| 1987 |
POU2F2 (OTF-2) was purified to homogeneity from B cells as a protein complex of three peptides (62, 61, and 58.5 kDa), each capable of binding the octamer sequence 5'-ATGCAAAT, and the purified factor activated transcription from a kappa light chain promoter in vitro, establishing it as a B cell-specific transcription factor for immunoglobulin genes. |
Affinity chromatography purification, SDS-PAGE renaturation/DNA binding assay, in vitro transcription assay |
Cell |
High |
3119226
|
| 1990 |
OTF-2 (POU2F2) contains two distinct transcriptional activation domains required jointly for high-level transcription: a C-terminal proline-rich domain and an upstream domain with intermingled proline, glutamine, and leucine residues; point mutations in either glutamine or leucine clusters abolished function, indicating structural constraints beyond amino acid composition alone. |
Site-directed mutagenesis of OTF-2 cDNA, transient transfection into non-lymphoid cells, reporter gene transcription assay |
The EMBO journal |
High |
2328729
|
| 1990 |
Purified OTF-1 and OTF-2 (POU2F2) have indistinguishable DNA-binding affinities and protein-DNA contacts on immunoglobulin or histone H2b promoters, and each can intrinsically activate transcription from these promoters to equivalent levels in OTF-depleted extracts; however, full immunoglobulin gene transcription in B-cell extracts requires an additional B-cell-specific regulatory component that cooperates with OTF-2. |
High-resolution DNase I footprinting, electrophoretic mobility shift assay (EMSA), in vitro transcription with OTF-depleted extracts, purified protein reconstitution |
Molecular and cellular biology |
High |
2123291
|
| 1990 |
OTF-2 (POU2F2) interacts with the octamer element of the MOPC 141 immunoglobulin heavy-chain promoter, with footprinting revealing contacts extending over the heptamer element; an additional novel B-cell factor (NTF) binding the N element (5'-GGAACCTCCCCC) cooperates with OTF-2 to drive high-level B-cell-specific transcription, suggesting protein-protein interactions between NTF and OTF-2. |
EMSA, DNase I footprinting, in vitro transcription assay with purified factors |
Molecular and cellular biology |
Medium |
2109187
|
| 1990 |
In a variant B-lymphoma cell line (1.3E2) defective in LPS-mediated kappa gene activation, neither NF-κB nor OTF-2 nuclear localization increases upon LPS stimulation, indicating that OTF-2 nuclear translocation is part of the LPS-activated transcriptional pathway for kappa light chain expression in B cells. |
Electrophoretic mobility shift assay on nuclear extracts, genetic variant cell line analysis |
Immunogenetics |
Medium |
1689272
|
| 1991 |
Anti-IgM antibody treatment of LPS-stimulated splenic B cells reduces OTF-2 (POU2F2) binding activity in nuclear extracts and alters its nuclear localization as detected by immunofluorescence, coinciding with suppression of IgH enhancer-driven transcription, placing OTF-2 downstream of surface Ig crosslinking signals. |
EMSA on nuclear extracts, in situ immunofluorescence with anti-OTF-2 antibodies, CAT reporter assay |
Nucleic acids research |
Medium |
1658749
|
| 1992 |
OTF-2 (POU2F2), but not OTF-1, positively activates transcription of the MHC class II gene DRA in vitro and in vivo; this activation requires an intact octamer element in the DRA promoter, as demonstrated by protein fractions enriched for OTF-2, recombinant OTF-2 produced by in vitro transcription/translation, and transient transfection with an OTF-2 expression vector. |
In vitro transcription with OTF-enriched fractions, in vitro transcription/translation of recombinant OTF-2, transient transfection with OTF-2 expression vector, octamer element mutation analysis |
The Journal of biological chemistry |
High |
1560002
|
| 2014 |
Mutations in POU2F2 (OCT2) found in follicular lymphoma affect its transcriptional and functional properties, as measured by luciferase reporter assays, biological analysis of stably transduced cell lines, and global expression profiling, indicating that loss-of-function mutations in POU2F2 contribute to lymphoma pathogenesis. |
Exome sequencing, luciferase reporter assay, stable cell line transduction, global expression profiling |
Blood |
Medium |
24435047
|
| 2015 |
In gastric cancer cells, POU2F2 expression is induced by NF-κB activation; in turn, POU2F2 directly binds the ROBO1 promoter and activates its transcription, thereby promoting gastric cancer cell metastasis; miR-218 suppresses this axis by simultaneously targeting POU2F2, ROBO1, and IKK-β. |
Luciferase reporter assay, EMSA, ChIP-PCR, gain/loss-of-function experiments in vitro and in vivo (experimental metastasis animal model) |
Gut |
High |
26019213
|
| 2020 |
In developing mouse retina, Pou2f2 (induced by Pou2f1) binds to a POU motif in the promoter of the rod-inducing factor Nrl to repress its expression; conditional inactivation of Pou2f2 in retinal progenitor cells increases Nrl expression and reduces cone photoreceptor production, while forced sustained Pou2f2 expression expands the cone production window. |
Promoter binding assay, conditional knockout mouse model (Cre-mediated), retroviral misexpression, quantification of cone vs. rod fate |
Development (Cambridge, England) |
High |
32878923
|
| 2019 |
In the developing mouse spinal cord, Pou2f2 expression in V2 interneurons is restricted by Onecut transcription factors; gain- or loss-of-function of Pou2f2 alters the position (distribution/migration) of V2 interneuron populations, placing Pou2f2 downstream of Onecut factors in a genetic pathway controlling interneuron diversification. |
Gain-of-function and loss-of-function experiments in mouse spinal cord, immunofluorescence for interneuron markers |
Frontiers in cellular neuroscience |
Medium |
31231191
|
| 2019 |
In the developing mouse spinal cord, Pou2f2 is expressed in dorsal interneurons under regulation by Onecut factors; overexpression or inactivation of Pou2f2 leads to alterations in dI2, dI3, and Phox2a-positive dI5 differentiation and defects in dI2–dI6 interneuron distribution. |
Gain-of-function and loss-of-function experiments, immunofluorescence for dorsal interneuron markers |
Frontiers in molecular neuroscience |
Medium |
31787878
|
| 2021 |
POU2F2 promotes glioblastoma cell proliferation and aerobic glycolysis by directly binding to and activating transcription of the PDPK1 promoter; reconstitution of PDPK1 in POU2F2-knockdown cells rescues AKT/mTOR pathway activity, glycolysis, and proliferation, placing POU2F2 upstream of PDPK1 in a PI3K/AKT/mTOR signaling cascade. |
ChIP assay, luciferase reporter assay, shRNA knockdown, PDPK1 reconstitution/rescue experiments, PDPK1/AKT interaction inhibitor, in vivo xenograft model |
Cell death & disease |
High |
33931589
|
| 2021 |
POU2F2 promotes lung cancer cell proliferation and motility by directly binding to and activating transcription of the AGO1 promoter, as demonstrated by ChIP and luciferase assays, with AGO1 knockdown abolishing the POU2F2-driven effects in vitro and in vivo. |
ChIP assay, luciferase reporter assay, shRNA knockdown, CCK-8/colony formation/Transwell assays, xenograft tumor model |
BMC pulmonary medicine |
Medium |
33832481
|
| 2023 |
POU2F2 is a critical transcription factor driving escape from oncogene-induced senescence (OIS); its binding activity to cis-regulatory elements increases as cells escape OIS, and it exploits a pre-coded enhancer landscape to activate transcriptional programs enabling senescence escape and acquisition of transformed cell features. |
Dynamic multidimensional profiling (chromatin accessibility, transcriptomics), ChIP/CUT&RUN for POU2F2 binding, functional OIS escape assays |
Cell genomics |
Medium |
37082139
|
| 2022 |
CBX7 downregulates POU2F2 expression in bladder cancer cells; POU2F2 in turn activates PD-L1 expression, establishing a CBX7/POU2F2/PD-L1 regulatory axis; depletion of CBX7 results in resistance to PD-1 blockade. |
RNA-seq, knockdown experiments, Western blot, functional PD-1 blockade resistance assay |
Biochemical and biophysical research communications |
Low |
35526483
|
| 2023 |
POU2F2 and CEBPB cooperatively and additively enhance EDN1 (endothelin 1) transcription in vascular smooth muscle cells by binding to an enhancer region of the Edn1 promoter (-1309 to -1279 bp); overexpression of either factor increases EDN1 expression, and POU2F2 knockdown reduces it. |
Promoter activity analysis (luciferase), overexpression/knockdown experiments, EDN1 secretion ELISA |
Journal of molecular endocrinology |
Medium |
36942826
|
| 2024 |
POU2F2 transcriptionally upregulates PTPRG-AS1 lncRNA in triple-negative breast cancer by binding to its promoter; PTPRG-AS1 then acts as a competing endogenous RNA to sponge miR-376c-3p, thereby upregulating SLC7A11 and inhibiting ferroptosis. |
ChIP assay, dual-luciferase reporter assay, MTT/colony formation assay, Fe2+/ROS measurement, in vivo tumor growth assay |
Epigenomics |
Medium |
38318853
|
| 2024 |
POU2F2 promotes PIK3CD transcription by directly binding to its promoter in B lymphocytes, thereby activating the Akt/mTOR signaling pathway and enhancing B cell proliferation; knockdown of POU2F2 suppresses B cell proliferation and IgG deposition in vivo. |
ChIP assay, luciferase reporter assay, shRNA knockdown, MTT/flow cytometry, IgG deposition assessment, Western blot |
Nephrology (Carlton, Vic.) |
Medium |
39401868
|
| 2024 |
POU2F2 acts as a transcriptional repressor of SLC3A2 in chondrocytes; lncRNA HOXA11-AS interacts with POU2F2 (identified by RNA pulldown, mass spectrometry, and ChIP) to block its repressor activity, thereby increasing SLC3A2 expression and inhibiting ferroptosis in osteoarthritis. |
RNA pulldown, mass spectrometry, ChIP, RNA sequencing, in vitro and in vivo OA models |
Cellular signalling |
Medium |
39251054
|
| 2025 |
POU2F2 positively regulates transcription of the MARCH1 E3 ubiquitin ligase gene by binding its promoter; MARCH1 in turn interacts with and promotes ubiquitination and degradation of the tumor suppressor MYCT1, thereby driving AML cell proliferation and inhibiting apoptosis and differentiation. |
Promoter binding assay (ChIP/luciferase inferred from context), gain/loss-of-function, co-immunoprecipitation, ubiquitination assay, in vivo AML mouse model |
Oncogene |
Medium |
40533483
|
| 2025 |
POU2F2 directly binds the PREX1 promoter and activates its transcription in AML cells, promoting mTOR pathway activation and AML malignant progression; PREX1 knockdown reverses POU2F2 overexpression-driven effects, establishing POU2F2 upstream of PREX1/mTOR in AML. |
Dual-luciferase assay, ChIP assay, Western blot, colony formation/CCK-8/Transwell assays, xenograft tumor model |
Journal of biochemical and molecular toxicology |
Medium |
40317800
|
| 2025 |
In the THBS1-mediated diabetic osteoporosis pathway, PPARγ (activated downstream of CD36) transcriptionally upregulates POU2F2, which then enhances osteoclastogenesis via c-FOS induction; genetic ablation of THBS1 or virtual screening inhibitor nasunin suppressed this CD36-PPARγ-POU2F2-c-FOS axis and reduced bone loss in T2D mice. |
ChIP-qPCR for PPARγ binding to POU2F2 promoter, Western blot, flow cytometry, TRAP staining, micro-CT, in vivo T2D mouse model, virtual screening |
Biochimica et biophysica acta. Molecular basis of disease |
Medium |
41407214
|
| 2025 |
In multiple myeloma, POU2F2 binds eccANKRD28 (an active enhancer eccDNA) and forms a protein complex with RUNX1 and RUNX2 to activate the promoters of oncogenes including IRF4, JUNB, IKZF3, RUNX3, and BCL2, driving bortezomib/lenalidomide resistance; CRISPR/Cas9-mediated elevation of eccANKRD28 desensitizes cells to treatment. |
H3K27ac ChIP-seq, scRNA-seq, scATAC-seq, CUT&Tag, CRISPR/Cas9, in vitro and in vivo drug resistance assays |
Advanced science (Weinheim, Baden-Wurttemberg, Germany) |
Medium |
40167268
|
| 2026 |
POU2F2 is a crucial transcription factor mediating MIF-driven activation of SPP1+ tumor-associated macrophages in colorectal cancer; BCL9L is identified as a direct downstream transcriptional target of POU2F2 in this context, and blocking MIF signaling abolishes SPP1+TAM activation in vitro and in vivo. |
scRNA-seq interaction analysis, TAM co-culture model, liver metastasis in vivo model, mechanistic studies identifying POU2F2 as transcriptional regulator of BCL9L |
International journal of biological sciences |
Low |
41800265
|
| 2026 |
POU2F2 directly binds to and activates the SPOCD1 promoter in lung adenocarcinoma cells (demonstrated by dual-luciferase, ChIP, and DNA pulldown assays), thereby enhancing PI3K/AKT pathway signaling and promoting cell proliferation; exercise suppresses POU2F2 expression, disrupting this axis. |
Dual-luciferase assay, ChIP assay, DNA pulldown, shRNA knockdown, CCK-8/EdU/flow cytometry/TUNEL assays, xenograft model with Ki67 IHC |
Clinical & translational oncology |
Medium |
41795741
|
| 2025 |
Genetic loss of Pou2f2 in mouse spinal cord results in impaired development of two early-born motor neuron columns and re-specification of anterolateral system projection neurons as a later-born subset, placing Pou2f2 in a conserved sequential transcription factor cascade (Onecut2 → Pou2f2 → Pou3f1) that controls chronological diversification of spinal neuron subtypes. |
Conditional/constitutive mouse knockout, immunofluorescence for motor neuron and projection neuron markers, genetic epistasis analysis |
bioRxivpreprint |
Medium |
bio_10.1101_2025.05.27.656404
|