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Oligodendrocyte transcription factor 2

This gene encodes a basic helix-loop-helix transcription factor which is expressed in oligodendroglial tumors of the brain. The protein is an essential regulator of ventral neuroectodermal progenitor cell fate. The gene is involved in a chromosomal translocation t(14;21)(q11.2;q22) associated with T-cell acute lymphoblastic leukemia. Its chromosomal location is within a region of chromosome 21 which has been suggested to play a role in learning deficits associated with Down syndrome. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, Olig1, Glial Fibrillary Acidic Protein, FATE, Phosphoglucomutase
Papers using Olig2 antibodies
2′, 3′-cyclic nucleotide 3′-phosphodiesterase, an oligodendrocyte-Schwann cell and myelin-associated enzyme of the nervous system.
Reh Thomas A., In PLoS ONE, 1988
... Briefly, Olig2 cDNA was ligated into multiple cloning sites of the retroviral vector pLHCX (Clontech, Mountain View, CA) ...
Papers on Olig2
NeuN(+) neuronal nuclei in non-human primate prefrontal cortex and subcortical white matter after clozapine exposure.
Akbarian et al., New York City, United States. In Schizophr Res, Feb 2016
Numbers and proportions of nuclei expressing the oligodendrocyte lineage marker, OLIG2, and cell-type specific RNA expression patterns, were maintained after antipsychotic drug exposure.
Trimethyltin chloride inhibits neuronal cell differentiation in zebrafish embryo neurodevelopment.
Park et al., Seoul, South Korea. In Neurotoxicol Teratol, Jan 2016
In this study, we confirmed the dose-dependent effects of TMT on neurodevelopmental stages through analysis of morphological changes and fluorescence assays using HuC-GFP and olig2-dsRed transgenic zebrafish embryos.
Motor neurons and oligodendrocytes arise from distinct cell lineages by progenitor recruitment.
Appel et al., Aurora, United States. In Genes Dev, Jan 2016
During spinal cord development, ventral neural progenitor cells that express the transcription factors Olig1 and Olig2, called pMN progenitors, produce motor neurons and then oligodendrocytes.
Differentiation of oligodendrocyte precursors is impaired in the prefrontal cortex in schizophrenia.
Woo et al., Belmont, United States. In Schizophr Res, Dec 2015
To address this hypothesis, we quantified cells that were immunoreactive for neural/glial antigen 2 (NG2), a selective marker for OPCs, and those that were immunoreactive for oligodendrocyte transcription factor 2 (OLIG2), an oligodendrocyte lineage marker that is expressed by OPCs and maturing oligodendrocytes.
Comprehensive Identification of Long Non-coding RNAs in Purified Cell Types from the Brain Reveals Functional LncRNA in OPC Fate Determination.
Wu et al., Stanford, United States. In Plos Genet, Dec 2015
OLIG2-binding sites in the upstream regulatory region of lnc-OPC were identified by ChIP (chromatin immunoprecipitation)-Sequencing and validated by luciferase assays.
Irradiation of primary human gliomas triggers dynamic and aggressive survival responses involving microvesicle signaling.
Limoli et al., Irvine, United States. In Environ Mol Mutagen, Dec 2015
Radiation-induced changes were exacerbated under chronic as compared to acute irradiation paradigms and promoted cellular reprogramming through enhanced expression of key transcription factors and regulators involved in differentiation and pluripotency (SOX2, POU3F2, SALL2, OLIG2, NANOG, POU5F1v1, MSI1).
Primary diffuse leptomeningeal glioneuronal tumors.
Park et al., Seoul, South Korea. In Brain Tumor Pathol, 2015
All three cases were diffusely positive for both GFAP and synaptophysin, and scattered positive for OLIG2 and NeuN, but negative for IDH-1 (H09).
Signaling molecules regulating phenotypic conversions of astrocytes and glial scar formation in damaged nerve tissues.
Koyama, Ōsaka, Japan. In Neurochem Int, 2014
The transcription factors: STAT3, OLIG2, SMAD, NF-κB, and Sp1 have been suggested to play regulatory roles in astrocytic activation and glial scar formation.
Reconstructing and reprogramming the tumor-propagating potential of glioblastoma stem-like cells.
Bernstein et al., United States. In Cell, 2014
Here, we identify a core set of neurodevelopmental TFs (POU3F2, SOX2, SALL2, and OLIG2) essential for GBM propagation.
Human iPSC-derived oligodendrocyte progenitor cells can myelinate and rescue a mouse model of congenital hypomyelination.
Goldman et al., Rochester, United States. In Cell Stem Cell, 2013
From three hiPSC lines, as well as from human embryonic stem cells (hESCs), we generated highly enriched OLIG2(+)/PDGFRα(+)/NKX2.2(+)/SOX10(+) human OPCs, which could be further purified using fluorescence-activated cell sorting.
Separated at birth? The functional and molecular divergence of OLIG1 and OLIG2.
Rowitch et al., Boston, United States. In Nat Rev Neurosci, 2012
The basic helix-loop-helix transcription factors oligodendrocyte transcription factor 1 (OLIG1) and OLIG2 are structurally similar and, to a first approximation, coordinately expressed in the developing CNS and postnatal brain.
Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma.
Pfister et al., Heidelberg, Germany. In Cancer Cell, 2012
We also demonstrate that the two H3F3A mutations give rise to GBMs in separate anatomic compartments, with differential regulation of transcription factors OLIG1, OLIG2, and FOXG1, possibly reflecting different cellular origins.
Antagonistic modulation of gliomagenesis by Pax6 and Olig2 in PDGF-induced oligodendroglioma.
Malatesta et al., Genova, Italy. In Int J Cancer, 2012
Olig2 is strictly required to maintain the malignancy of oligodendroglioma cells.
[A flow cytometric postmortem brain study for major depressive disorders: implication for oligodendroglial differentiation and functions].
Tatebayashi et al., Tokyo, Japan. In Nihon Shinkei Seishin Yakurigaku Zasshi, 2012
Anisotropic frozen brain tissue was transformed into an isotropic suspension of nuclei; the numbers and fluorescent intensities of 7-AAD(+), a DNA marker, were quantified; and the nuclei were immunolabeled for the neuronal and oligodendroglial nuclear markers, NeuN and olig2, respectively.
Markers of survival and metastatic potential in childhood CNS primitive neuro-ectodermal brain tumours: an integrative genomic analysis.
Huang et al., Toronto, Canada. In Lancet Oncol, 2012
FINDINGS: We identified three molecular subgroups of CNS PNETs that were distinguished by primitive neural (group 1), oligoneural (group 2), and mesenchymal lineage (group 3) gene-expression signatures with differential expression of cell-lineage markers LIN28 and OLIG2.
Olig2-dependent developmental fate switch of NG2 cells.
Nishiyama et al., United States. In Development, 2012
The findings indicated that NG2+ polydendrocytes in the embryonic and early postnatal brain exhibit developmental fate switch from oligodendrocytes to astrocytes in vivo upon removal of Olig2.
OLIG2 over-expression impairs proliferation of human Down syndrome neural progenitors.
Sheen et al., Boston, United States. In Hum Mol Genet, 2012
OLIG2 over-expression inhibits neural progenitor proliferation through changes in potassium channel activity, thereby contributing to the reduced neuronal numbers and brain size in DS.
Modification of pax6 and olig2 expression in adult hippocampal neurogenesis selectively induces stem cell fate and alters both neuronal and glial populations.
Peterson et al., North Chicago, United States. In Stem Cells, 2012
Pax6 decreases the number of Neuron-Glia 2 progenitor cells and prevents oligodendrocytic lineage commitment, while repression of Olig2 results in an expanded astrocytic lineage.
olig2-Expressing hindbrain cells are required for migrating facial motor neurons.
Appel et al., Aurora, United States. In Dev Dyn, 2012
these data raise the possibility that cells expressing olig2 are intermediate targets that help guide facial motor neuron migration.
The evolution of Olig genes and their roles in myelination.
Richardson et al., London, United Kingdom. In Neuron Glia Biol, 2008
The transcription factors OLIG1 and OLIG2, master regulators of OL development, presumably also played a seminal role during the evolution of the genetic programme leading to myelination in the CNS.
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