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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
Tetracycline-regulated expression of OLIG2 gene in human dental pulp stem cells lead to mouse sciatic nerve regeneration upon transplantation.
Esmaeili-Mahani et al., Tehrān, Iran. In Neuroscience, 01 Nov 2015
Oligodendrocyte lineage transcription factor 2 (OLIG2) plays an important role in the oligodendrogenic pathway.
Yu et al., Qingdao, China. In Depress Anxiety, 31 Oct 2015
BACKGROUND: Oligodendrocyte transcription factor 2 (OLIG2) is primarily concentrated in the brain and spinal cord ventricular zone, where this protein stimulates oligodendrocytes and specific neurons, determines motor neuron and oligodendrocyte differentiation, and sustains replication in early development.
Alterations in hippocampal myelin and oligodendrocyte precursor cells during epileptogenesis.
Jiang et al., Chongqing, China. In Brain Res, 30 Oct 2015
The transcription factors olig1 and olig2, which play crucial roles in regulating OPC proliferation, differentiation and remyelination, were up-regulated during the early phases (the acute and latent phases) followed by a sharp decline in their expression during the chronic and late chronic phases.
Neuronal labeling patterns in the spinal cord of adult transgenic Zebrafish.
Drapeau et al., Montréal, Canada. In Dev Neurobiol, 26 Oct 2015
We used well-known transgenic lines in which expression of green fluorescent protein (GFP) is driven by promoters to hb9 and isl1 in motoneurons, alx/chx10 and evx1 interneurons, ngn1 in sensory neurons and olig2 in oligodendrocytes, as well as antibodies for neurons (HuC/D, NF and SV2) and glia (GFAP).
Sonic hedgehog functions upstream of disrupted-in-schizophrenia 1 (disc1): implications for mental illness.
Wood et al., Sheffield, United Kingdom. In Biol Open, 24 Oct 2015
We show that disc1 is prominently expressed in olig2-positive midline progenitor cells that are absent in smo mutants, while cyclopamine treatment blocks disc1 expression in these cells and mimics the effect of disc1 knock down on OPC specification.
Influence of oriented nanofibrous PCL scaffolds on quantitative gene expression during neural differentiation of mouse embryonic stem cells.
Hosseinkhani et al., Tehrān, Iran. In J Biomed Mater Res A, 10 Sep 2015
Analysis also showed higher expression of dorso-ventral neural markers (Isl1/2 and Lim1/2) than motor neuron progenitor markers (Pax6, Nkx6.1 and olig2) in aligned nanofibers than in the T group.
Primary diffuse leptomeningeal glioneuronal tumors.
Park et al., Seoul, South Korea. In Brain Tumor Pathol, Jan 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).
Reconstructing and reprogramming the tumor-propagating potential of glioblastoma stem-like cells.
Bernstein et al., United States. In Cell, May 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.
Behavior of neural stem cells in the Alzheimer brain.
Shetty et al., Durham, United States. In Cell Mol Life Sci, 2008
Furthermore, fibrillary Abeta and down-regulation of oligodendrocyte-lineage transcription factor-2 (OLIG2) may cause the death of these nonfunctional neurons.
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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