Affinage

OLIG2

Oligodendrocyte transcription factor 2 · UniProt Q13516

Length
323 aa
Mass
32.4 kDa
Annotated
2026-06-10
100 papers in source corpus 38 papers cited in narrative 38 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

OLIG2 is a basic helix-loop-helix transcription factor that operates as a master regulator of ventral neural progenitor identity, coupling neuronal and glial subtype specification within a combinatorial transcriptional code (PMID:11567617, PMID:11955447). Genetic loss-of-function establishes it as essential for both motoneuron and oligodendrocyte lineage specification: Olig2-null progenitors fail to generate these cell types and are instead diverted toward astrocytic and interneuron fates (PMID:12121626, PMID:11955447), a requirement conserved in zebrafish downstream of Hedgehog signaling (PMID:12167410). OLIG2 functions principally as a transcriptional repressor (PMID:11567617, PMID:10737801), directly repressing the cell cycle inhibitor p21/CDKN1A to drive progenitor and glioma proliferation (PMID:17296553) and repressing Hes5 to time motor neuron differentiation (PMID:29389974). A central theme is that distinct OLIG2 activities are gated by post-translational modification. Phosphorylation of an amino-terminal triple serine motif (S10/S13/S14) by a sequentially priming GSK3/CK2/CDK1/2 kinase cascade maintains promitotic, antineural function and partitions OLIG2 into transcriptionally active open chromatin in proximity to p53 (PMID:21382551, PMID:28355568, PMID:24948806), while SUMOylation at K27/K76/K112 cooperates with this phosphorylation to suppress p53-mediated genotoxic responses by occluding p53 from the Cdkn1a promoter (PMID:32483381). Independently, phosphorylation of S147 in the HLH domain switches OLIG2 from homodimers to Neurogenin2-containing heterodimers, providing the molecular basis for the motor-neuron versus oligodendrocyte fate decision (PMID:21382552). In the oligodendrocyte program, OLIG2 acts as a prepatterning factor that recruits the SWI/SNF remodeler Smarca4/Brg1 to lineage-specific enhancers (PMID:23332759), recruits SETDB1 to impose H3K9me3-mediated repression of Sox11 (PMID:35301318), and heterodimerizes with Tcf4 to activate myelin gene enhancers and drive terminal differentiation and myelination (PMID:32266943, PMID:36198499). OLIG2 forms a physical complex with Nkx2.2 underlying cross-repressive patterning of the pMN-p3 boundary (PMID:14573534), and its phosphorylation state controls glioma proliferation, PDGFRα-driven proneural identity, and TGF-β2-dependent invasion, making it a driver and therapeutic node in glioma (PMID:17296553, PMID:27165742, PMID:27396340).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 2000 Medium

    Before its neural role was known, the question was what BHLHB1/OLIG2 does transcriptionally; identifying it via a leukemic translocation showed it acts as a bHLH repressor of E2A activity.

    Evidence Translocation breakpoint cloning and E2A reporter assays in NIH 3T3 and Jurkat cells

    PMID:10737801

    Open questions at the time
    • No neural context or physiological targets identified
    • Repression mechanism on E2A not mapped to specific domains
  2. 2001 High

    The central question of how a single factor could specify both neurons and glia was addressed by showing Olig2 acts as a context-dependent repressor whose output depends on co-expressed transcription factors.

    Evidence In vivo gain-of-function misexpression in chick spinal cord with repressor and Neurogenin assays

    PMID:11567617

    Open questions at the time
    • Direct DNA targets not identified
    • Molecular basis of the fate switch unknown at this stage
  3. 2002 High

    Whether Olig2 is genuinely required for these lineages was settled by knockout and double-mutant mice, establishing it as essential for motoneuron and oligodendrocyte specification and showing pMN progenitors default to astrocytes/interneurons in its absence.

    Evidence Olig2 and Olig1/Olig2 knockout mice with lineage tracing; zebrafish loss/gain-of-function with Hedgehog epistasis

    PMID:11955447 PMID:12121626 PMID:12167410

    Open questions at the time
    • Partial Olig1/Olig3 compensation complicates interpretation
    • Direct molecular targets driving fate choice not defined
  4. 2003 Medium

    To explain the patterning logic of the pMN-p3 boundary, Olig2 was shown to form a specific physical complex with Nkx2.2, providing a biochemical basis for cross-repression.

    Evidence Co-immunoprecipitation, yeast two-hybrid, and deletion mapping with in vivo cross-repression assays

    PMID:14573534

    Open questions at the time
    • Complex alone insufficient to induce OPCs
    • Single lab; structural basis of interaction not resolved
  5. 2004 Medium

    The mechanism by which Olig2 suppresses astrocyte fate was addressed by showing it disrupts the p300-STAT3 coactivator complex required for LIF-induced astrocyte gene activation.

    Evidence Overexpression in neuroepithelial cells, GFAP-luciferase, and p300-STAT3 co-IP

    PMID:14576772

    Open questions at the time
    • Direct binding partner among p300/STAT3 not defined
    • Single lab
  6. 2005 High

    Whether Olig2 acts as an intrinsic fate determinant postnatally was tested in the SVZ, showing its repressor function is necessary and sufficient to direct progenitors toward pan-glial fates.

    Evidence In vivo dominant-interfering and wild-type Olig2 expression in postnatal SVZ with fate analysis

    PMID:16093378

    Open questions at the time
    • Repressed neuronal target genes not enumerated
  7. 2006 Medium

    Downstream regulatory architecture was extended by showing Olig2 induces Sox10 and Nkx2.2 in a dosage-dependent, reciprocally regulated network, and that Olig2 lineages also contribute to cholinergic neurons.

    Evidence Chick in ovo overexpression with epistasis and dosage experiments; lineage tracing and ChAT analysis in Olig2-KO basal forebrain

    PMID:16537079 PMID:17098222

    Open questions at the time
    • Directness of Sox10/Nkx2.2 induction not all established by ChIP
    • Cholinergic role based on partial (~40%) reduction
  8. 2007 High

    How Olig2 links lineage to proliferation, and its postnatal astrocyte role, were established by direct p21 repression in progenitors/gliomas and by conditional ablation compromising white matter astrocytes.

    Evidence ChIP of p21 promoter with conditional glioma model; conditional Olig2 KO with multiple Cre lines and fate mapping; injury-induced nucleocytoplasmic translocation tied to astrocytic conversion

    PMID:17296553 PMID:17428828 PMID:17510983

    Open questions at the time
    • Mechanism of injury-induced translocation not molecularly defined
    • Region-specific astrocyte requirement (white vs gray matter) unexplained
  9. 2008 Medium

    Upstream control of Olig2 itself was addressed by showing Smad-containing complexes directly bind and regulate the Olig2 promoter under FGF/BMP signaling.

    Evidence ChIP of Olig2 promoter, MAPK inhibition, and SMAD1 nuclear localization assays in spinal cord cultures

    PMID:18682850

    Open questions at the time
    • Single lab
    • Quantitative contribution to in vivo Olig2 expression unclear
  10. 2011 High

    The long-standing puzzle of how one factor selects motor neuron versus oligodendrocyte fate, and proliferative versus differentiation states, was resolved by two phospho-regulatory mechanisms: S147 phosphorylation controls dimer partner choice and the triple serine motif controls promitotic function.

    Evidence Phospho-specific antibodies, site mutagenesis (S147A, triple serine), transgenic mice, and dimerization assays across chick, mouse, and P19 systems

    PMID:21382551 PMID:21382552

    Open questions at the time
    • S147 kinase only tentatively assigned (possibly PKA)
    • Genome-wide consequences of each phospho-state not yet mapped
  11. 2012 High

    Whether Olig2 actively maintains oligodendrocyte over astrocyte fate in NG2 cells was tested by cell-type-specific deletion, showing loss switches NG2 cells to astrocytes in dorsal but not ventral regions.

    Evidence Constitutive and inducible Olig2 KO in NG2 cells with genetic fate mapping

    PMID:22627280

    Open questions at the time
    • Regional difference (neocortex vs ventral forebrain) mechanistically unexplained
  12. 2013 High

    How Olig2 reorganizes chromatin to drive the oligodendrocyte program was established by showing it acts as a prepatterning factor recruiting Smarca4/Brg1 to stage-specific enhancers genome-wide.

    Evidence Multi-stage ChIP-seq, conditional Smarca4/Brg1 KO, and enhancer functional analysis

    PMID:23332759

    Open questions at the time
    • Direct physical Olig2-Brg1 contact vs co-occupancy not fully distinguished
    • Stage-specific cofactor switching not detailed
  13. 2013 Medium

    Stage-specific requirements for Olig2 in differentiation versus myelination were initially examined, suggesting deletion in immature OLs enhances maturation via Olig1 compensation — a result later overturned.

    Evidence Stage-specific conditional KO (CNPase-Cre, PLP-Cre) with Olig1 rescue in vitro

    PMID:23658182

    Open questions at the time
    • Directly contradicted by PMID 36198499
    • Reliance on a single Cre strategy per stage
  14. 2014 Medium

    The chromatin and partner basis of Olig2's promitotic and self-renewal functions were detailed: phospho-Olig2 localizes to open chromatin near p53, Olig2 co-activates proliferation genes while blocking neuronal/quiescence genes, and upstream repressors (Prox1) restrict its expression.

    Evidence Chromatin fractionation and proximity ligation to p53; DNase-seq/ChIP-seq in NS cells; Prox1 ChIP and gain/loss-of-function on Olig2 enhancers

    PMID:24948806 PMID:25294244 PMID:25411508

    Open questions at the time
    • Functional consequence of Olig2-p53 proximity not directly demonstrated in these studies
    • Single labs
  15. 2016 High

    Olig2's role in glioma was sharpened by showing phospho-state controls TGF-β2-driven invasion, that Olig2 maintains PDGFRα-driven proneural identity, and that loss sensitizes tumors to EGFR inhibition.

    Evidence Phosphomimetic/deficient mutants with invasion assays and pathway inhibitors; ChIP-seq and conditional deletion in proneural glioma with EGFR inhibitor epistasis; Brg1 repression of Olig2 promoter

    PMID:27067865 PMID:27165742 PMID:27396340

    Open questions at the time
    • Direct Olig2 target genes driving TGF-β2 induction not fully mapped
    • Translation to human glioma subtypes incomplete
  16. 2016 High

    A direct injury-response target was identified by showing Olig2 binds and activates the Gpr17 locus following demyelination, regulating oligodendrocyte survival via cAMP and Xaf1.

    Evidence ChIP-seq in oligodendrocytes, Gpr17 KO, pharmacological inhibition, and cAMP measurement after lysolecithin injury

    PMID:27733608

    Open questions at the time
    • Whether Gpr17 regulation is activating or context-dependent not fully resolved
  17. 2018 Medium

    How Olig2 times motor neuron generation was addressed by showing it directly represses Hes1/Hes5 just prior to MN differentiation via a conserved Hes5 regulatory element.

    Evidence Single-cell RNA-seq, expression-dynamics reconstruction, and Hes5 regulatory element analysis

    PMID:29389974

    Open questions at the time
    • Direct binding shown by regulatory element analysis rather than full biochemical validation
    • Single lab
  18. 2020 Medium

    Two PTM-dependent and injury-related functions were defined: SUMOylation cooperates with phosphorylation to suppress p53 genotoxic responses by occluding p53 from Cdkn1a, and Olig2 drives semaphorin-mediated axon retraction after spinal cord injury; Tcf4 was also identified as the preferred oligodendrocyte heterodimer partner.

    Evidence SUMO site mutagenesis with ChIP at Cdkn1a; Olig2 ChIP at semaphorin enhancers with conditional KO; Tcf4/Tcf3/Tcf12 mutants with co-IP and myelin enhancer assays

    PMID:32266943 PMID:32483381 PMID:32564090

    Open questions at the time
    • SUMO and semaphorin findings each single-lab
    • Interplay between SUMO and phospho marks not structurally resolved
  19. 2022 High

    The chromatin-repressive mechanism of differentiation was extended by showing Olig2 recruits SETDB1 to silence Sox11 via H3K9me3, while rigorous multi-Cre deletion resolved the earlier contradiction by establishing that Olig2 is required for OL maturation/myelination at all stages.

    Evidence OLIG2-SETDB1 co-IP, H3K9me3 ChIP, and Sox11 rescue experiments; multiple conditional KO lines (Plp1/Mobp/Mog-Cre) with ChIP-seq and lineage tracing; Ddx20 identified as an Olig2-binding stabilizer in NPCs

    PMID:34974536 PMID:35301318 PMID:36198499

    Open questions at the time
    • Whether SETDB1 recruitment is direct contact or bridged is not fully resolved
    • Ddx20 interaction validated in a single lab
  20. 2024 Medium

    Functional redundancy among proneural factors in tumorigenesis was addressed by showing ASCL1 and OLIG2 cross-bind each other's loci and act redundantly to drive GBM formation and tumor cell heterogeneity.

    Evidence Somatic SVZ progenitor GBM model, scRNA-seq, and ASCL1/OLIG2 ChIP-seq co-occupancy with loss-of-function readouts

    PMID:39609428

    Open questions at the time
    • Direct ASCL1-OLIG2 physical interaction not established
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how the combinatorial PTM code (S147 phosphorylation, triple serine phosphorylation, and SUMOylation) is integrated in real time to switch OLIG2 among its repressive, promitotic, and lineage-instructive states, and what governs the kinase signaling inputs in vivo.
  • No structural model of multiply-modified OLIG2
  • Upstream signals controlling S147 kinase and SUMO machinery in vivo undefined
  • Temporal coordination of PTMs with partner switching not mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 4 GO:0140110 transcription regulator activity 4
Localization
GO:0005634 nucleus 3 GO:0000228 nuclear chromosome 2
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-1643685 Disease 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1640170 Cell Cycle 3 R-HSA-4839726 Chromatin organization 2
Partners
ASCL1DDX20NEUROG2NKX2.2SETDB1SMARCA4TCF4TP53

Evidence

Reading pass · 38 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 Olig2 functions as a transcriptional repressor; coexpression of Olig2 with Nkx2.2 in the spinal cord promotes ectopic and precocious oligodendrocyte differentiation, while misexpression of Olig2 alone derepresses Neurogenins and promotes motoneuron differentiation. This dual action depends on spatiotemporal changes in expression domains of interacting transcription factors. In vivo gain-of-function misexpression in chick spinal cord; reporter/transcriptional repressor assays; forced expression of Neurogenin1 to block the effect Neuron High 11567617
2002 Olig2 is essential for motoneuron and oligodendrocyte lineage specification; Olig2−/− mice lack motoneurons and oligodendrocytes, and pMN progenitors instead generate astrocytes (expressing S100β). Olig1 and Olig3 are expressed in cells that should have expressed Olig2, showing partial compensation. Homozygous Olig2 knockout mouse; histological and marker analysis of spinal cord Current biology : CB High 11955447 12121626
2002 In Olig1/Olig2 double-mutant mice, motoneurons are largely eliminated and oligodendrocyte differentiation is abolished; pMN progenitors instead generate V2 interneurons and then astrocytes. Olig genes couple neuronal and glial subtype specification as part of a combinatorial transcriptional code with proneural genes. Olig1/2 double-mutant mice; lineage tracing Cell High 11955447
2002 Loss of olig2 function in zebrafish prevents primary motor neuron and oligodendrocyte development, while olig2 overexpression promotes excess primary motor neurons and oligodendrocytes. Hedgehog signaling is required upstream of olig2 expression for oligodendrocyte development. Zebrafish loss-of-function (morpholino) and overexpression; genetic epistasis with Hedgehog pathway mutants Developmental biology High 12167410
2002 Olig2 and Nkx2.2 are expressed in adjacent non-overlapping domains during neurogenesis, then co-expressed in oligodendrocyte progenitors (OLPs). Antisense inhibition of both Olig2 and Nkx2.2 has an additive inhibitory effect on OLP differentiation and PLP expression, demonstrating a cooperative role. Expression analysis in chick and mouse; antisense oligonucleotide knockdown in culture; comparison with PDGFA−/− embryos Development (Cambridge, England) Medium 11830569
2003 Olig2 protein forms a physical complex with Nkx2.2 protein in mammalian cells and in a yeast two-hybrid assay. This interaction is specific: Olig2 does not bind Nkx6.1, and Nkx2.2 does not interact with NeuroD. The Olig2-Nkx2.2 physical complex underlies the cross-repressive interaction establishing the pMN-p3 boundary; the complex alone is insufficient to induce OPCs. Co-immunoprecipitation in mammalian cells; yeast two-hybrid; deletion mapping; cross-repression assays in vivo The Journal of neuroscience Medium 14573534
2004 OLIG2 inhibits LIF-induced astrocytic differentiation by abolishing complex formation between transcriptional coactivator p300 and STAT3 (activated by LIF). Enforced OLIG2 expression in neuroepithelial cells blocks astrocyte-specific GFAP promoter activation; OLIG2 protein disappears from nuclei during astrocytic differentiation. Overexpression in mouse neuroepithelial cells; GFAP promoter-luciferase assay; co-immunoprecipitation of p300-STAT3 complex; immunofluorescence Cell death and differentiation Medium 14576772
2004 Olig2 is expressed throughout the oligodendrocyte lineage and in all diffuse gliomas; OLIG2 protein is restricted to oligodendroglia and their progenitors in normal human brain, as established by antibody validated by Western blot (single band at predicted MW, no cross-reactivity with Olig1). Polyclonal antibody development; Western blot; immunohistochemistry on human brain tissue and tumors The American journal of pathology Medium 15111318
2005 Olig2 repressor function is both sufficient and necessary to prevent neuronal differentiation and to direct SVZ progenitors toward astrocytic and oligodendrocytic (pan-glial) fates in the postnatal SVZ. This identifies Olig2 as the first intrinsic fate determinant shown to operate in early postnatal SVZ. In vivo expression of normal and dominant-interfering forms of Olig2 in postnatal SVZ; cell fate analysis The Journal of neuroscience High 16093378
2006 Olig2 induces Sox10 and Nkx2.2 expression and precocious oligodendrocyte differentiation in chick spinal cord; Sox10 functions downstream of Olig2 but can also modulate Olig2 expression (reciprocal regulation). Control of oligodendrocyte differentiation by Olig2, Sox10, and Nkx2.2 is dosage-dependent. In ovo overexpression in chick spinal cord; genetic epistasis analysis; haploinsufficiency and overdosage experiments Developmental biology Medium 17098222
2007 Olig2 directly represses p21(WAF1/CIP1) in neural progenitors and gliomas, linking Olig2-regulated lineage-restricted pathway to proliferation. Olig2 function is required for proliferation of neural progenitors and glioma formation in a genetically relevant murine model. Conditional murine glioma model; ChIP for p21 promoter; Olig2 loss-of-function in neural progenitors with proliferation and tumor formation readouts Neuron High 17296553
2007 Conditional ablation of Olig2 in the cortex and spinal cord severely compromises white matter astrocyte formation. Postnatal Olig2 function is required for astrocyte differentiation in the cerebral white matter, but astrocytes in cortical gray matter still form (with sustained GFAP upregulation). Cell type-specific fate-mapping confirmed abnormal astrocyte formation is attributable to Olig2 loss in developing astrocytes and their precursors. Conditional Olig2 knockout mice with temporal and cell-type specific Cre; fate-mapping analysis; histological marker analysis Development (Cambridge, England) High 17428828
2007 After stab wound brain injury, Olig2 undergoes nucleocytoplasmic translocation in glial progenitors during the first week post-injury, correlating with astrocytic differentiation. This translocation and astrocytic conversion (NG2 downregulation, GFAP upregulation) can be recapitulated by serum or BMP in vitro and is blocked by Notch-1 inhibition with gamma-secretase inhibitor DAPT. In vivo stab wound in rats; transgenic mouse models; in vitro BMP/serum exposure; gamma-secretase inhibitor DAPT treatment; immunostaining for Olig2 localization Journal of neuroscience research Medium 17510983
2008 FGF prevents BMP-induced nuclear localization of C-term-phosphorylated SMAD1 in a MAPK-dependent manner, correlating with OLIG2 upregulation and OPC generation. SMAD4 associates with a Smad binding site in the Olig2 promoter and dissociates upon differentiation, indicating direct transcriptional regulation of the Olig2 promoter by Smad-containing complexes. Chromatin immunoprecipitation (ChIP) of Olig2 promoter; MAPK inhibition; SMAD1 nuclear localization assays; FGF2 treatment of dorsal spinal cord cultures PloS one Medium 18682850
2009 In zebrafish, Olig2 acts upstream of Sim1 to specify diencephalic dopaminergic neurons. Olig2 and Sim1 are co-expressed in a subset of diencephalic progenitors; loss of either impairs dopaminergic development; Olig2 regulates Sim1 expression; and gain of Sim1 function rescues DA differentiation deficits caused by Olig2 knockdown. Zebrafish loss-of-function (morpholino); gain-of-function (overexpression); epistasis rescue experiment; in situ hybridization and immunostaining Developmental dynamics Medium 19253397
2011 Serine 147 in the helix-loop-helix domain of OLIG2 is phosphorylated during motor neuron production and dephosphorylated at the onset of OLP genesis. S147A mutation abolishes MN production without preventing OLP production. Wild-type OLIG2 forms stable homodimers, whereas unphosphorylated OLIG2(S147A) preferentially forms heterodimers with Neurogenin 2 or other bHLH partners, providing a molecular basis for the MN-OLP fate switch. Phosphorylation is possibly mediated by protein kinase A. Phospho-specific antibody characterization; S147A transgenic mice; chick in ovo electroporation; P19 cell culture; protein-protein interaction studies (homodimer vs. heterodimer preference) Neuron High 21382552
2011 Proliferative/antineural function of Olig2 is controlled by phosphorylation of a conserved triple serine motif (S10, S13, S14) in the amino-terminal domain. In the phosphorylated state, Olig2 maintains promitotic (antineural) functions relevant to both normal neural progenitors and glioma cells. Phospho-specific antibody; mutagenesis of triple serine motif; in vivo progenitor proliferation assays; genetically defined murine glioma model Neuron High 21382551
2012 Olig2 expression is spontaneously downregulated in NG2 cells as they differentiate into astrocytes. Constitutive or perinatal deletion of Olig2 specifically in NG2 cells in the neocortex and corpus callosum (but not ventral forebrain) switches their fate from oligodendrocytes to astrocytes, with concomitant severe reduction in oligodendrocytes and myelin. Conditional Olig2 knockout in NG2 cells (constitutive and tamoxifen-inducible Cre); genetic fate mapping; histological analysis Development (Cambridge, England) High 22627280
2013 Olig2 functions as a prepatterning factor that directs the ATP-dependent SWI/SNF chromatin-remodeling enzyme Smarca4/Brg1 to oligodendrocyte-specific enhancers genome-wide. Activation of Smarca4/Brg1 at the differentiation onset is necessary and sufficient to initiate and promote oligodendrocyte lineage progression. Olig2-Smarca4/Brg1 co-occupancy at stage-specific cis-regulatory elements controls the transcriptional program for oligodendrocyte differentiation and myelination. ChIP-seq (genome-wide, multi-stage); conditional Smarca4/Brg1 knockout; functional enhancer analysis; chromatin epigenetic marking Cell High 23332759
2013 Deletion of Olig2 in OPCs (CNPase-Cre) significantly inhibits differentiation and causes hypomyelination; deletion in immature OLs (inducible PLP-Cre) reportedly enhances maturation and accelerates myelination/remyelination, mediated by compensatory upregulation (~3-fold) of Olig1. Olig1 overexpression in OPCs in a null Olig2 background rescues the differentiation phenotype. Stage-specific conditional Olig2 knockout (CNPase-Cre and inducible PLP-Cre); Olig1 expression analysis; rescue by Olig1 overexpression in vitro The Journal of neuroscience Medium 23658182
2014 Phosphorylated Olig2 (triple serine motif) is preferentially localized to a transcriptionally active 'open' chromatin compartment with coregulator proteins, while unphosphorylated Olig2 (as in mature white matter) is in a transcriptionally inactive condensed chromatin fraction. Phosphorylation brings Olig2 within 30 nm of p53 within the open chromatin compartment (proximity ligation assay), providing a molecular basis for Olig2's promitotic function opposing p53. Chromatin fractionation; phospho-specific antibody; proximity ligation assay; co-purification of Olig2 with coregulators from chromatin fractions The Journal of neuroscience Medium 24948806
2014 OLIG2 contributes to neural stem cell self-renewal by concurrently activating pro-proliferation genes and preventing activation of genes promoting neuronal differentiation and quiescence, as established by ChIP-seq genome-wide occupancy and functional validation in NS cells. DNase-seq; histone modification ChIP-seq; OLIG2 ChIP-seq; functional knockdown/overexpression in NS cells with self-renewal and differentiation readouts Genome research Medium 25294244
2016 Unphosphorylated OLIG2 (at S10, S13, S14) induces TGF-β2 expression and promotes invasive mesenchymal properties in glioma cells both in vitro and in vivo. Inhibition of the TGF-β2 pathway blocks OLIG2-dependent invasion. Ectopic phosphomimetic Olig2 is sufficient to block TGF-β2-mediated invasion and reduce expression of invasion genes ZEB1 and CD44. Phosphomimetic and phosphodeficient OLIG2 mutant expression; in vitro migration/invasion assays; in vivo xenograft; TGF-β2 pathway inhibitor treatment; gene expression analysis Cell reports Medium 27396340
2016 Olig2 directly activates cell-proliferation machinery to promote tumorigenesis and maintains PDGFR-α expression. Deletion of Olig2 causes a tumor phenotypic shift from proneural (PDGFRα-high) toward astroglia-associated (EGFR-high) gene expression, sensitizing glioma cells to EGFR inhibitors. Genome occupancy (ChIP-seq) and expression profiling in Olig2-deleted proneural glioma cells; conditional Olig2 deletion in tumor model; EGFR inhibitor treatment; lifespan analysis Cancer cell High 27165742
2016 After lysolecithin-induced demyelination injury, Olig2 is upregulated in oligodendrocytes and transcriptionally targets the Gpr17 locus (demonstrated by ChIP-seq). Gpr17 activation inhibits oligodendrocyte survival by reducing intracellular cAMP and inducing pro-apoptotic gene Xaf1; Gpr17 inhibition elevated Epac1 expression and promoted oligodendrocyte differentiation. ChIP-seq in oligodendrocytes; Gpr17 global and oligodendrocyte-specific KO; pharmacological Gpr17 inhibition; intracellular cAMP measurement; gene expression analysis The Journal of neuroscience High 27733608
2017 Phosphorylation of the triple serine motif (S10, S13, S14) in Olig2 is driven by a sequentially priming cascade requiring three kinases: GSK3α/β, CK2, and CDK1/2 — collectively necessary and sufficient to phosphorylate the motif. Phosphorylation of the motif creates a highly charged 'acid blob' in the Olig2 amino terminus. Small molecule inhibitors of this kinase cascade reduce glioma cell growth. Mass spectrometry phospho-site mapping; kinase inhibitor studies; reconstitution of phosphorylation cascade in vitro; mutagenesis of individual serines; glioma cell growth assays Cell reports High 28355568
2018 Single-cell transcriptomics and gene expression reconstruction reveal that Olig2 represses Hes1 and Hes5 expression just prior to motor neuron differentiation, coordinating the spatial and temporal pattern of MN generation. Olig2 repression of Hes5 appears direct, via a conserved regulatory element within the Hes5 locus that restricts expression from MN progenitors. Single-cell RNA sequencing; gene expression dynamics reconstruction; regulatory element analysis of Hes5 locus PLoS biology Medium 29389974
2020 Olig2 is conjugated by SUMO1 at three lysine residues (K27, K76, K112). SUMOylation is required for Olig2 to suppress p53-mediated cell cycle arrest and apoptosis induced by genotoxic damage, and both SUMOylation and triple serine motif (TSM) phosphorylation are required for the antiapoptotic function. Olig2 SUMOylation enhances its genomic targeting ability and occludes p53 recruitment to the Cdkn1a promoter. SUMO site mutagenesis; co-immunoprecipitation; ChIP showing Olig2 and p53 occupancy at Cdkn1a promoter; TMZ genotoxic challenge assays; cell cycle/apoptosis readouts Cell death and differentiation Medium 32483381
2020 After spinal cord injury, Olig2+ cells drive upregulation of semaphorins Sema5a and Sema6d, promoting corticospinal axon retraction. Olig2 binds to putative enhancer regions of semaphorin genes (by ChIP). Conditional deletion of Olig2 in the spinal cord reduces semaphorin expression and alleviates axon retraction. ChIP for Olig2 binding to semaphorin gene enhancers; conditional Olig2 deletion in spinal cord; genetic deletion of semaphorins and receptors; axon retraction quantification Cerebral cortex Medium 32564090
2020 Tcf4 is the preferred heterodimerization partner of Olig2 in oligodendrocytes. Tcf4 is required in a cell-autonomous manner for terminal oligodendrocyte differentiation and myelination in vivo and ex vivo. Genetic and functional studies on myelin gene enhancer regions confirmed the relevance of the Olig2-Tcf4 physical interaction. Mouse mutants (Tcf4, Tcf3, Tcf12 knockouts); co-immunoprecipitation/heterodimerization assays; organotypic slice culture; enhancer functional assays for myelin genes Nucleic acids research Medium 32266943
2022 OLIG2 recruits histone methyltransferase SETDB1 to the Sox11 gene locus, leading to H3K9me3-mediated repression of Sox11 expression during differentiation of OPCs into immature oligodendrocytes. Tissue-specific Setdb1 depletion causes hypomyelination and remyelination defects; knockdown of Sox11 rescues the hypomyelination phenotype caused by Olig2 loss. Co-immunoprecipitation (OLIG2-SETDB1); ChIP for H3K9me3 at Sox11 locus; tissue-specific Setdb1 conditional KO; Sox11 siRNA knockdown in rat primary OPCs; Sox11 oligodendrocyte lineage KO in mice Nature communications High 35301318
2022 Olig2 ablation in immature oligodendrocytes (using Plp1, Mobp, or Mog promoter-driven Cre lines) causes defects in OL maturation and myelination and does not enhance remyelination. Olig2 targets the enhancers of key myelination-related genes in immature and mature OLs (genome occupancy analysis). This directly contradicts an earlier report (PMID:23658182) claiming Olig2 deletion in immature OLs enhances myelination. Multiple conditional Olig2 KO mouse lines (Plp1-Cre, Mobp-Cre, Mog-Cre); ChIP-seq genome occupancy in immature and mature OLs; lysolecithin demyelination model; lineage tracing with reporters The Journal of neuroscience High 36198499
2022 Ddx20 is a novel Olig2-binding protein. Olig2 contributes to NPC proliferation through Ddx20 protein stabilization; Ddx20 knockout causes apoptosis and cell cycle arrest in NPCs and OPCs via potentiation of p53 (both DNA damage-dependent and -independent), including SMN complex disruption and abnormal Mdm2 mRNA splicing. Protein interaction screen identifying Ddx20; CNS-specific Ddx20 conditional KO; Olig2 null NPC analysis; Ddx20 protein stability assays; Mdm2 splicing analysis; p53 pathway readouts Cell death and differentiation Medium 34974536
2024 ASCL1 and OLIG2 function redundantly and are both required for brain tumor formation in a mouse SVZ progenitor GBM model. ASCL1 and OLIG2 bind each other's loci and to downstream target genes, with OLIG2 co-regulating tumor cell types and migration. High ASCL1 specifies highly migratory NSC/astrocyte-like tumor cells. Somatic mutation induction in SVZ progenitors; scRNA-seq; ChIP-seq for ASCL1 and OLIG2 co-occupancy; loss-of-function with tumor formation and migration readouts Nature communications Medium 39609428
2000 OLIG2 (then designated BHLHB1) inhibits E2A-mediated transcriptional activation in NIH 3T3 fibroblasts and Jurkat T cells when expressed ectopically following activation by the t(14;21) translocation placing the TCR alpha locus enhancer near the BHLHB1 locus. Chromosomal translocation breakpoint cloning; ectopic expression; E2A transcription reporter assays in NIH 3T3 and Jurkat T cells Proceedings of the National Academy of Sciences of the United States of America Medium 10737801
2006 A subset of cells derived from Olig2-expressing progenitors in the basal forebrain at E12.5 expresses ChAT (choline acetyltransferase). The number of ChAT+ cells is reduced by ~40% in Olig2 knockout mouse basal forebrain with no evidence of elevated apoptosis or reduced proliferation, indicating a role for Olig2 in cholinergic differentiation. Tamoxifen-inducible Cre-mediated lineage tracing in Olig2 locus; ChAT immunostaining; Olig2 knockout analysis Developmental biology Medium 16537079
2016 Brg1 (SWI/SNF subunit) interacts with a proximal Olig2 promoter and represses Olig2 transcription in the mouse cortex at E14 (where OPCs are absent) but not in the ganglionic eminence (where OPCs form). Brg1-null NPCs show precocious Olig2 expression in the cortex, but fail to differentiate into OPCs, establishing that Brg1 both represses Olig2 and is required for downstream OPC differentiation. ChIP for Brg1 at Olig2 promoter; Brg1 conditional knockout; comparison of Olig2 expression between cortex and ganglionic eminence Developmental biology Medium 27067865
2014 Prox1 directly binds to the proximal promoter and K23 enhancer of the Olig2 gene locus in vivo (ChIP in mouse neural tube) and suppresses Olig2 expression, thereby controlling MN versus V2 interneuron identity. Prox1 gain- and loss-of-function in mouse NPCs and chick neural tube confirm it is sufficient and necessary for Olig2 repression. ChIP in mouse neural tube for Prox1 binding to Olig2 promoter and K23 enhancer; plasmid-based transcriptional reporter assays; gain- and loss-of-function in mouse NPCs and chick neural tube The Journal of neuroscience Medium 25411508

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 The bHLH transcription factors OLIG2 and OLIG1 couple neuronal and glial subtype specification. Cell 847 11955447
2001 The bHLH transcription factor Olig2 promotes oligodendrocyte differentiation in collaboration with Nkx2.2. Neuron 478 11567617
2002 The basic helix-loop-helix factor olig2 is essential for the development of motoneuron and oligodendrocyte lineages. Current biology : CB 416 12121626
2007 Olig2-regulated lineage-restricted pathway controls replication competence in neural stem cells and malignant glioma. Neuron 415 17296553
2004 The oligodendroglial lineage marker OLIG2 is universally expressed in diffuse gliomas. Journal of neuropathology and experimental neurology 348 15198128
2013 Olig2 targets chromatin remodelers to enhancers to initiate oligodendrocyte differentiation. Cell 308 23332759
2002 olig2 is required for zebrafish primary motor neuron and oligodendrocyte development. Developmental biology 252 12167410
2004 Increased expression of Nkx2.2 and Olig2 identifies reactive oligodendrocyte progenitor cells responding to demyelination in the adult CNS. Molecular and cellular neurosciences 245 15519240
2004 Regionalization and fate specification in neurospheres: the role of Olig2 and Pax6. Molecular and cellular neurosciences 226 15080895
2005 Olig2 directs astrocyte and oligodendrocyte formation in postnatal subventricular zone cells. The Journal of neuroscience : the official journal of the Society for Neuroscience 210 16093378
2010 Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome. Nature neuroscience 180 20639873
2002 Dual origin of spinal oligodendrocyte progenitors and evidence for the cooperative role of Olig2 and Nkx2.2 in the control of oligodendrocyte differentiation. Development (Cambridge, England) 177 11830569
2007 A crucial role for Olig2 in white matter astrocyte development. Development (Cambridge, England) 168 17428828
2006 Induction of oligodendrocyte differentiation by Olig2 and Sox10: evidence for reciprocal interactions and dosage-dependent mechanisms. Developmental biology 160 17098222
2019 OLIG2 Drives Abnormal Neurodevelopmental Phenotypes in Human iPSC-Based Organoid and Chimeric Mouse Models of Down Syndrome. Cell stem cell 152 31130512
2006 Olig2-positive progenitors in the embryonic spinal cord give rise not only to motoneurons and oligodendrocytes, but also to a subset of astrocytes and ependymal cells. Developmental biology 149 16581057
2015 Gain of Olig2 function in oligodendrocyte progenitors promotes remyelination. Brain : a journal of neurology 133 25564492
2004 Anti-human Olig2 antibody as a useful immunohistochemical marker of normal oligodendrocytes and gliomas. The American journal of pathology 123 15111318
2009 NG2+/Olig2+ cells are the major cycle-related cell population of the adult human normal brain. Brain pathology (Zurich, Switzerland) 119 19486010
2012 Olig2-dependent developmental fate switch of NG2 cells. Development (Cambridge, England) 110 22627280
2011 Phosphorylation regulates OLIG2 cofactor choice and the motor neuron-oligodendrocyte fate switch. Neuron 109 21382552
2011 Phosphorylation state of Olig2 regulates proliferation of neural progenitors. Neuron 103 21382551
2016 Olig2-Dependent Reciprocal Shift in PDGF and EGF Receptor Signaling Regulates Tumor Phenotype and Mitotic Growth in Malignant Glioma. Cancer cell 101 27165742
2013 Stage-specific deletion of Olig2 conveys opposing functions on differentiation and maturation of oligodendrocytes. The Journal of neuroscience : the official journal of the Society for Neuroscience 96 23658182
2004 Negative regulatory effect of an oligodendrocytic bHLH factor OLIG2 on the astrocytic differentiation pathway. Cell death and differentiation 86 14576772
2007 An olig2 reporter gene marks oligodendrocyte precursors in the postembryonic spinal cord of zebrafish. Developmental dynamics : an official publication of the American Association of Anatomists 84 17969181
1992 Oligo(2'-O-methyl)ribonucleotides. Effective probes for duplex DNA. FEBS letters 83 1633847
2018 Olig2-Lineage Astrocytes: A Distinct Subtype of Astrocytes That Differs from GFAP Astrocytes. Frontiers in neuroanatomy 82 29497365
2003 Expression of FGF receptors 1, 2, 3 in the embryonic and postnatal mouse brain compared with Pdgfralpha, Olig2 and Plp/dm20: implications for oligodendrocyte development. Developmental neuroscience 81 12966207
2016 Olig2-Targeted G-Protein-Coupled Receptor Gpr17 Regulates Oligodendrocyte Survival in Response to Lysolecithin-Induced Demyelination. The Journal of neuroscience : the official journal of the Society for Neuroscience 79 27733608
2012 TricycloDNA-modified oligo-2'-deoxyribonucleotides reduce scavenger receptor B1 mRNA in hepatic and extra-hepatic tissues--a comparative study of oligonucleotide length, design and chemistry. Nucleic acids research 78 22467214
2021 Using the lineage determinants Olig2 and Sox10 to explore transcriptional regulation of oligodendrocyte development. Developmental neurobiology 73 34480425
2007 Evidence that nucleocytoplasmic Olig2 translocation mediates brain-injury-induced differentiation of glial precursors to astrocytes. Journal of neuroscience research 72 17510983
2003 Expression of the oligodendroglial lineage-associated markers Olig1 and Olig2 in different types of human gliomas. Journal of neuropathology and experimental neurology 72 14575240
2007 Cannabinoids modulate Olig2 and polysialylated neural cell adhesion molecule expression in the subventricular zone of post-natal rats through cannabinoid receptor 1 and cannabinoid receptor 2. The European journal of neuroscience 71 17880390
2006 Involvement of the Olig2 transcription factor in cholinergic neuron development of the basal forebrain. Developmental biology 71 16537079
2022 The Oligodendrocyte Transcription Factor 2 OLIG2 regulates transcriptional repression during myelinogenesis in rodents. Nature communications 68 35301318
2009 Olig2+ precursors produce abducens motor neurons and oligodendrocytes in the zebrafish hindbrain. The Journal of neuroscience : the official journal of the Society for Neuroscience 64 19244509
2018 Olig2 and Hes regulatory dynamics during motor neuron differentiation revealed by single cell transcriptomics. PLoS biology 63 29389974
2000 The t(14;21)(q11.2;q22) chromosomal translocation associated with T-cell acute lymphoblastic leukemia activates the BHLHB1 gene. Proceedings of the National Academy of Sciences of the United States of America 63 10737801
2010 OLIG2 is differentially expressed in pediatric astrocytic and in ependymal neoplasms. Journal of neuro-oncology 57 21193945
2005 Olig2 expression, GFAP, p53 and 1p loss analysis contribute to glioma subclassification. Neuropathology and applied neurobiology 57 15634232
2002 Non-overlapping expression of Olig3 and Olig2 in the embryonic neural tube. Mechanisms of development 56 11960707
2003 Cross-repressive interaction of the Olig2 and Nkx2.2 transcription factors in developing neural tube associated with formation of a specific physical complex. The Journal of neuroscience : the official journal of the Society for Neuroscience 55 14573534
2016 Post-translational Modifications of OLIG2 Regulate Glioma Invasion through the TGF-β Pathway. Cell reports 54 27396340
2012 OLIG2 over-expression impairs proliferation of human Down syndrome neural progenitors. Human molecular genetics 54 22343408
2014 Characterization of the neural stem cell gene regulatory network identifies OLIG2 as a multifunctional regulator of self-renewal. Genome research 51 25294244
2008 Induction of Olig2 precursors by FGF involves BMP signalling blockade at the Smad level. PloS one 51 18682850
2021 Region-specific distribution of Olig2-expressing astrocytes in adult mouse brain and spinal cord. Molecular brain 50 33618751
2020 Transcription factor Tcf4 is the preferred heterodimerization partner for Olig2 in oligodendrocytes and required for differentiation. Nucleic acids research 50 32266943
2010 FGF-receptor signalling controls neural cell diversity in the zebrafish hindbrain by regulating olig2 and sox9. Development (Cambridge, England) 50 20023158
1996 Oligo-2'-fluoro-2'-deoxynucleotide N3'-->P5' phosphoramidates: synthesis and properties. Nucleic acids research 49 8760881
2016 Lineage-Restricted OLIG2-RTK Signaling Governs the Molecular Subtype of Glioma Stem-like Cells. Cell reports 47 27626655
2012 Diagnostic implications of IDH1-R132H and OLIG2 expression patterns in rare and challenging glioblastoma variants. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 45 23041832
2006 NG2 and Olig2 expression provides evidence for phenotypic deregulation of cultured central nervous system and peripheral nervous system neural precursor cells. Stem cells (Dayton, Ohio) 43 17053213
2009 Quantitative analysis of mitotic Olig2 cells in adult human brain and gliomas: implications for glioma histogenesis and biology. Glia 41 18837053
2016 Distinct cortical and sub-cortical neurogenic domains for GABAergic interneuron precursor transcription factors NKX2.1, OLIG2 and COUP-TFII in early fetal human telencephalon. Brain structure & function 40 27905023
2006 Induced expression of Olig2 is sufficient for oligodendrocyte specification but not for motoneuron specification and astrocyte repression. Molecular and cellular neurosciences 40 17035043
2017 Harnessing OLIG2 function in tumorigenicity and plasticity to target malignant gliomas. Cell cycle (Georgetown, Tex.) 39 28806136
2012 Effects of Olig2-overexpressing neural stem cells and myelin basic protein-activated T cells on recovery from spinal cord injury. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics 39 22173726
2016 Brg1 directly regulates Olig2 transcription and is required for oligodendrocyte progenitor cell specification. Developmental biology 36 27067865
2008 Olig2-induced neural stem cell differentiation involves downregulation of Wnt signaling and induction of Dickkopf-1 expression. PloS one 35 19093005
2010 Expression of the transcription factor Olig2 in proliferating cells in the adult zebrafish telencephalon. Developmental dynamics : an official publication of the American Association of Anatomists 34 20981834
2006 Expression of the basic helix-loop-factor Olig2 in the developing retina: Olig2 as a new marker for retinal progenitors and late-born cells. Gene expression patterns : GEP 34 16815098
2021 One-step Reprogramming of Human Fibroblasts into Oligodendrocyte-like Cells by SOX10, OLIG2, and NKX6.2. Stem cell reports 33 33770499
2022 Shh and Olig2 sequentially regulate oligodendrocyte differentiation from hiPSCs for the treatment of ischemic stroke. Theranostics 32 35547747
2017 The transcription factor Olig2 is important for the biology of diffuse intrinsic pontine gliomas. Neuro-oncology 32 28339768
2009 Neural protein Olig2 acts upstream of the transcriptional regulator Sim1 to specify diencephalic dopaminergic neurons. Developmental dynamics : an official publication of the American Association of Anatomists 31 19253397
2020 Olig2 SUMOylation protects against genotoxic damage response by antagonizing p53 gene targeting. Cell death and differentiation 30 32483381
2018 Age-Dependent Decline in Fate Switch from NG2 Cells to Astrocytes After Olig2 Deletion. The Journal of neuroscience : the official journal of the Society for Neuroscience 30 29382710
2017 A Sequentially Priming Phosphorylation Cascade Activates the Gliomagenic Transcription Factor Olig2. Cell reports 30 28355568
2015 Human Dental Pulp Stem Cells Differentiate into Oligodendrocyte Progenitors Using the Expression of Olig2 Transcription Factor. Cells, tissues, organs 29 25966902
2007 Differential regulation of basic helix-loop-helix factors Mash1 and Olig2 by beta-amyloid accelerates both differentiation and death of cultured neural stem/progenitor cells. The Journal of biological chemistry 29 17488716
2024 Transcription factors ASCL1 and OLIG2 drive glioblastoma initiation and co-regulate tumor cell types and migration. Nature communications 27 39609428
2016 Molecular mechanisms of OLIG2 transcription factor in brain cancer. Oncotarget 27 27447975
2005 OLIG2 (BHLHB1), a bHLH transcription factor, contributes to leukemogenesis in concert with LMO1. Cancer research 27 16103065
2016 Olig2 regulates Purkinje cell generation in the early developing mouse cerebellum. Scientific reports 26 27469598
2009 Olig2 transcription factor in the developing and injured forebrain; cell lineage and glial development. Molecules and cells 26 19390819
2014 Pten loss in Olig2 expressing neural progenitor cells and oligodendrocytes leads to interneuron dysplasia and leukodystrophy. Stem cells (Dayton, Ohio) 25 24395742
2014 Differentiation of neurosphere-derived rat neural stem cells into oligodendrocyte-like cells by repressing PDGF-α and Olig2 with triiodothyronine. Tissue & cell 25 25200619
2012 Modification of pax6 and olig2 expression in adult hippocampal neurogenesis selectively induces stem cell fate and alters both neuronal and glial populations. Stem cells (Dayton, Ohio) 25 22162276
2019 OLIG2 is a marker of the fusion protein-driven neurodevelopmental transcriptional signature in alveolar rhabdomyosarcoma. Human pathology 24 31299267
2014 Prox1 regulates Olig2 expression to modulate binary fate decisions in spinal cord neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 24 25411508
2013 Olig2/Plp-positive progenitor cells give rise to Bergmann glia in the cerebellum. Cell death & disease 24 23492777
2012 Antagonistic modulation of gliomagenesis by Pax6 and Olig2 in PDGF-induced oligodendroglioma. International journal of cancer 24 22514120
2011 Differential and cooperative actions of Olig1 and Olig2 transcription factors on immature proliferating cells after contusive spinal cord injury. Glia 24 21538562
2008 Olig2 and CD99 are useful negative markers for the diagnosis of brain tumors. Clinical neuropathology 24 18552083
2022 Olig2 Ablation in Immature Oligodendrocytes Does Not Enhance CNS Myelination and Remyelination. The Journal of neuroscience : the official journal of the Society for Neuroscience 23 36198499
2014 An amino terminal phosphorylation motif regulates intranuclear compartmentalization of Olig2 in neural progenitor cells. The Journal of neuroscience : the official journal of the Society for Neuroscience 23 24948806
2004 Analysis of the bHLH transcription factors Olig1 and Olig2 in brain tumors. Journal of neuro-oncology 23 15164981
2022 Ddx20, an Olig2 binding factor, governs the survival of neural and oligodendrocyte progenitor cells via proper Mdm2 splicing and p53 suppression. Cell death and differentiation 22 34974536
2011 All the embryo's a stage, and Olig2 in its time plays many parts. Neuron 22 21382543
2006 A novel function of OLIG2 to suppress human glial tumor cell growth via p27Kip1 transactivation. Journal of cell science 22 16554441
2016 Accelerated generation of oligodendrocyte progenitor cells from human induced pluripotent stem cells by forced expression of Sox10 and Olig2. Science China. Life sciences 21 27785726
2015 Disruption of neurogenesis and cortical development in transgenic mice misexpressing Olig2, a gene in the Down syndrome critical region. Neurobiology of disease 21 25747816
2022 Sonic Hedgehog Pathway Modulation Normalizes Expression of Olig2 in Rostrally Patterned NPCs With Trisomy 21. Frontiers in cellular neuroscience 20 35058753
2020 Olig2-Induced Semaphorin Expression Drives Corticospinal Axon Retraction After Spinal Cord Injury. Cerebral cortex (New York, N.Y. : 1991) 20 32564090
2017 Local injection of Lenti-Olig2 at lesion site promotes functional recovery of spinal cord injury in rats. CNS neuroscience & therapeutics 20 28452182
2015 Tetracycline-regulated expression of OLIG2 gene in human dental pulp stem cells lead to mouse sciatic nerve regeneration upon transplantation. Neuroscience 20 26254831
2014 Characterization of Olig2 expression during cerebellar development. Gene expression patterns : GEP 20 24594479

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