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Oligodendrocyte transcription factor 2

Olig2
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, FATE, Glial Fibrillary Acidic Protein, ACID
Papers using Olig2 antibodies
2′, 3′-cyclic nucleotide 3′-phosphodiesterase, an oligodendrocyte-Schwann cell and myelin-associated enzyme of the nervous system.
Supplier
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
Prox1 regulates olig2 expression to modulate binary fate decisions in spinal cord neurons.
New
Politis et al., Frankfurt am Main, Germany. In J Neurosci, 19 Dec 2014
Olig2 is a key transcription factor in these networks by inducing motor neuron (MN) specification and inhibiting interneuron identity.
Identification of OLIG2 as the most specific glioblastoma stem cell marker starting from comparative analysis of data from similar DNA chip microarray platforms.
New
Salmon et al., Brussels, Belgium. In Tumour Biol, 12 Dec 2014
Finally, among the eight genes, oligodendrocyte lineage transcription factor 2 (OLIG2) was characterised by the most different expression level in the "GSC model" compared to the "differentiated tumour cells model".
Characterization of the neural stem cell gene regulatory network identifies OLIG2 as a multi-functional regulator of self-renewal.
New
Martynoga et al., Singapore, Singapore. In Genome Res, 07 Nov 2014
We validate our predictions by functional analysis of the bHLH TF OLIG2.
Signaling molecules regulating phenotypic conversions of astrocytes and glial scar formation in damaged nerve tissues.
Review
New
Koyama, Ōsaka, Japan. In Neurochem Int, Sep 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.
Efficient generation of myelinating oligodendrocytes from primary progressive multiple sclerosis patients by induced pluripotent stem cells.
New
Fossati et al., New York City, United States. In Stem Cell Reports, Sep 2014
Key elements of our protocol include adherent cultures, dual SMAD inhibition, and addition of retinoids from the beginning of differentiation, which lead to increased yields of OLIG2 progenitors and high numbers of OPCs within 75 days.
Reconstructing and reprogramming the tumor-propagating potential of glioblastoma stem-like cells.
New
Impact
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.
Prominin-1 (CD133) defines both stem and non-stem cell populations in CNS development and gliomas.
New
Ligon et al., Boston, United States. In Plos One, Dec 2013
In adult human brain, PROM1 cells are rarely positive for OLIG2, but express astroglial markers GFAP and SOX2.
Identification of molecular pathways facilitating glioma cell invasion in situ.
New
Fine et al., Bethesda, United States. In Plos One, Dec 2013
OLIG2, a proliferation regulator and glioma progenitor cell marker upregulated in IGCs was found to function in enhancing migration and stemness of GSCs.
Human iPSC-derived oligodendrocyte progenitor cells can myelinate and rescue a mouse model of congenital hypomyelination.
New
Impact
Goldman et al., Rochester, United States. In Cell Stem Cell, Mar 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.
Review
Impact
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.
Impact
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.
GeneRIF
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].
Review
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.
Impact
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
Review
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.
Review
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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