA-affinity precipitation), and LINC01564 lncRNA binds the 3'UTR of POU2F1 mRNA to stabilize it (confirmed by RIP and RNA pulldown), forming a positive regulatory loop. |
RIP, RNA pulldown, ChIP assay, MTT, invasion/clonogenic assay, in vivo metastasis model |
Journal of translational medicine |
Medium |
35562740
|
| 2021 |
A CHD-associated SNP rs492554 and linked SNP rs12406992 map within a POU2F1 binding motif in the SESN2 regulatory region; the protective T allele shows preferential binding affinity to POU2F1 by EMSA and luciferase assay. POU2F1 knockdown suppresses luciferase expression driven by the T-C haplotype, demonstrating POU2F1 acts as an allele-specific transcriptional activator of SESN2. |
EMSA, luciferase reporter assay, POU2F1 knockdown, eQTL analysis |
Frontiers in cell and developmental biology |
Medium |
34249922
|
| 2024 |
POU2F1 directly binds the miR-29b1/a cluster promoter (shown by ChIP and luciferase) to repress miR-29b-3p and miR-29a-3p transcription. This elevates PIK3R1 and PIK3R3 (direct targets of these miRNAs), activating PI3K/Akt/mTOR signaling to promote gastric cancer cell invasion and metastasis. Co-immunoprecipitation demonstrated PIK3R1-PIK3R3 interaction. |
ChIP assay, luciferase reporter assay, co-immunoprecipitation, Transwell invasion assay, in vivo metastasis model, miRNA/target validation |
Chinese medical journal |
Medium |
39183556
|
| 2019 |
The nucleotide sequence and position of substitutions at PORE (palindromic octamer-related element) and MORE (more PORE) sites determines whether Oct-1/POU2F1 binds as a monomer, homodimer, or multimer. Specific substitutions suppress dimer formation while others stimulate it, demonstrating that DNA sequence conformation of the binding site controls the character of POU2F1-DNA interaction. |
EMSA with nucleotide substitution series in PORE/MORE sites |
Molekuliarnaia biologiia |
Medium |
31184608
|
| 1994 |
OTF-1 (POU2F1) and NFI binding sites on the stably integrated MMTV LTR are permanently occupied in vivo in NIH3T3 and GR cells that exhibit hormone-independent MMTV expression, as shown by in vivo DMS footprinting, with guanine contacts identical to those identified by in vitro methylation interference. |
In vivo dimethyl sulfate (DMS) footprinting, in vitro methylation interference assay |
Cellular & molecular biology research |
Medium |
7787882
|
| 2024 |
Bovine Oct1/POU2F1 acts as a pro-viral factor for BoHV-1 replication: CRISPR/Cas9 Oct1 knockout in MDBK cells significantly reduces viral gene expression (all three temporal gene classes) and viral replication, a phenotype rescued by re-expression of wild-type Oct1. |
CRISPR/Cas9 knockout, viral infection at high and low MOI, viral gene expression analysis, rescue overexpression |
Viruses |
Medium |
39459888
|
| 2025 |
POU2F1 directly activates LDHA transcription in pituitary adenoma cells (confirmed by dual-luciferase reporter and ChIP assays), promoting proliferation, invasion, migration, sphere formation, and aerobic glycolysis. LDHA overexpression ameliorates PI3K/AKT pathway inactivation induced by POU2F1 silencing, placing POU2F1 upstream of LDHA and PI3K/AKT. |
Dual-luciferase reporter assay, ChIP assay, knockdown/overexpression, in vivo xenograft |
Brain research |
Medium |
40819704
|
| 2026 |
POU2F1 promotes chemoresistance in colorectal cancer by stimulating MCT4 expression, thereby reducing cytosolic lactate and decreasing lactylation of PPP1R11. Reduced PPP1R11 lactylation destabilizes PPP1R11 E3 ligase activity, preventing MDR2 ubiquitination and degradation, thus stabilizing MDR2 and conferring chemoresistance. |
Knockdown/overexpression, MCT4 and PPP1R11 lactylation assays, MDR2 ubiquitination assay, in vivo tumor model |
Advanced science |
Medium |
41793212
|
| 2026 |
POU2F1 directly activates transcription of DHCR24 and ELOVL2 (confirmed by ChIP and luciferase assays), driving cholesterol biosynthesis and lipid metabolic remodeling in endometrial cancer. POU2F1 knockdown reduces DHCR24 and ELOVL2 levels, proliferation, migration, and invasion, effects reversed by DHCR24/ELOVL2 restoration. |
ChIP assay, luciferase reporter assay, knockdown/overexpression, xenograft model |
Cancer & metabolism |
Medium |
41947242
|
| 2026 |
USP18 deubiquitinase stabilizes POU2F1 by removing its ubiquitin chains; the lncRNA ABHD11-AS1 suppresses USP18 translation by binding EIF4E and disrupting its phase separation, leading to increased POU2F1 ubiquitination and proteasomal degradation in CRC cells. |
Co-immunoprecipitation, ubiquitination assay, EIF4E phase separation assay, siRNA knockdown, Western blotting |
International journal of biological sciences |
Medium |
42157946
|