Affinage

POU2F1

POU domain, class 2, transcription factor 1 · UniProt P14859

Length
743 aa
Mass
76.5 kDa
Annotated
2026-04-28
100 papers in source corpus 44 papers cited in narrative 44 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

POU2F1 (Oct-1) is a ubiquitously expressed POU-domain transcription factor that binds octamer and TAATGARAT DNA motifs to activate or repress transcription in a context-dependent manner, functioning as a switchable stabilizer of repressed, poised, and inducible chromatin states across diverse cellular processes including cell cycle progression, DNA damage response, metabolic reprogramming, immune memory, and oncogenesis. Its bipartite POU domain searches DNA via rotation-coupled sliding (homeodomain) and intersegment transfer (POU-specific domain), with flanking cis-element sequences inducing conformational changes that gate cofactor recruitment — including VP16/HCF for HSV transactivation, OCA-B/OBF1 for immunoglobulin gene activation and CD4+ T cell memory, Jmjd1a/KDM3A for H3K9me2 demethylation at poised loci, and the NuRD complex for repression (PMID:21555551, PMID:8001121, PMID:10541551, PMID:21051540, PMID:26481684). Oct-1 is extensively post-translationally regulated: cell-cycle-phase-specific phosphorylation by cdc2 and Nek6 controls mitotic chromatin exclusion and centrosomal/kinetochore localization followed by APC/C-mediated K11-linked polyubiquitination, DNA-PK phosphorylation mediates DNA damage survival, O-GlcNAcylation integrates metabolic signals, and BRCA1-BARD1 E3 ligase activity promotes Oct-1 ubiquitylation and degradation to restrain glycolytic reprogramming (PMID:1887216, PMID:21897860, PMID:17213819, PMID:23580612, PMID:29330289). Oct-1 directly represses tumor suppressors (p15INK4b, NPR3) and activates metabolic enzymes (ALDOA, ACSL3) and stress-response genes (GADD45, FILIP1L), with conditional deletion in intestinal stem cells impairing injury recovery and modulating tumorigenesis in opposing directions depending on oncogenic context (PMID:17316622, PMID:31059499, PMID:34997215, PMID:27270436).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1988 High

    Establishing that Oct-1 mediates HSV IE gene activation not by direct viral-factor DNA binding but by serving as a platform for VP16-induced multiprotein complex assembly on TAATGARAT elements answered how a ubiquitous host factor could be co-opted for virus-specific transcription.

    Evidence Affinity purification of OTF-1/OTF-2 with EMSA and complementation in depleted extracts

    PMID:2842768

    Open questions at the time
    • Identity of the additional cellular factor in the VP16-Oct1 complex (later identified as HCF) was unknown
    • Whether VP16-Oct1 interaction required specific DNA conformations was unresolved
  2. 1990 High

    Demonstrating that Oct-1's POU domain stimulates adenovirus DNA replication through a mechanism distinct from its transcription activation domain revealed that Oct-1 has separable replication-stimulatory and transcriptional functions, broadening its role beyond transcription.

    Evidence Vaccinia-expressed Oct-1 deletion mutants in in vitro adenovirus DNA replication and DNA-binding assays

    PMID:2347308

    Open questions at the time
    • Mechanism by which POU domain stimulates replication initiation not defined
    • Whether replication function is physiologically relevant for cellular DNA replication unknown
  3. 1990 High

    Showing that purified Oct-1 and Oct-2 bind identically to both H2B and immunoglobulin promoters but that full Ig activation requires a B-cell-specific cofactor established that promoter selectivity arises from cofactor interaction rather than differential DNA binding.

    Evidence Purification from HeLa/B cells; DNase I footprinting; in vitro transcription reconstitution with depleted extracts

    PMID:2123291

    Open questions at the time
    • Identity of the B-cell-specific cofactor (later OCA-B) not yet known
  4. 1994 High

    Discovery that a flanking cis-element induces a POU domain conformational change required for VP16 recognition resolved how the same octamer-binding protein achieves cofactor selectivity at different genomic sites.

    Evidence Site-directed mutagenesis of flanking element and homeodomain residues; EMSA and VP16 complex formation

    PMID:8001121

    Open questions at the time
    • Structural basis of the conformational change at atomic resolution was not yet available
    • Whether similar conformational gating governs other cofactor interactions unknown
  5. 1991 High

    Identifying a complex temporal program of Oct-1 phosphorylation across the cell cycle, with mitotic phosphorylation by a cdc2-related kinase, established that Oct-1 activity is dynamically regulated by cell-cycle kinases rather than being constitutive.

    Evidence Cell cycle synchronization; 2D phosphopeptide mapping; kinase activity correlation

    PMID:1887216

    Open questions at the time
    • Specific phosphorylation sites not mapped
    • Functional consequences of individual phosphorylation events unknown
  6. 1999 High

    The crystal structure of the OCA-B/Oct-1 POU/DNA ternary complex revealed the atomic basis for cofactor selectivity: OCA-B contacts a hydrophobic pocket on the POU-specific domain and makes sequence-specific DNA contacts, explaining how a short peptide achieves both protein and DNA recognition.

    Evidence X-ray crystallography at 3.2 Å resolution

    PMID:10541551

    Open questions at the time
    • How OCA-B binding translates to transcriptional activation mechanistically was not resolved
    • Structure of full-length OCA-B or its activation domain unknown
  7. 1998 High

    Demonstrating that Oct-1 accesses its binding site on histone H3/H4 tetramer particles but not full nucleosomes, and that SWI/SNF remodeling generates tetramer-like accessibility, placed Oct-1 within the chromatin remodeling framework and defined its nucleosome access requirements.

    Evidence In vitro chromatin reconstitution with recombinant histones; site-directed hydroxyl radical mapping; SWI/SNF remodeling

    PMID:9614938

    Open questions at the time
    • Whether Oct-1 actively recruits SWI/SNF or passively benefits from its action was unclear
  8. 2007 High

    Two parallel discoveries — that DNA-PK phosphorylates 13 N-terminal Oct-1 residues required for DNA-damage survival, and that Oct-1 silences p15INK4b via SMRT/HDAC1 recruitment — established Oct-1 as both a DNA damage response effector and an HDAC-dependent cell cycle gene repressor.

    Evidence IR-induced phosphorylation assays with Ser/Thr→Ala mutagenesis and Oct-1−/− MEF rescue; ChIP for SMRT/HDAC1 at p15 promoter in WT vs Oct-1−/− MEFs

    PMID:17213819 PMID:17316622

    Open questions at the time
    • Which of the 13 DNA-PK sites are individually critical was not resolved
    • Whether HDAC-dependent repression extends genome-wide or is locus-specific unknown
  9. 2009 High

    Showing that oxidative and genotoxic stress dynamically alter Oct-1 phosphorylation to redirect its DNA-binding selectivity to stress-responsive targets in vivo demonstrated that post-translational modification functions as a target-gene switch rather than simply modulating binding affinity.

    Evidence In vivo phosphorylation analysis; POU domain phosphosite mutagenesis; ChIP under stress conditions

    PMID:19171782

    Open questions at the time
    • Kinases responsible for stress-induced POU domain phosphorylation not fully identified
    • Whether stress-induced retargeting is conserved across cell types unresolved
  10. 2010 High

    Identifying Oct-1 as a switchable chromatin platform — recruiting Jmjd1a/KDM3A to remove H3K9me2 for anti-repression at some loci while recruiting NuRD for repression at others — unified its dual activator/repressor activities under a single mechanistic framework of context-dependent cofactor switching.

    Evidence ChIP for histone marks and cofactors in fibroblasts, T cells, and colon cancer cells with siRNA knockdown

    PMID:21051540

    Open questions at the time
    • Signal that dictates Jmjd1a vs NuRD recruitment at a given locus not identified
    • Whether switching occurs dynamically at a single locus or is preset not established
  11. 2011 High

    Discovery that Nek6 phosphorylates Oct-1 S335 during mitosis, excluding it from chromatin and targeting it to centrosomes/kinetochores where APC/C adds K11-linked polyubiquitin chains, revealed a non-transcriptional mitotic function and a novel post-translational regulatory circuit.

    Evidence Phospho-specific antibodies; immunofluorescence; Xenopus egg extract spindle assay; co-IP with APC1; ubiquitin linkage analysis

    PMID:21897860

    Open questions at the time
    • Precise mitotic function at spindle poles/kinetochores not defined
    • Whether K11-polyubiquitin leads to degradation or signaling unknown
    • Spindle defects shown only in Xenopus extracts, not mammalian cells
  12. 2011 High

    NMR characterization of Oct-1's DNA search mechanism revealed that POU(HD) slides rotationally along DNA while POU(S) mediates intersegment transfer, explaining how the bipartite domain achieves efficient target search on genomic DNA.

    Evidence Residual dipolar coupling and paramagnetic relaxation enhancement NMR with specific and nonspecific DNA complexes

    PMID:21555551

    Open questions at the time
    • In vivo relevance of the two-mode search mechanism not tested
    • Influence of chromatin context on search dynamics unknown
  13. 2013 Medium

    Mapping O-GlcNAcylation sites (T255, S728) on Oct-1 and showing they control both repression under growth conditions and activation under starvation at the Gadd45a locus identified Oct-1 as a metabolic signal integrator whose activity is tuned by nutrient-sensitive sugar modification.

    Evidence O-GlcNAc site mapping; mutagenesis; ChIP; reporter assays

    PMID:23580612

    Open questions at the time
    • How O-GlcNAcylation mechanistically switches Oct-1 between repressive and activating modes not defined
    • Whether O-GlcNAc and phosphorylation cross-regulate at these sites unknown
  14. 2015 High

    Demonstrating that Oct-1 and OCA-B are required for CD4+ memory T cell generation and maintain poised chromatin (low H3K9me2) at ~50 target genes via Jmjd1a recruitment translated the in vitro cofactor-switching model into an in vivo immune function with therapeutic implications.

    Evidence Adoptive transfer in vivo memory assays; ChIP-seq; conditional OCA-B knockout; H3K9me2 ChIP-qPCR

    PMID:26481684

    Open questions at the time
    • Whether Oct-1/OCA-B are required for CD8+ memory as well not addressed
    • Mechanism by which poised state is selectively re-activated upon antigen re-encounter unclear
  15. 2017 High

    Showing that BRCA1-BARD1 E3 ligase ubiquitylates Oct-1 for degradation to restrain glycolysis, with BRCA1 E3 mutations elevating Oct-1 and skewing metabolism, established a direct BRCA1–Oct-1 metabolic regulatory axis relevant to breast cancer pathogenesis.

    Evidence BRCA1 E3 ligase mutants; CRISPR Oct-1 deletion epistasis; ubiquitylation assays; metabolic profiling; xenograft assays

    PMID:29330289

    Open questions at the time
    • Specific Oct-1 transcriptional targets driving glycolytic shift not fully delineated
    • Whether this axis operates in normal mammary epithelium not tested
  16. 2016 High

    Genome-wide ChIP-seq revealing Oct-1 co-occupancy with androgen receptor at enhancers/promoters in prostate cancer, with pharmacological disruption by pyrrole-imidazole polyamides blocking tumor growth, established Oct-1 as a collaborative oncogenic transcription factor and potential therapeutic target in CRPC.

    Evidence ChIP-seq; polyamide treatment; xenograft tumor growth assays

    PMID:27270436

    Open questions at the time
    • Whether Oct-1 recruits AR or vice versa not resolved
    • Selectivity of polyamides for Oct-1 sites vs other AT-rich binding proteins not fully assessed
  17. 2019 High

    Two studies revealed opposing Oct-1 roles in disease: Oct-1 drives atherosclerosis by activating the LOX-1 scavenger receptor (regulated by CKIP-1/REGγ-mediated degradation), while in intestinal stem cells Oct-1 deletion impairs injury recovery yet modulates tumorigenesis in an oncogenic-context-dependent manner.

    Evidence Co-IP of CKIP-1/REGγ/Oct-1; Ckip-1 KO mice with bone marrow transplantation; conditional Oct-1 gut KO in DSS colitis and Apc-LOH tumor models; ChIP-seq

    PMID:30683852 PMID:31059499

    Open questions at the time
    • How Oct-1 switches between tumor-suppressive and oncogenic roles depending on Apc status mechanistically undefined
    • Specific Oct-1 targets mediating LOX-1 independent atherosclerotic effects not explored
  18. 2024 High

    Identifying Oct-1 as a host co-activator of HSV-1 lytic transcription that is silenced by neuronal miR-9 to enforce latency closed a decades-long loop from the original VP16-Oct1 observations, providing a mechanism for the cell-type-specific switch between lytic and latent infection.

    Evidence Functional miRNA screen; lentiviral miR-9 expression in Neuro-2a, iPSC-derived and primary neurons; ChIP-seq; ATAC-seq; RNA-seq

    PMID:38443365

    Open questions at the time
    • Whether miR-9 regulation of Oct-1 operates at additional non-viral loci in neurons not explored
    • Contribution of Oct-1 vs Onecut factors to latency/reactivation balance not quantitatively resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the signal(s) determining whether Oct-1 recruits activating (Jmjd1a) versus repressive (NuRD) cofactors at a given locus; the precise mitotic function of phospho-Oct-1 at centrosomes and kinetochores; whether the conformational gating mechanism demonstrated for VP16 generalizes to other cofactor interactions; and how the interplay among phosphorylation, O-GlcNAcylation, and ubiquitination integrates to set Oct-1 target gene selectivity genome-wide.
  • No systematic structural or proteomic analysis of Oct-1 cofactor switching determinants
  • Mitotic function beyond Xenopus extract phenotype untested in mammalian systems
  • Comprehensive PTM crosstalk map lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 12 GO:0003677 DNA binding 9
Localization
GO:0005634 nucleus 6 GO:0005694 chromosome 2 GO:0005815 microtubule organizing center 1
Pathway
R-HSA-74160 Gene expression (Transcription) 11 R-HSA-1643685 Disease 5 R-HSA-1640170 Cell Cycle 3 R-HSA-4839726 Chromatin organization 3 R-HSA-73894 DNA Repair 3 R-HSA-168256 Immune System 2
Complex memberships
NuRD complexOCA-B/Oct-1 complexVP16/HCF/Oct-1 complex

Evidence

Reading pass · 44 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1988 OTF-1 (POU2F1) binds the TAATGARAT sequence (overlapping the octamer motif) and the herpesvirus transactivator Vmw65 (VP16) induces formation of a higher-order complex that includes OTF-1 and at least one additional cellular factor; VP16 does not bind DNA directly but interacts with OTF-1 to stimulate HSV IE gene transcription. Affinity purification of OTF-1/OTF-2; band-shift (EMSA) assay; complementation experiments with OTF-1-depleted nuclear extracts Proceedings of the National Academy of Sciences of the United States of America High 2842768
1990 The 160-amino-acid POU domain of Oct-1 is sufficient to stimulate adenovirus DNA replication in vitro in an octamer-dependent manner; the POU-specific subdomain is required for full activity, whereas the homeodomain alone has weak DNA-binding activity and paradoxically inhibits replication; the DNA replication-stimulating domain does not coincide with the transcription activation domain, indicating distinct mechanisms. Vaccinia expression system overproduction of Oct-1, Oct-2, and deletion mutants; in vitro adenovirus DNA replication assay; DNA-binding assays The EMBO journal High 2347308
1990 Purified OTF-1 and OTF-2 show indistinguishable DNA-binding affinities and contacts on both the H2B and immunoglobulin promoters; each can activate transcription from either promoter in OTF-depleted extracts, but full immunoglobulin gene activation requires an additional B-cell-specific component that interacts with the OTFs. Purification of OTF-1/OTF-2 from HeLa and B cells; high-resolution DNase I footprinting; mobility shift/competition assays; in vitro transcription reconstitution with OTF-depleted extracts Molecular and cellular biology High 2123291
1991 Oct1 undergoes a complex temporal program of phosphorylation during the cell cycle; a p34cdc2-related kinase active during mitosis is responsible for at least one mitotic phosphorylation, and multiple kinases and phosphatases appear to be involved in generating distinct phosphopeptides at specific cell cycle phases. Cell cycle synchronization; 2D phosphopeptide mapping; kinase activity assays Science (New York, N.Y.) High 1887216
1994 A flanking cis-element adjacent to the octamer core induces a conformational change in the Oct-1 POU domain–DNA complex; this conformation is required for Vmw65 (VP16) recognition. A single substitution in the flanking signal prevents VP16 interaction without affecting overall POU binding, and a homeodomain residue mutation reverts the complex to a conformation not recognized by VP16. Site-directed mutagenesis of flanking cis element and homeodomain residues; EMSA; VP16 complex formation assays Cell High 8001121
1994 In B cells lacking Oct2, the ubiquitous Oct1 can activate octamer-containing promoters to normal levels via a novel B-cell-specific complex containing Oct1; a second B-cell activity interacts specifically with Oct2 to confer function from distal enhancer positions, demonstrating context-dependent functional selectivity. Reporter gene transfection in Oct2-deficient B cell lines; EMSA to detect Oct1-containing B-cell complex The EMBO journal Medium 8157005
1996 Oct-1 and Oct-2 DNA-binding site specificity is regulated in vitro by protein kinase A, protein kinase C, and casein kinase 2 in a binding-site-specific manner; inhibition of cellular phosphatases also modulates binding, and the kinase effects are phosphatase-dependent, indicating that the balance of kinase/phosphatase activity controls Oct-1 DNA-binding selectivity. In vitro kinase treatment of nuclear extracts; EMSA with three distinct octamer/TAATGARAT motifs; phosphatase inhibitor studies The Biochemical journal Medium 8645173
1997 The POU domain of either Oct-1 or Oct-2 is sufficient to activate transcription from both Ig and H2B promoters in B cells; in combination with specific distal enhancers, Oct-1 is preferentially more potent and this preference depends on a region external to the POU domain. Altered DNA-binding specificity mutants of Oct-1 and Oct-2; reporter gene assays in B cells with varied promoter/enhancer combinations The EMBO journal High 9384588
1997 VP16 is phosphorylated by casein kinase II (CKII) at Ser375 in vitro and in nuclear extracts; Ser375 is the critical residue required for complex formation with Oct-1 and HCF, and its substitution to alanine abolishes CKII phosphorylation and virtually eliminates Oct-1/HCF complex formation and transactivation in vivo. In vitro CKII phosphorylation of purified wild-type and mutant VP16; complex formation assays; transactivation assays The EMBO journal High 9171355
1998 OTF1 (Oct-1) can bind to its cognate site on a histone H3/H4 tetramer particle (but not on the full octamer particle) assembled on the MMTV promoter; SWI/SNF remodeling of the octamer particle generates a DNase I pattern indistinguishable from the tetramer, suggesting that SWI/SNF promotes Oct-1 access by removing H2A/H2B. In vitro chromatin reconstitution with recombinant histones; site-directed hydroxyl radical mapping; DNase I footprinting; transcription factor binding assays; SWI/SNF remodeling assay Journal of molecular biology High 9614938
1999 Crystal structure of a ternary complex (OCA-B peptide / Oct-1 POU domain / octamer DNA) at 3.2 Å resolution reveals that OCA-B binds in the major groove near the center of the octamer, forming hydrogen bonds with the adenine at position 5 of the DNA; a short OCA-B α-helix contacts a hydrophobic pocket on the POU-specific domain, providing structural basis for cofactor selectivity in immunoglobulin transcription. X-ray crystallography at 3.2 Å Genes & development High 10541551
1999 Oct-1 functionally interacts with retinoid X receptor (RXR) via the POU homeodomain (not POU-specific domain) and RXR's C/D domains; Oct-1 reduces TR/RXR binding to thyroid hormone response elements (TREs) and represses T3-dependent transcription by altering DNA-binding ability of TR/RXR heterodimers. In vitro pull-down with RXR deletion mutants; EMSA; transient transfection reporter assays in COS1 cells The Journal of biological chemistry Medium 10383413
1999 Oct1 and YY1 bind to a novel negative regulatory element at positions -90 to -79 of the human IL-5 promoter; substitution mutations abolishing their binding significantly increase IL-5 promoter activity in activated T cells, establishing Oct1 as a transcriptional repressor at this locus. DNase I footprinting; EMSA; site-directed mutagenesis; reporter gene transfection in T cells The Journal of allergy and clinical immunology Medium 10359895
2000 Isothermal titration calorimetry of Oct-1 POU domain binding to the octamer reveals a large negative heat capacity change exceeding empirical predictions from buried surface area; proteolysis studies indicate this discrepancy arises from partial folding of the POU domain upon DNA binding; six charged protein-DNA phosphate contacts are identified. Isothermal titration calorimetry; limited proteolysis of free vs. DNA-bound protein Biochemistry Medium 10858307
2001 The Oct-1 N-terminal activation region plus POU domain (residues 1–445) is sufficient for in vitro transcription stimulation from an immunoglobulin promoter with Bob1 (OCA-B) and from the HSV ICPO promoter with VP16; the activation domains of Oct-1 and Bob1 are largely unstructured and do not physically interact, implying their synergy requires co-recruitment of common factors. Recombinant protein expression and purification; in vitro transcription assay; NMR/spectroscopic characterization of activation domain structure Biochemistry Medium 11380252
2002 BRCA1 activates the GADD45 promoter through OCT-1 and CAAT motifs; BRCA1 physically associates with transcription factors Oct-1 and NF-YA (which bind these motifs) as shown by biotin-streptavidin pull-down and co-immunoprecipitation; immunodepletion of Oct-1 or NF-YA, or mutation of their binding sites, disrupts BRCA1 binding to the GADD45 promoter. Biotin-streptavidin pull-down; co-immunoprecipitation; site-directed mutagenesis; chromatin immunoprecipitation; reporter assays The Journal of biological chemistry High 11777930
2003 STAT5A/B and Oct-1 form a stable complex on the cyclin D1 proximal promoter; cytokine-activated STAT5 requires an adjacent octamer element constitutively occupied by Oct-1 for stable recruitment in vitro; STAT5 interacts with Oct-1 in vivo via a carboxy-terminal STAT5 motif similar to known Oct-1 POU-interacting motifs found in OBF-1/Bob and SNAP190. EMSA; co-immunoprecipitation in vivo; reporter assays; mutational analysis of promoter elements Molecular and cellular biology High 14645506
2003 OBF1 stabilizes Oct1 POU dimer–DNA interactions on PORE-type sequences, alleviates DNA sequence requirements for Oct1 dimerization, and overrides Oct1 interface mutations that abolish PORE-mediated dimerization; the PORE-type Oct1/Oct2 dimer (not monomer) is the primary OBF1 target. In vitro EMSA with purified proteins; mutagenesis of Oct1 dimer interface; reporter gene assays in B cells The EMBO journal High 12727885
2005 Prolactin decreases Oct-1 binding to the proximal cyclin D1 promoter (via a region spanning -254 to -180), and this decreased binding correlates with increased PRL-responsiveness; proximal promoter activity remains Stat5-dependent, identifying an inhibitory role for Oct-1 at this locus that is relieved by cytokine signaling. EMSA; promoter deletion and mutational analysis; reporter assays in multiple cell lines Molecular and cellular endocrinology Medium 15885880
2006 Sox2 and Oct-1 (Pou2f1) interact cooperatively on composite Sox/Oct DNA-binding sites to transactivate the Pax6 lens ectoderm enhancer; genetic combination of Sox2 and Pou2f1 mutant alleles causes failure of lens and nasal placode induction phenocopying Pax6 null embryos; the same composite binding sites are essential for Pax6 enhancer activity in vivo. Genetic epistasis (compound heterozygous mouse mutants); in vitro transactivation assays; transgenic mouse enhancer assays; identification of cooperative DNA-binding sites Developmental biology High 17140559
2007 DNA-PK phosphorylates a cluster of 13 Ser/Thr residues within the N-terminal transcriptional regulatory domain of Oct-1 following ionizing radiation; these phosphorylations are required for Oct-1-mediated cell survival after DNA damage; Ser/Thr-to-Ala substitution eliminates IR-induced phosphorylation and prevents rescue of Oct-1−/− MEF survival. In vivo phosphorylation assays after IR; site-directed mutagenesis (Ser/Thr → Ala); rescue of Oct-1−/− MEFs; ChIP for RNA PolII/TBP/H4Ac at H2B promoter Oncogene High 17213819
2007 Oct-1 binds the p15(INK4b) promoter in vitro and in vivo; the Oct-1 binding site functions as a silencer; SMRT and HDAC1 are present at the p15 proximal promoter; Oct-1−/− MEFs show elevated p15 protein; HDAC inhibitor activates p15 in wild-type but not Oct-1−/− MEFs, establishing HDAC-dependent transcriptional repression of p15 by Oct-1. EMSA; ChIP; HDAC inhibitor treatment; comparison of wild-type vs. Oct-1−/− MEFs FEBS letters High 17316622
2009 Oct1 is dynamically phosphorylated in vivo following oxidative and genotoxic stress; stress regulates the DNA-sequence selectivity of both Oct1 and Oct4; mutation of conserved phosphorylation target residues in the DNA-binding domain confirms their role in regulating binding selectivity; ChIP shows stress-inducible association of Oct1 with a distinct set of in vivo targets. In vivo phosphorylation analysis; mutagenesis of Oct1/Oct4 POU domain residues; ChIP; Oct1 target gene screen under stress conditions Genes & development High 19171782
2009 Oct-1 functions as a repressor of Cdx-2 (proglucagon gene activator) in pancreatic and intestinal endocrine cells; cAMP elevation activates EPAC, leading to enhanced Oct-1 phosphorylation and nuclear exclusion, reducing Oct-1 and co-repressor association with the Cdx-2 promoter and increasing proglucagon/proinsulin mRNA. ChIP; pharmacological cAMP elevation; subcellular fractionation; reporter assays The Journal of biological chemistry Medium 19617623
2010 Oct1 recruits the Jmjd1a/KDM3A lysine demethylase to remove inhibitory H3K9me2 marks and block repression at Polr2a and Ahcy target loci in fibroblasts; at the Il2 locus in T cells and Cdx2 locus in colon cancer cells, Oct1 recruits the NuRD chromatin-remodeling complex to promote repression, but can switch to Jmjd1a recruitment for anti-repression — establishing Oct1 as a switchable stabilizer of repressed and inducible states. ChIP for histone marks and co-factors; siRNA knockdown; purified T cells and colon cancer cell lines The Journal of biological chemistry High 21051540
2010 Oct1 is required for mTOR-induced G1 cell cycle arrest: Oct1−/− MEFs bypass G1 arrest induced by glucose/amino acid starvation or rapamycin; Oct1 controls transcription of CDK inhibitor p27(Kip1) downstream of mTOR, and Oct1-null cells fail to upregulate p27(Kip1) in response to mTOR inhibition. Oct1−/− MEFs; cell cycle analysis; rapamycin treatment; glucose/amino acid starvation; qRT-PCR and protein expression of p27(Kip1) Cell cycle (Georgetown, Tex.) High 20935455
2011 Oct1 is phosphorylated at S335 by the NIMA-related kinase Nek6 during M-phase, which excludes Oct1 from mitotic chromatin and concentrates phospho-Oct1 at centrosomes, mitotic spindle poles, kinetochores, and the midbody; phospho-Oct1 is subsequently modified by non-canonical K11-linked polyubiquitin chains added by the anaphase-promoting complex (APC1 interacts with Oct1-pS335); Oct1 depletion causes spindle morphogenesis defects in Xenopus egg extracts. siRNA knockdown; phospho-specific antibodies; immunofluorescence; Xenopus egg extract spindle assay; co-immunoprecipitation with APC1; ubiquitin linkage-specific analysis PloS one High 21897860
2011 NMR (residual dipolar coupling and paramagnetic relaxation enhancement) characterization of Oct1 DNA search reveals that the POU(HD) domain searches DNA primarily by rotation-coupled sliding (intramolecular translocation) while the POU(S) domain acts as an antenna to promote intersegment transfer via a bridged intermediate; cross-talk between POU(S) and POU(HD) ensures efficient sampling of DNA. Residual dipolar coupling (RDC) NMR; paramagnetic relaxation enhancement (PRE) NMR; specific and nonspecific DNA complexes Proceedings of the National Academy of Sciences of the United States of America High 21555551
2013 Oct1 is modified by O-linked β-N-acetylglucosamine (O-GlcNAc) at T255 and S728; under anchorage-independent overgrowth conditions, O-GlcNAcylation correlates with increased Oct1 binding to the Gadd45a promoter and transcriptional repression; upon acute nutrient starvation, Oct1 mediates Gadd45a activation; both O-GlcNAc sites are important for both repression and activation, identifying Oct1 as a metabolic/stress signal integrator. O-GlcNAc site mapping; mutagenesis of O-GlcNAc sites; ChIP; reporter assays; identification of ubiquitination sites FASEB journal Medium 23580612
2015 Oct1 and its cofactor OCA-B are selectively required for in vivo generation of CD4+ memory T cells and their response to antigen reencounter; mechanistically, OCA-B recruits the histone demethylase Jmjd1a to maintain poised (H3K9me2-low) states at target loci including Il2, Ifng, and Zbtb32 in resting but previously stimulated CD4+ T cells; ChIPseq identifies ~50 direct Oct1/OCA-B target genes. In vivo T cell memory assays (adoptive transfer); ChIPseq; ChIP-qPCR for H3K9me2; gene expression analysis; OCA-B conditional knockout The Journal of experimental medicine High 26481684
2015 ACK1 phosphorylates AKT (Thr308/Ser473) to activate the AKT pathway, which upregulates POU2F1 transcription factor; POU2F1 then directly binds the promoter of ECD (ecdysoneless homologue) to drive ECD expression, thereby promoting EMT, migration, and invasion in gastric cancer cells. SILAC proteomics; ChIP for POU2F1 at ECD promoter; reporter assays; overexpression/knockdown; in vivo metastasis assay The Journal of pathology Medium 25678401
2016 Oct1 is recruited to the FILIP1L promoter following doxorubicin treatment (TOP2 poison) and facilitates FILIP1L expression, which mediates apoptosis; FILIP1L induction is specific to TOP2-targeting drugs (not UV or TOP2 catalytic inhibitors), establishing Oct1 as a mediator of genotoxic-stress-induced pro-apoptotic transcription. shRNA screen; ChIP showing Oct1 relocalization to FILIP1L promoter; reporter assays; drug specificity comparisons PloS one Medium 22900064
2016 Oct1 is recruited to androgen receptor (AR)-binding enhancer/promoter regions genome-wide in prostate cancer cells (ChIP-seq); Oct1 facilitates AR signaling and a major Oct1/AR co-regulated target is ACSL3; pyrrole-imidazole polyamides targeting the Oct1-binding sequence block Oct1 chromatin association, suppress ACSL3 induction, and inhibit castration-resistant tumor growth in vivo. ChIP-seq; ChIP-qPCR; polyamide treatment; xenograft tumor growth assays Oncogene High 27270436
2017 POU2F1 directly binds the ALDOA promoter to enhance its transcriptional activity, upregulating aldolase A and thereby enhancing aerobic glycolysis and the pentose phosphate pathway in colon cancer cells; this POU2F1-ALDOA axis reduces oxidative stress, promotes proliferation, and decreases oxaliplatin sensitivity. ChIP for POU2F1 at ALDOA promoter; reporter assays; gain/loss of function with functional metabolic readouts Oncogene Medium 34997215
2017 BRCA1 promotes Oct1 ubiquitylation and degradation via its N-terminal E3 ubiquitin ligase activity (with BARD1); BRCA1 E3 ligase mutation elevates Oct1 protein and skews cells toward glycolysis; mutation of two ubiquitylated Oct1 lysines insulates Oct1 against BRCA1-mediated destabilization; CRISPR Oct1 deletion reverts the glycolytic phenotype caused by BRCA1 E3 mutation. BRCA1 E3 ligase mutants; CRISPR Oct1 deletion; ubiquitylation assays; metabolic profiling; RNAseq; xenograft assays Molecular cancer research : MCR High 29330289
2017 POU2F1 binds promoters of fibrosis repressors IL1R2, CD69, and TGIF2 in cardiac fibroblasts (shown by ChIP); pathological substrate stiffness upregulates POU2F1, which represses these fibrosis repressors, promoting cardiac fibroblast-to-myofibroblast differentiation; POU2F1 knockdown upregulates the repressors and attenuates differentiation. ChIP for POU2F1 at repressor promoters; polyacrylamide hydrogel stiffness model; gain/loss of function; mouse myocardial infarction model Science China. Life sciences Medium 32617828
2017 POU2F1 directly suppresses NPR3 promoter activity by binding the -900 to -800 bp region (dual-luciferase and site-directed mutagenesis); loss of NPR3 (suppressed by POU2F1) activates the PI3K/AKT pathway to promote osteosarcoma cell proliferation. Dual-luciferase reporter assay; site-directed mutagenesis of POU2F1 binding site; gain/loss of function; PI3K/AKT pathway readouts Cellular signalling Medium 34229087
2017 OCT1 is an AR collaborative transcription factor in CRPC cells; ChIP-seq in 22Rv1 CRPC cells reveals expanded OCT1 binding regions vs. LNCaP, with CRPC-specific target genes including ANLN (anillin); ANLN knockdown impairs cell growth and cell cycle progression, identifying it as a functional Oct1/AR co-regulated target in advanced prostate cancer. ChIP-seq; microarray; ChIP-qPCR; siRNA knockdown; cell cycle analysis Endocrinology Medium 30649323
2019 CKIP-1 interacts with the proteasome activator REGγ and targets Oct-1 for degradation, thereby suppressing Oct-1-driven transcription of the scavenger receptor LOX-1; Ckip-1 deficiency in macrophages specifically upregulates LOX-1 (not CD36 or SR-A), increases lipoprotein uptake and foam cell formation, and accelerates atherosclerosis in mice. Co-immunoprecipitation of CKIP-1/REGγ/Oct-1; protein stability assays; ChIP for Oct-1 at LOX-1 promoter; Ckip-1 KO mice; bone marrow transplantation Nature communications High 30683852
2019 Oct1/Pou2f1 deletion in mouse colon stem cells selectively blocks recovery from dextran sodium sulfate injury and reduces tumorigenicity in a chemical carcinogen model, while loss of one or both Oct1 alleles progressively increases tumor burden in an Apc loss-of-heterozygosity model; Oct1 ChIP-seq in HCT116 cells identifies targets associated with mitotic stability, metabolism, and stress response. Conditional Oct1 deletion in gut stem cells; DSS colitis model; chemical and Apc-LOH tumor models; ChIP-seq PLoS genetics High 31059499
2021 The lncRNA MIR210HG interacts directly with OCT1 in the nucleus of GBM cells; this interaction promotes OCT1-mediated transcription of IGFBP2 and FGFR1, driving hypoxic GBM stemness, invasion, and temozolomide resistance. RNA immunoprecipitation (direct OCT1-MIR210HG interaction); nuclear fractionation; RNA-seq; gene knockdown; in vitro and in vivo growth assays Cancer science Medium 34897892
2021 YES1 kinase phosphorylates OCT1 on tyrosine residues (identified by unbiased phospho-proteomics); pharmacological or genetic inhibition of YES1 reduces OCT1 transporter activity (SLC22A1) and modulates hepatic isobutyryl-L-carnitine levels in vivo, demonstrating post-translational regulation of OCT1 by tyrosine phosphorylation. Phospho-proteomics screen; genetic/pharmacological YES1 inhibition; targeted metabolomics for OCT1 biomarker Frontiers in pharmacology Medium 33790797
2022 Exercise training activates AMPK, which downregulates C/EBPβ, the transcription factor that drives POU2F1 expression; POU2F1 overexpression nullifies exercise-training benefits on cardiac fibrosis; C/EBPβ binds and activates the POU2F1 promoter (validated by dual-luciferase reporter assay), establishing the AMPK→C/EBPβ→POU2F1 axis in cardiac fibroblasts. Dual-luciferase reporter assay for C/EBPβ binding to POU2F1 promoter; AAV9-mediated POU2F1 overexpression in vivo; AMPK agonist/inhibitor; RNA-seq Journal of sport and health science Medium 36374849
2024 Neuronal miR-9 targets Oct-1 (and Onecut family members) to repress HSV-1 lytic gene activation and promote latency; knockdown of Oct-1 via miR-9 reduces HSV-1 replication, while overexpression of Oct-1 (or Onecutproteins) increases HSV-1 replication and reactivation; Oct-1 is thus a host co-activator of HSV transcription regulated by neuronal miR-9. Functional miRNA screen; luciferase-expressing HSV-1; lentiviral miR-9 expression; siRNA knockdown; overexpression in Neuro-2a, iPSC-derived neurons, and primary mouse neurons; ChIP-seq; ATAC-seq; RNA-seq Nature communications High 38443365

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1988 A herpesvirus trans-activating protein interacts with transcription factor OTF-1 and other cellular proteins. Proceedings of the National Academy of Sciences of the United States of America 361 2842768
2005 Adhesion and proliferation of OCT-1 osteoblast-like cells on micro- and nano-scale topography structured poly(L-lactide). Biomaterials 197 15701374
2014 OCT1 is a high-capacity thiamine transporter that regulates hepatic steatosis and is a target of metformin. Proceedings of the National Academy of Sciences of the United States of America 188 24961373
2001 Reduced hepatic uptake and intestinal excretion of organic cations in mice with a targeted disruption of the organic cation transporter 1 (Oct1 [Slc22a1]) gene. Molecular and cellular biology 171 11463829
2000 Localization of organic cation transporters OCT1 and OCT2 in rat kidney. American journal of physiology. Renal physiology 163 10997918
1990 The DNA binding domain (POU domain) of transcription factor oct-1 suffices for stimulation of DNA replication. The EMBO journal 136 2347308
1991 Differential phosphorylation of the transcription factor Oct1 during the cell cycle. Science (New York, N.Y.) 134 1887216
2002 BRCA1 regulates GADD45 through its interactions with the OCT-1 and CAAT motifs. The Journal of biological chemistry 114 11777930
2011 Mitochondrial protein turnover: role of the precursor intermediate peptidase Oct1 in protein stabilization. Molecular biology of the cell 103 21525245
2010 Interaction between polymorphisms in the OCT1 and MATE1 transporter and metformin response. Pharmacogenetics and genomics 103 19898263
1990 Activation of octamer-containing promoters by either octamer-binding transcription factor 1 (OTF-1) or OTF-2 and requirement of an additional B-cell-specific component for optimal transcription of immunoglobulin promoters. Molecular and cellular biology 102 2123291
2022 The POU2F1-ALDOA axis promotes the proliferation and chemoresistance of colon cancer cells by enhancing glycolysis and the pentose phosphate pathway activity. Oncogene 101 34997215
2009 A general mechanism for transcription regulation by Oct1 and Oct4 in response to genotoxic and oxidative stress. Genes & development 97 19171782
2006 Sox2 and Pou2f1 interact to control lens and olfactory placode development. Developmental biology 94 17140559
2000 Developmentally regulated expression of organic ion transporters NKT (OAT1), OCT1, NLT (OAT2), and Roct. American journal of physiology. Renal physiology 87 10751225
2011 Double-transfected MDCK cells expressing human OCT1/MATE1 or OCT2/MATE1: determinants of uptake and transcellular translocation of organic cations. British journal of pharmacology 86 20883471
2013 Organic cation transporter 1 (OCT1/mOct1) is localized in the apical membrane of Caco-2 cell monolayers and enterocytes. Molecular pharmacology 79 23680637
1999 Crystal structure of an OCA-B peptide bound to an Oct-1 POU domain/octamer DNA complex: specific recognition of a protein-DNA interface. Genes & development 77 10541551
2003 STAT5 and Oct-1 form a stable complex that modulates cyclin D1 expression. Molecular and cellular biology 76 14645506
1994 Site-specific conformational alteration of the Oct-1 POU domain-DNA complex as the basis for differential recognition by Vmw65 (VP16). Cell 73 8001121
2015 ACK1 promotes gastric cancer epithelial-mesenchymal transition and metastasis through AKT-POU2F1-ECD signalling. The Journal of pathology 70 25678401
2016 The Oct1 transcription factor and epithelial malignancies: Old protein learns new tricks. Biochimica et biophysica acta 66 26877236
2019 DLX6-AS1/miR-204-5p/OCT1 positive feedback loop promotes tumor progression and epithelial-mesenchymal transition in gastric cancer. Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association 64 31463827
1994 Differential transactivation potential of Oct1 and Oct2 is determined by additional B cell-specific activities. The EMBO journal 64 8157005
2012 Transcription factor Oct1 is a somatic and cancer stem cell determinant. PLoS genetics 61 23144633
1996 AP-1 and Oct-1 transcription factors down-regulate the expression of the human PIT1/GHF1 gene. The Journal of biological chemistry 61 8943298
1997 Using altered specificity Oct-1 and Oct-2 mutants to analyze the regulation of immunoglobulin gene transcription. The EMBO journal 58 9384588
1991 Characterization of two Drosophila POU domain genes, related to oct-1 and oct-2, and the regulation of their expression patterns. Mechanisms of development 58 1685891
2017 E6/E7-P53-POU2F1-CTHRC1 axis promotes cervical cancer metastasis and activates Wnt/PCP pathway. Scientific reports 57 28303973
2002 Analysis of octamer-binding transcription factors Oct2 and Oct1 and their coactivator BOB.1/OBF.1 in lymphomas. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 57 11904338
2019 CKIP-1 limits foam cell formation and inhibits atherosclerosis by promoting degradation of Oct-1 by REGγ. Nature communications 56 30683852
2019 Variation in the Plasma Membrane Monoamine Transporter (PMAT) (Encoded by SLC29A4) and Organic Cation Transporter 1 (OCT1) (Encoded by SLC22A1) and Gastrointestinal Intolerance to Metformin in Type 2 Diabetes: An IMI DIRECT Study. Diabetes care 54 30885951
2010 Oct1 is a switchable, bipotential stabilizer of repressed and inducible transcriptional states. The Journal of biological chemistry 53 21051540
2009 Organic cation transporters OCT1, 2, and 3 mediate high-affinity transport of the mutagenic vital dye ethidium in the kidney proximal tubule. American journal of physiology. Renal physiology 53 19357179
2005 Prolactin signals via Stat5 and Oct-1 to the proximal cyclin D1 promoter. Molecular and cellular endocrinology 49 15885880
1998 The mouse mammary tumour virus promoter positioned on a tetramer of histones H3 and H4 binds nuclear factor 1 and OTF1. Journal of molecular biology 49 9614938
2016 miR-449a promotes liver cancer cell apoptosis by downregulation of Calpain 6 and POU2F1. Oncotarget 48 26375440
2015 Oct1 and OCA-B are selectively required for CD4 memory T cell function. The Journal of experimental medicine 46 26481684
2013 Role of the plasma membrane transporter of organic cations OCT1 and its genetic variants in modern liver pharmacology. BioMed research international 46 23984399
2016 The Nonmetabolized β-Blocker Nadolol Is a Substrate of OCT1, OCT2, MATE1, MATE2-K, and P-Glycoprotein, but Not of OATP1B1 and OATP1B3. Molecular pharmaceutics 42 26702643
1997 A single serine residue at position 375 of VP16 is critical for complex assembly with Oct-1 and HCF and is a target of phosphorylation by casein kinase II. The EMBO journal 42 9171355
2016 The human organic cation transporter OCT1 mediates high affinity uptake of the anticancer drug daunorubicin. Scientific reports 40 26861753
2007 DNA-PK phosphorylation sites on Oct-1 promote cell survival following DNA damage. Oncogene 40 17213819
2020 lncRNA CRNDE promotes the proliferation and metastasis by acting as sponge miR-539-5p to regulate POU2F1 expression in HCC. BMC cancer 39 32252678
2017 Methyl CpG level at distal part of heat-shock protein promoter HSP70 exhibits epigenetic memory for heat stress by modulating recruitment of POU2F1-associated nucleosome-remodeling deacetylase (NuRD) complex. Journal of neurochemistry 38 28278364
2016 Targeting Oct1 genomic function inhibits androgen receptor signaling and castration-resistant prostate cancer growth. Oncogene 37 27270436
1999 Functional interaction between Oct-1 and retinoid X receptor. The Journal of biological chemistry 36 10383413
2016 Organic Cation Transporter 1 (OCT1) mRNA expression in hepatocellular carcinoma as a biomarker for sorafenib treatment. BMC cancer 35 26872727
2018 PBPK Model of Morphine Incorporating Developmental Changes in Hepatic OCT1 and UGT2B7 Proteins to Explain the Variability in Clearances in Neonates and Small Infants. CPT: pharmacometrics & systems pharmacology 34 29920988
2017 Effects of genetic polymorphisms on the OCT1 and OCT2-mediated uptake of ranitidine. PloS one 34 29236753
2011 Intra- and intermolecular translocation of the bi-domain transcription factor Oct1 characterized by liquid crystal and paramagnetic NMR. Proceedings of the National Academy of Sciences of the United States of America 33 21555551
2021 Hypoxia-inducible lncRNA MIR210HG interacting with OCT1 is involved in glioblastoma multiforme malignancy. Cancer science 31 34897892
2009 POU homeodomain protein Oct-1 functions as a sensor for cyclic AMP. The Journal of biological chemistry 31 19617623
1999 Binding of YY1 and Oct1 to a novel element that downregulates expression of IL-5 in human T cells. The Journal of allergy and clinical immunology 31 10359895
2000 Characterization of sequence-specific DNA binding by the transcription factor Oct-1. Biochemistry 30 10858307
2019 Oct1/Pou2f1 is selectively required for colon regeneration and regulates colon malignancy. PLoS genetics 29 31059499
1996 Oct-1 [corrected] and Oct-2 DNA-binding site specificity is regulated in vitro by different kinases. The Biochemical journal 29 8645173
2017 POU2F1 promotes growth and metastasis of hepatocellular carcinoma through the FAT1 signaling pathway. American journal of cancer research 28 28861323
2013 Hepatocyte nuclear factor 1 regulates the expression of the organic cation transporter 1 via binding to an evolutionary conserved region in intron 1 of the OCT1 gene. The Journal of pharmacology and experimental therapeutics 28 23922447
1993 Chromosomal structure and expression of the human OTF1 locus encoding the Oct-1 protein. Genomics 28 8314572
2013 Glucocorticoid receptor regulates organic cation transporter 1 (OCT1, SLC22A1) expression via HNF4α upregulation in primary human hepatocytes. Pharmacological reports : PR 27 24399729
2011 Dynamic regulation of Oct1 during mitosis by phosphorylation and ubiquitination. PloS one 27 21897860
2004 Seven novel single nucleotide polymorphisms in the human SLC22A1 gene encoding organic cation transporter 1 (OCT1). Drug metabolism and pharmacokinetics 27 15499200
2024 Neuronal miR-9 promotes HSV-1 epigenetic silencing and latency by repressing Oct-1 and Onecut family genes. Nature communications 26 38443365
2024 The full spectrum of SLC22 OCT1 mutations illuminates the bridge between drug transporter biophysics and pharmacogenomics. Molecular cell 26 38703769
2004 Cloning, genomic organization, expression, and effect on beta-casein promoter activity of a novel isoform of the mouse Oct-1 transcription factor. Gene 26 14729276
2019 Integrative Genomic Analysis of OCT1 Reveals Coordinated Regulation of Androgen Receptor in Advanced Prostate Cancer. Endocrinology 25 30649323
2021 Isobutyrylcarnitine as a Biomarker of OCT1 Activity and Interspecies Differences in its Membrane Transport. Frontiers in pharmacology 24 34040533
2017 POU2F1 over-expression correlates with poor prognoses and promotes cell growth and epithelial-to-mesenchymal transition in hepatocellular carcinoma. Oncotarget 24 28489585
2013 Regulation of Oct1/Pou2f1 transcription activity by O-GlcNAcylation. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 24 23580612
2004 Transcriptional regulation of murine Slc22a1 (Oct1) by peroxisome proliferator agonist receptor-alpha and -gamma. American journal of physiology. Gastrointestinal and liver physiology 24 15458920
2022 Exercise training attenuates angiotensin II-induced cardiac fibrosis by reducing POU2F1 expression. Journal of sport and health science 23 36374849
2021 LncRNA NEAT1 Promotes Inflammatory Response in Sepsis via the miR-31-5p/POU2F1 Axis. Inflammation 23 33710444
2011 Genetic analysis of OCT1 gene polymorphisms in an Indian population. Indian journal of human genetics 23 22345987
2001 Expression of the Oct-1 transcription factor and characterization of its interactions with the Bob1 coactivator. Biochemistry 23 11380252
1999 Reconstitution of the protein kinase A response of the rat prolactin promoter: differential effects of distinct Pit-1 isoforms and functional interaction with Oct-1. Molecular endocrinology (Baltimore, Md.) 23 9973253
1992 Identification of sites for distinct DNA binding proteins including Oct-1 and Oct-2 in the Cr2 gene. Journal of immunology (Baltimore, Md. : 1950) 23 1534100
2021 Influence of YES1 Kinase and Tyrosine Phosphorylation on the Activity of OCT1. Frontiers in pharmacology 22 33790797
2021 NPR3, transcriptionally regulated by POU2F1, inhibits osteosarcoma cell growth through blocking the PI3K/AKT pathway. Cellular signalling 22 34229087
2020 Pathological matrix stiffness promotes cardiac fibroblast differentiation through the POU2F1 signaling pathway. Science China. Life sciences 22 32617828
2019 LncRNA SND1-IT1 accelerates the proliferation and migration of osteosarcoma via sponging miRNA-665 to upregulate POU2F1. European review for medical and pharmacological sciences 22 31799644
2014 OCT-1, ABCB1, and ABCG2 Expression in Imatinib-Resistant Chronic Myeloid Leukemia Treated with Dasatinib or Nilotinib. Chonnam medical journal 22 25568846
2011 Maternal Oct1/2 is required for Nodal and Vg1/Univin expression during dorsal-ventral axis specification in the sea urchin embryo. Developmental biology 22 21782809
2021 Pterostilbene leads to DNMT3B-mediated DNA methylation and silencing of OCT1-targeted oncogenes in breast cancer cells. The Journal of nutritional biochemistry 21 34242723
2019 Highly Variable Pharmacokinetics of Tyramine in Humans and Polymorphisms in OCT1, CYP2D6, and MAO-A. Frontiers in pharmacology 21 31736764
2016 Oct-1, to go or not to go? That is the PolII question. Biochimica et biophysica acta 21 27063953
2007 Oct-1 is involved in the transcriptional repression of the p15(INK4b) gene. FEBS letters 21 17316622
2003 OBF1 enhances transcriptional potential of Oct1. The EMBO journal 21 12727885
2022 LncRNA AC026401.3 interacts with OCT1 to intensify sorafenib and lenvatinib resistance by activating E2F2 signaling in hepatocellular carcinoma. Experimental cell research 20 36084669
2019 Slc7a11 Modulated by POU2F1 is Involved in Pigmentation in Rabbit. International journal of molecular sciences 20 31137576
2019 The human organic cation transporter OCT1 and its role as a target for drug responses. Drug metabolism reviews 20 31564168
2018 OCT1-Mediated Metformin Uptake Regulates Pancreatic Stellate Cell Activity. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 20 29949790
2011 Effect of cryopreservation on the activity of OATP1B1/3 and OCT1 in isolated human hepatocytes. Chemico-biological interactions 20 21356203
2012 Sensitivity to TOP2 targeting chemotherapeutics is regulated by Oct1 and FILIP1L. PloS one 19 22900064
2010 Oct1 is required for mTOR-induced G1 cell cycle arrest via the control of p27(Kip1) expression. Cell cycle (Georgetown, Tex.) 19 20935455
2010 Association of the POU class 2 homeobox 1 gene (POU2F1) with susceptibility to Type 2 diabetes in Chinese populations. Diabetic medicine : a journal of the British Diabetic Association 19 21059098
2017 Daidzein promotes proliferation and differentiation in osteoblastic OCT1 cells via activation of the BMP-2/Smads pathway. Die Pharmazie 18 29441895
2016 Role of OCT-1 and partner proteins in T cell differentiation. Biochimica et biophysica acta 18 27126747
2018 BRCA1 through Its E3 Ligase Activity Regulates the Transcription Factor Oct1 and Carbohydrate Metabolism. Molecular cancer research : MCR 17 29330289
2017 Enforcement of developmental lineage specificity by transcription factor Oct1. eLife 17 28537559