OLIG2: Difference between revisions

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{{Infobox_gene}}
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'''Oligodendrocyte transcription factor (OLIG2)''' is a basic helix-loop-helix ([[bHLH]]) transcription factor encoded by the ''Olig2'' gene. The protein is of 329 amino acids in length, 32kDa in size and contains 1 basic helix-loop-helix DNA-binding domain.<ref>{{cite web|url=http://atlasgeneticsoncology.org/Genes/OLIG2ID236.html | title = OLIG2 | work = Atlas of Genetics and Cytogenetics in Oncology and Hematology }}</ref> It is one of the three members of the bHLH family. The other two members are [[OLIG1]] and OLIG3. The expression of OLIG2 is mostly restricted in [[central nervous system]], where it acts as both an anti-neurigenic and a neurigenic factor at different stages of development. OLIG2 is well known for determining [[motor neuron]] and [[oligodendrocyte]] differentiation, as well as its role in sustaining replication in early development. It is mainly involved in diseases such as brain tumor and [[Down syndrome]].
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== Function ==
{{GNF_Protein_box
OLIG2 is mostly expressed in restricted domains of the brain and [[spinal cord]] ventricular zone which give rise to oligodendrocytes and specific types of neurons. In the spinal cord, the pMN region sequentially generates motor neurons and oligodendrocytes. During embryogenesis, OLIG2 first directs motor neuron fate by establishing a ventral domain of motor neuron progenitors and promoting neuronal differentiation. OLIG2 then switches to promoting the formation of oligodendrocyte precursors and oligodendrocyte differentiation at later stages of development. Apart from functioning as a neurogenic factor in specification and the differentiation of motor neurons and oligodendrocytes, OLIG2 also functions as an anti-neurogenic factor at early time points in pMN progenitors to sustain the cycling progenitor pool. This side of anti-neurogenicity of OLIG2 later plays a bigger role in malignancies like [[glioma]].<ref>{{cite journal | vauthors = Gaber ZB, Novitch BG | title = All the embryo's a stage, and Olig2 in its time plays many parts | journal = Neuron | volume = 69 | issue = 5 | pages = 833–5 | date = Mar 2011 | pmid = 21382543 | pmc =  | doi = 10.1016/j.neuron.2011.02.037 }}</ref>
| image = 
| image_source =
| PDB =  
| Name = Oligodendrocyte lineage transcription factor 2
| HGNCid = 9398
| Symbol = OLIG2
| AltSymbols =; BHLHB1; OLIGO2; PRKCBP2; RACK17
| OMIM = 606386
| ECnumber = 
| Homologene = 4241
| MGIid = 1355331
| GeneAtlas_image1 = PBB_GE_OLIG2_213824_at_tn.png
| GeneAtlas_image2 = PBB_GE_OLIG2_213825_at_tn.png
| Function = {{GNF_GO|id=GO:0003677 |text = DNA binding}} {{GNF_GO|id=GO:0003705 |text = RNA polymerase II transcription factor activity, enhancer binding}} {{GNF_GO|id=GO:0005515 |text = protein binding}} {{GNF_GO|id=GO:0030528 |text = transcription regulator activity}} {{GNF_GO|id=GO:0042803 |text = protein homodimerization activity}}
| Component = {{GNF_GO|id=GO:0005634 |text = nucleus}} {{GNF_GO|id=GO:0005737 |text = cytoplasm}}
| Process = {{GNF_GO|id=GO:0000122 |text = negative regulation of transcription from RNA polymerase II promoter}} {{GNF_GO|id=GO:0006355 |text = regulation of transcription, DNA-dependent}} {{GNF_GO|id=GO:0007275 |text = multicellular organismal development}} {{GNF_GO|id=GO:0007399 |text = nervous system development}} {{GNF_GO|id=GO:0042552 |text = myelination}} {{GNF_GO|id=GO:0048663 |text = neuron fate commitment}} {{GNF_GO|id=GO:0048709 |text = oligodendrocyte differentiation}}
| Orthologs = {{GNF_Ortholog_box
    | Hs_EntrezGene = 10215
    | Hs_Ensembl = ENSG00000205927
    | Hs_RefseqProtein = NP_005797
    | Hs_RefseqmRNA = NM_005806
    | Hs_GenLoc_db = 
    | Hs_GenLoc_chr = 21
    | Hs_GenLoc_start = 33320023
    | Hs_GenLoc_end = 33323374
    | Hs_Uniprot = Q13516
    | Mm_EntrezGene = 50913
    | Mm_Ensembl = ENSMUSG00000039830
    | Mm_RefseqmRNA = NM_016967
    | Mm_RefseqProtein = NP_058663
    | Mm_GenLoc_db =   
    | Mm_GenLoc_chr = 16
    | Mm_GenLoc_start = 91114409
    | Mm_GenLoc_end = 91117536
    | Mm_Uniprot = Q542S0
  }}
}}
'''Oligodendrocyte lineage transcription factor 2''', also known as '''OLIG2''', is a human [[gene]].<ref name="entrez">{{cite web | title = Entrez Gene: OLIG2 oligodendrocyte lineage transcription factor 2| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=10215| accessdate = }}</ref>


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The role of [[phosphorylation]] has been highlighted recently to account for the multifaceted functions of OLIG2 in differentiation and proliferation. Studies showed that the phosphorylation state of OLIG2 at Ser30 determines the fate of cortical progenitor cells, in which cortical progenitor cells will either differentiate into astrocytes or remain as neuronal progenitors.<ref>{{cite journal | vauthors = Setoguchi T, Kondo T | title = Nuclear export of OLIG2 in neural stem cells is essential for ciliary neurotrophic factor-induced astrocyte differentiation | journal = The Journal of Cell Biology | volume = 166 | issue = 7 | pages = 963–8 | date = Sep 2004 | pmid = 15452140 | pmc = 2172021 | doi = 10.1083/jcb.200404104 }}</ref> Phosphorylation at a triple serine motif (Ser10, Ser13 and Ser14) on the other hand was shown to regulate the proliferative function of OLIG2.<ref>{{cite journal | vauthors = Sun Y, Meijer DH, Alberta JA, Mehta S, Kane MF, Tien AC, Fu H, Petryniak MA, Potter GB, Liu Z, Powers JF, Runquist IS, Rowitch DH, Stiles CD | title = Phosphorylation state of Olig2 regulates proliferation of neural progenitors | journal = Neuron | volume = 69 | issue = 5 | pages = 906–17 | date = Mar 2011 | pmid = 21382551 | pmc = 3065213 | doi = 10.1016/j.neuron.2011.02.005 }}</ref> Another phosphorylation site Ser147 predicted by bioinformatics was found to regulate motor neuron development by regulating the binding between OLIG2 and NGN2.<ref>{{cite journal | vauthors = Li H, de Faria JP, Andrew P, Nitarska J, Richardson WD | title = Phosphorylation regulates OLIG2 cofactor choice and the motor neuron-oligodendrocyte fate switch | journal = Neuron | volume = 69 | issue = 5 | pages = 918–29 | date = Mar 2011 | pmid = 21382552 | pmc = 3093612 | doi = 10.1016/j.neuron.2011.01.030 }}</ref> Further, OLIG2 contains a ST box composed of a string of 12 contiguous serine and threonine residues at position Ser77-Ser88. It is believed that phosphorylation at ST box is biologically functional,<ref>{{cite journal | vauthors = Huillard E, Ziercher L, Blond O, Wong M, Deloulme JC, Souchelnytskyi S, Baudier J, Cochet C, Buchou T | title = Disruption of CK2beta in embryonic neural stem cells compromises proliferation and oligodendrogenesis in the mouse telencephalon | journal = Molecular and Cellular Biology | volume = 30 | issue = 11 | pages = 2737–49 | date = Jun 2010 | pmid = 20368359 | pmc = 2876519 | doi = 10.1128/MCB.01566-09 }}</ref> yet the role of it still remains to be elucidated in vivo.<ref>{{cite journal | vauthors = Sun Y, Meijer DH, Alberta JA, Mehta S, Kane MF, Tien AC, Fu H, Petryniak MA, Potter GB, Liu Z, Powers JF, Runquist IS, Rowitch DH, Stiles CD | title = Phosphorylation state of Olig2 regulates proliferation of neural progenitors | journal = Neuron | volume = 69 | issue = 5 | pages = 906–17 | date = Mar 2011 | pmid = 21382551 | pmc = 3065213 | doi = 10.1016/j.neuron.2011.02.005 }}</ref>
{{PBB_Summary
| section_title =  
| summary_text = 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.<ref name="entrez">{{cite web | title = Entrez Gene: OLIG2 oligodendrocyte lineage transcription factor 2| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=10215| accessdate = }}</ref>
}}


==References==
OLIG2 has also been implicated in bovine horn ontogenesis. It was the only gene in the bovine ''polled'' locus to show differential expression between the putative horn bud and the frontal forehead skin.<ref>{{cite journal | vauthors = Allais-Bonnet A, Grohs C, Medugorac I, Krebs S, Djari A, Graf A, Fritz S, Seichter D, Baur A, Russ I, Bouet S, Rothammer S, Wahlberg P, Esquerré D, Hoze C, Boussaha M, Weiss B, Thépot D, Fouilloux MN, Rossignol MN, van Marle-Köster E, Hreiðarsdóttir GE, Barbey S, Dozias D, Cobo E, Reversé P, Catros O, Marchand JL, Soulas P, Roy P, Marquant-Leguienne B, Le Bourhis D, Clément L, Salas-Cortes L, Venot E, Pannetier M, Phocas F, Klopp C, Rocha D, Fouchet M, Journaux L, Bernard-Capel C, Ponsart C, Eggen A, Blum H, Gallard Y, Boichard D, Pailhoux E, Capitan A | title = Novel insights into the bovine polled phenotype and horn ontogenesis in Bovidae | journal = PLOS ONE | volume = 8 | issue = 5 | pages = e63512 | year = 2013 | pmid = 23717440 | pmc = 3661542 | doi = 10.1371/journal.pone.0063512 }}</ref>
{{reflist|2}}
 
==Further reading==
== Clinical Significance ==
{{refbegin | 2}}
 
{{PBB_Further_reading
=== OLIG2 in Cancer ===
| citations =
OLIG2 is well recognized for its importance in cancer research, particularly in brain tumors and [[leukemia]]. OLIG2 is universally expressed in glioblastoma and other diffuse gliomas ([[astrocytomas]], [[oligodendrogliomas]] and [[oligoastrocytomas]]), and is a useful positive diagnostic marker of these brain tumors.<ref>{{cite journal | vauthors = Ligon KL, Alberta JA, Kho AT, Weiss J, Kwaan MR, Nutt CL, Louis DN, Stiles CD, Rowitch DH | title = The oligodendroglial lineage marker OLIG2 is universally expressed in diffuse gliomas | journal = Journal of Neuropathology and Experimental Neurology | volume = 63 | issue = 5 | pages = 499–509 | date = May 2004 | pmid = 15198128 | doi=10.1093/jnen/63.5.499}}</ref> In particular, OLIG2 is selectively expressed in a subgroup of glioma cells that are highly tumorigenic,<ref>{{cite journal | vauthors = Ligon KL, Huillard E, Mehta S, Kesari S, Liu H, Alberta JA, Bachoo RM, Kane M, Louis DN, Depinho RA, Anderson DJ, Stiles CD, Rowitch DH | title = Olig2-regulated lineage-restricted pathway controls replication competence in neural stem cells and malignant glioma | journal = Neuron | volume = 53 | issue = 4 | pages = 503–17 | date = Feb 2007 | pmid = 17296553 | pmc = 1810344 | doi = 10.1016/j.neuron.2007.01.009 }}</ref> and is shown to be required for proliferation of human glioma cells implanted in the brain of [[severe combined immunodeficiency]] (SCID) mice.<ref>{{cite journal | vauthors = Mehta S, Huillard E, Kesari S, Maire CL, Golebiowski D, Harrington EP, Alberta JA, Kane MF, Theisen M, Ligon KL, Rowitch DH, Stiles CD | title = The central nervous system-restricted transcription factor Olig2 opposes p53 responses to genotoxic damage in neural progenitors and malignant glioma | journal = Cancer Cell | volume = 19 | issue = 3 | pages = 359–71 | date = Mar 2011 | pmid = 21397859 | pmc = 3070398 | doi = 10.1016/j.ccr.2011.01.035 }}</ref>
*{{cite journal  | author=Wang J, Jani-Sait SN, Escalon EA, ''et al.'' |title=The t(14;21)(q11.2;q22) chromosomal translocation associated with T-cell acute lymphoblastic leukemia activates the BHLHB1 gene. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=97 |issue= 7 |pages= 3497-502 |year= 2000 |pmid= 10737801 |doi=  }}
 
*{{cite journal  | author=Hattori M, Fujiyama A, Taylor TD, ''et al.'' |title=The DNA sequence of human chromosome 21. |journal=Nature |volume=405 |issue= 6784 |pages= 311-9 |year= 2000 |pmid= 10830953 |doi= 10.1038/35012518 }}
Though the molecular mechanism behind this tumorigenesis is not entirely clear, more studies have recently been published pinpointing diverse evidence and potential roles for OLIG2 in glioma progression.  It is believed that OLIG2 promotes neural stem cell and progenitor cell proliferation by opposing [[p53]] pathway, which potentially contributes to glioma progression. OLIG2 has been shown to directly repress the p53 tumor-suppressor pathway effector p21<sup>WAF1/CIP1</sup>,<ref>{{cite journal | vauthors = Ligon KL, Huillard E, Mehta S, Kesari S, Liu H, Alberta JA, Bachoo RM, Kane M, Louis DN, Depinho RA, Anderson DJ, Stiles CD, Rowitch DH | title = Olig2-regulated lineage-restricted pathway controls replication competence in neural stem cells and malignant glioma | journal = Neuron | volume = 53 | issue = 4 | pages = 503–17 | date = Feb 2007 | pmid = 17296553 | pmc = 1810344 | doi = 10.1016/j.neuron.2007.01.009 }}</ref> suppress p53 [[acetylation]] and impede the binding of p53 to several [[enhancer (genetics)|enhancer]] sites.<ref>{{cite journal | vauthors = Mehta S, Huillard E, Kesari S, Maire CL, Golebiowski D, Harrington EP, Alberta JA, Kane MF, Theisen M, Ligon KL, Rowitch DH, Stiles CD | title = The central nervous system-restricted transcription factor Olig2 opposes p53 responses to genotoxic damage in neural progenitors and malignant glioma | journal = Cancer Cell | volume = 19 | issue = 3 | pages = 359–71 | date = Mar 2011 | pmid = 21397859 | pmc = 3070398 | doi = 10.1016/j.ccr.2011.01.035 }}</ref> It is further found that the phosphorylation of triple-serine motif in OLIG2 is present in several glioma lines and is more tumorigenic than the unphosphorylated status.<ref>{{cite journal | vauthors = Sun Y, Meijer DH, Alberta JA, Mehta S, Kane MF, Tien AC, Fu H, Petryniak MA, Potter GB, Liu Z, Powers JF, Runquist IS, Rowitch DH, Stiles CD | title = Phosphorylation state of Olig2 regulates proliferation of neural progenitors | journal = Neuron | volume = 69 | issue = 5 | pages = 906–17 | date = Mar 2011 | pmid = 21382551 | pmc = 3065213 | doi = 10.1016/j.neuron.2011.02.005 }}</ref> In a study using the U12-1 cell line for controlled expression of OLIG2, researchers showed that OLIG2 can suppress the proliferation of U12-1 by transactivating the ''p27<sup>Kip1</sup>'' gene<ref>{{cite journal | vauthors = Tabu K, Ohnishi A, Sunden Y, Suzuki T, Tsuda M, Tanaka S, Sakai T, Nagashima K, Sawa H | title = A novel function of OLIG2 to suppress human glial tumor cell growth via p27Kip1 transactivation | journal = Journal of Cell Science | volume = 119 | issue = Pt 7 | pages = 1433–41 | date = Apr 2006 | pmid = 16554441 | pmc =  | doi = 10.1242/jcs.02854 }}</ref> and can inhibit the motility of the cell by activating [[RhoA]].<ref>{{cite journal | vauthors = Tabu K, Ohba Y, Suzuki T, Makino Y, Kimura T, Ohnishi A, Sakai M, Watanabe T, Tanaka S, Sawa H | title = Oligodendrocyte lineage transcription factor 2 inhibits the motility of a human glial tumor cell line by activating RhoA | journal = Molecular Cancer Research | volume = 5 | issue = 10 | pages = 1099–109 | date = Oct 2007 | pmid = 17951409 | pmc =  | doi = 10.1158/1541-7786.MCR-07-0096 }}</ref>
*{{cite journal  | author=Marie Y, Sanson M, Mokhtari K, ''et al.'' |title=OLIG2 as a specific marker of oligodendroglial tumour cells. |journal=Lancet |volume=358 |issue= 9278 |pages= 298-300 |year= 2001 |pmid= 11498220 |doi= }}
 
*{{cite journal  | author=Lu QR, Park JK, Noll E, ''et al.'' |title=Oligodendrocyte lineage genes (OLIG) as molecular markers for human glial brain tumors. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=98 |issue= 19 |pages= 10851-6 |year= 2001 |pmid= 11526205 |doi= 10.1073/pnas.181340798 }}
Besides glioma, OLIG2 is also involved in leukemogenesis. The ''Olig2'' gene was actually first identified in a study in T-cell [[acute lymphoblastic leukemia]], in which the expression of OLIG2 was found elevated after t(14;21)(q11.2;q22) [[chromosomal translocation]].<ref>{{cite journal | vauthors = Birdsall B, Griffiths DV, Roberts GC, Feeney J, Burgen A | title = 1H nuclear magnetic resonance studies of Lactobacillus casei dihydrofolate reductase: effects of substrate and inhibitor binding on the histidine residues | journal = Proceedings of the Royal Society of London. Series B, Biological Sciences | volume = 196 | issue = 1124 | pages = 251–65 | date = Mar 1977 | pmid = 16268 | doi = 10.1098/rspb.1977.0040 }}</ref> The overexpression of OLIG2 was later shown present in malignancies beyond glioma and leukemia, such as breast cancer, [[melanoma]] and [[non-small cell lung carcinoma]] cell lines.<ref>{{cite journal | vauthors = Lin YW, Deveney R, Barbara M, Iscove NN, Nimer SD, Slape C, Aplan PD | title = OLIG2 (BHLHB1), a bHLH transcription factor, contributes to leukemogenesis in concert with LMO1 | journal = Cancer Research | volume = 65 | issue = 16 | pages = 7151–8 | date = Aug 2005 | pmid = 16103065 | pmc = 1681523 | doi = 10.1158/0008-5472.CAN-05-1400 }}</ref> It also has been shown that up-regulation of OLIG2 together with [[LMO1]] and Notch1 helps to provide proliferation signals.
*{{cite journal | author=Strausberg RL, Feingold EA, Grouse LH, ''et al.'' |title=Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue= 26 |pages= 16899-903 |year= 2003 |pmid= 12477932 |doi= 10.1073/pnas.242603899 }}
 
*{{cite journal | author=Sun T, Dong H, Wu L, ''et al.'' |title=Cross-repressive interaction of the Olig2 and Nkx2.2 transcription factors in developing neural tube associated with formation of a specific physical complex. |journal=J. Neurosci. |volume=23 |issue= 29 |pages= 9547-56 |year= 2003 |pmid= 14573534 |doi= }}
=== OLIG2 in Neural Diseases ===
*{{cite journal  | author=Fukuda S, Kondo T, Takebayashi H, Taga T |title=Negative regulatory effect of an oligodendrocytic bHLH factor OLIG2 on the astrocytic differentiation pathway. |journal=Cell Death Differ. |volume=11 |issue= 2 |pages= 196-202 |year= 2004 |pmid= 14576772 |doi= 10.1038/sj.cdd.4401332 }}
OLIG2 is also associated with Down syndrome, as it locates at chromosome 21 within or near the Down syndrome critical region on the long arm. This region is believed to contribute to the cognitive defects of Down syndrome. The substantial increase in the number of forebrain inhibitory neurons often observed in Ts65dn mouse (a murine model of trisomy 21) could lead to imbalance between excitation and inhibition and behavioral abnormalities. However, genetic reduction of OLIG2 and OLIG1 from three copies to two rescued the overproduction of interneurons, indicating the pivotal role of OLIG2 expression level in Down syndrome.<ref>{{cite journal | vauthors = Chakrabarti L, Best TK, Cramer NP, Carney RS, Isaac JT, Galdzicki Z, Haydar TF | title = Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome | journal = Nature Neuroscience | volume = 13 | issue = 8 | pages = 927–34 | date = Aug 2010 | pmid = 20639873 | pmc = 3249618 | doi = 10.1038/nn.2600 }}</ref> The association between OLIG2 and neural diseases (i.e. [[schizophrenia]] and [[Alzheimer]]’s disease) are under scrutiny, as several [[single nucleotide polymorphisms]] (SNPs) associated with these diseases in OLIG2 were identified by genome-wide association work.<ref>{{cite journal | vauthors = Georgieva L, Moskvina V, Peirce T, Norton N, Bray NJ, Jones L, Holmans P, Macgregor S, Zammit S, Wilkinson J, Williams H, Nikolov I, Williams N, Ivanov D, Davis KL, Haroutunian V, Buxbaum JD, Craddock N, Kirov G, Owen MJ, O'Donovan MC | title = Convergent evidence that oligodendrocyte lineage transcription factor 2 (OLIG2) and interacting genes influence susceptibility to schizophrenia | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 103 | issue = 33 | pages = 12469–74 | date = Aug 2006 | pmid = 16891421 | pmc = 1567903 | doi = 10.1073/pnas.0603029103 }}</ref><ref>{{cite journal | vauthors = Sims R, Hollingworth P, Moskvina V, Dowzell K, O'Donovan MC, Powell J, Lovestone S, Brayne C, Rubinsztein D, Owen MJ, Williams J, Abraham R | title = Evidence that variation in the oligodendrocyte lineage transcription factor 2 (OLIG2) gene is associated with psychosis in Alzheimer's disease | journal = Neuroscience Letters | volume = 461 | issue = 1 | pages = 54–9 | date = Sep 2009 | pmid = 19477230 | pmc =  | doi = 10.1016/j.neulet.2009.05.051 }}</ref>
*{{cite journal | author=Ota T, Suzuki Y, Nishikawa T, ''et al.'' |title=Complete sequencing and characterization of 21,243 full-length human cDNAs. |journal=Nat. Genet. |volume=36 |issue= 1 |pages= 40-5 |year= 2004 |pmid= 14702039 |doi= 10.1038/ng1285 }}
 
*{{cite journal | author=Ligon KL, Alberta JA, Kho AT, ''et al.'' |title=The oligodendroglial lineage marker OLIG2 is universally expressed in diffuse gliomas. |journal=J. Neuropathol. Exp. Neurol. |volume=63 |issue= 5 |pages= 499-509 |year= 2004 |pmid= 15198128 |doi= }}
OLIG2 also plays a functional role in neural repair. Studies showed that the number of OLIG2-expressing cells increased in the lesion after cortical stab-wound injury, supporting the role for OLIG2 in reactive [[gliosis]].<ref>{{cite journal | vauthors = Buffo A, Vosko MR, Ertürk D, Hamann GF, Jucker M, Rowitch D, Götz M | title = Expression pattern of the transcription factor Olig2 in response to brain injuries: implications for neuronal repair | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 102 | issue = 50 | pages = 18183–8 | date = Dec 2005 | pmid = 16330768 | pmc = 1312388 | doi = 10.1073/pnas.0506535102 }}</ref> OLIG2 was also implicated in generating reactive [[astrocytes]] possibly in a transient re-expression manner, but the mechanisms are unclear.<ref>{{cite journal | vauthors = Buffo A, Rite I, Tripathi P, Lepier A, Colak D, Horn AP, Mori T, Götz M | title = Origin and progeny of reactive gliosis: A source of multipotent cells in the injured brain | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 105 | issue = 9 | pages = 3581–6 | date = Mar 2008 | pmid = 18299565 | pmc = 2265175 | doi = 10.1073/pnas.0709002105 }}</ref>
*{{cite journal  | author=Gerhard DS, Wagner L, Feingold EA, ''et al.'' |title=The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121-7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504 }}
 
*{{cite journal | author=Hori Y, Gu X, Xie X, Kim SK |title=Differentiation of insulin-producing cells from human neural progenitor cells. |journal=PLoS Med. |volume=2 |issue= 4 |pages= e103 |year= 2006 |pmid= 15839736 |doi= 10.1371/journal.pmed.0020103 }}
== References ==
*{{cite journal  | author=Lin YW, Deveney R, Barbara M, ''et al.'' |title=OLIG2 (BHLHB1), a bHLH transcription factor, contributes to leukemogenesis in concert with LMO1. |journal=Cancer Res. |volume=65 |issue= 16 |pages= 7151-8 |year= 2005 |pmid= 16103065 |doi= 10.1158/0008-5472.CAN-05-1400 }}
{{reflist|33em}}
*{{cite journal | author=Jakovcevski I, Zecevic N |title=Olig transcription factors are expressed in oligodendrocyte and neuronal cells in human fetal CNS. |journal=J. Neurosci. |volume=25 |issue= 44 |pages= 10064-73 |year= 2006 |pmid= 16267213 |doi= 10.1523/JNEUROSCI.2324-05.2005 }}
 
*{{cite journal  | author=Kimura K, Wakamatsu A, Suzuki Y, ''et al.'' |title=Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. |journal=Genome Res. |volume=16 |issue= 1 |pages= 55-65 |year= 2006 |pmid= 16344560 |doi= 10.1101/gr.4039406 }}
== Further reading ==
*{{cite journal | author=Sun T, Hafler BP, Kaing S, ''et al.'' |title=Evidence for motoneuron lineage-specific regulation of Olig2 in the vertebrate neural tube. |journal=Dev. Biol. |volume=292 |issue= 1 |pages= 152-64 |year= 2006 |pmid= 16469306 |doi= 10.1016/j.ydbio.2005.12.047 }}
{{refbegin|33em}}
*{{cite journal | author=Tabu K, Ohnishi A, Sunden Y, ''et al.'' |title=A novel function of OLIG2 to suppress human glial tumor cell growth via p27Kip1 transactivation. |journal=J. Cell. Sci. |volume=119 |issue= Pt 7 |pages= 1433-41 |year= 2006 |pmid= 16554441 |doi= 10.1242/jcs.02854 }}
* {{cite journal | vauthors = Sun T, Dong H, Wu L, Kane M, Rowitch DH, Stiles CD | title = Cross-repressive interaction of the Olig2 and Nkx2.2 transcription factors in developing neural tube associated with formation of a specific physical complex | journal = The Journal of Neuroscience | volume = 23 | issue = 29 | pages = 9547–56 | date = Oct 2003 | pmid = 14573534 | doi = }}
*{{cite journal | author=Wissmüller S, Kosian T, Wolf M, ''et al.'' |title=The high-mobility-group domain of Sox proteins interacts with DNA-binding domains of many transcription factors. |journal=Nucleic Acids Res. |volume=34 |issue= 6 |pages= 1735-44 |year= 2006 |pmid= 16582099 |doi= 10.1093/nar/gkl105 }}
* {{cite journal | vauthors = Fukuda S, Kondo T, Takebayashi H, Taga T | title = Negative regulatory effect of an oligodendrocytic bHLH factor OLIG2 on the astrocytic differentiation pathway | journal = Cell Death and Differentiation | volume = 11 | issue = 2 | pages = 196–202 | date = Feb 2004 | pmid = 14576772 | doi = 10.1038/sj.cdd.4401332 }}
*{{cite journal | author=Ligon KL, Kesari S, Kitada M, ''et al.'' |title=Development of NG2 neural progenitor cells requires Olig gene function. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=103 |issue= 20 |pages= 7853-8 |year= 2006 |pmid= 16682644 |doi= 10.1073/pnas.0511001103 }}
* {{cite journal | vauthors = Ligon KL, Alberta JA, Kho AT, Weiss J, Kwaan MR, Nutt CL, Louis DN, Stiles CD, Rowitch DH | title = The oligodendroglial lineage marker OLIG2 is universally expressed in diffuse gliomas | journal = Journal of Neuropathology and Experimental Neurology | volume = 63 | issue = 5 | pages = 499–509 | date = May 2004 | pmid = 15198128 | doi =  10.1093/jnen/63.5.499}}
*{{cite journal  | author=Georgieva L, Moskvina V, Peirce T, ''et al.'' |title=Convergent evidence that oligodendrocyte lineage transcription factor 2 (OLIG2) and interacting genes influence susceptibility to schizophrenia. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=103 |issue= 33 |pages= 12469-74 |year= 2006 |pmid= 16891421 |doi= 10.1073/pnas.0603029103 }}
* {{cite journal | vauthors = Hori Y, Gu X, Xie X, Kim SK | title = Differentiation of insulin-producing cells from human neural progenitor cells | journal = PLoS Medicine | volume = 2 | issue = 4 | pages = e103 | date = Apr 2005 | pmid = 15839736 | pmc = 1087208 | doi = 10.1371/journal.pmed.0020103 }}
*{{cite journal  | author=Ruf N, Martelli M, Weschke B, Uhlenberg B |title=Oligodendroglial transcription factor (OLIG1 and OLIG2) mutations are not associated with Pelizaeus-Merzbacher-like leukodystrophy. |journal=Am. J. Med. Genet. B Neuropsychiatr. Genet. |volume=144 |issue= 3 |pages= 365-6 |year= 2007 |pmid= 17171653 |doi= 10.1002/ajmg.b.30434 }}
* {{cite journal | vauthors = Lin YW, Deveney R, Barbara M, Iscove NN, Nimer SD, Slape C, Aplan PD | title = OLIG2 (BHLHB1), a bHLH transcription factor, contributes to leukemogenesis in concert with LMO1 | journal = Cancer Research | volume = 65 | issue = 16 | pages = 7151–8 | date = Aug 2005 | pmid = 16103065 | pmc = 1681523 | doi = 10.1158/0008-5472.CAN-05-1400 }}
}}
* {{cite journal | vauthors = Jakovcevski I, Zecevic N | title = Olig transcription factors are expressed in oligodendrocyte and neuronal cells in human fetal CNS | journal = The Journal of Neuroscience | volume = 25 | issue = 44 | pages = 10064–73 | date = Nov 2005 | pmid = 16267213 | doi = 10.1523/JNEUROSCI.2324-05.2005 }}
* {{cite journal | vauthors = Kimura K, Wakamatsu A, Suzuki Y, Ota T, Nishikawa T, Yamashita R, Yamamoto J, Sekine M, Tsuritani K, Wakaguri H, Ishii S, Sugiyama T, Saito K, Isono Y, Irie R, Kushida N, Yoneyama T, Otsuka R, Kanda K, Yokoi T, Kondo H, Wagatsuma M, Murakawa K, Ishida S, Ishibashi T, Takahashi-Fujii A, Tanase T, Nagai K, Kikuchi H, Nakai K, Isogai T, Sugano S | title = Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes | journal = Genome Research | volume = 16 | issue = 1 | pages = 55–65 | date = Jan 2006 | pmid = 16344560 | pmc = 1356129 | doi = 10.1101/gr.4039406 }}
* {{cite journal | vauthors = Sun T, Hafler BP, Kaing S, Kitada M, Ligon KL, Widlund HR, Yuk DI, Stiles CD, Rowitch DH | title = Evidence for motoneuron lineage-specific regulation of Olig2 in the vertebrate neural tube | journal = Developmental Biology | volume = 292 | issue = 1 | pages = 152–64 | date = Apr 2006 | pmid = 16469306 | doi = 10.1016/j.ydbio.2005.12.047 }}
* {{cite journal | vauthors = Tabu K, Ohnishi A, Sunden Y, Suzuki T, Tsuda M, Tanaka S, Sakai T, Nagashima K, Sawa H | title = A novel function of OLIG2 to suppress human glial tumor cell growth via p27Kip1 transactivation | journal = Journal of Cell Science | volume = 119 | issue = Pt 7 | pages = 1433–41 | date = Apr 2006 | pmid = 16554441 | doi = 10.1242/jcs.02854 }}
* {{cite journal | vauthors = Wissmüller S, Kosian T, Wolf M, Finzsch M, Wegner M | title = The high-mobility-group domain of Sox proteins interacts with DNA-binding domains of many transcription factors | journal = Nucleic Acids Research | volume = 34 | issue = 6 | pages = 1735–44 | year = 2006 | pmid = 16582099 | pmc = 1421504 | doi = 10.1093/nar/gkl105 }}
* {{cite journal | vauthors = Ligon KL, Kesari S, Kitada M, Sun T, Arnett HA, Alberta JA, Anderson DJ, Stiles CD, Rowitch DH | title = Development of NG2 neural progenitor cells requires Olig gene function | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 103 | issue = 20 | pages = 7853–8 | date = May 2006 | pmid = 16682644 | pmc = 1472534 | doi = 10.1073/pnas.0511001103 }}
* {{cite journal | vauthors = Georgieva L, Moskvina V, Peirce T, Norton N, Bray NJ, Jones L, Holmans P, Macgregor S, Zammit S, Wilkinson J, Williams H, Nikolov I, Williams N, Ivanov D, Davis KL, Haroutunian V, Buxbaum JD, Craddock N, Kirov G, Owen MJ, O'Donovan MC | title = Convergent evidence that oligodendrocyte lineage transcription factor 2 (OLIG2) and interacting genes influence susceptibility to schizophrenia | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 103 | issue = 33 | pages = 12469–74 | date = Aug 2006 | pmid = 16891421 | pmc = 1567903 | doi = 10.1073/pnas.0603029103 }}
* {{cite journal | vauthors = Ruf N, Martelli M, Weschke B, Uhlenberg B | title = Oligodendroglial transcription factor (OLIG1 and OLIG2) mutations are not associated with Pelizaeus-Merzbacher-like leukodystrophy | journal = American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics | volume = 144B | issue = 3 | pages = 365–6 | date = Apr 2007 | pmid = 17171653 | doi = 10.1002/ajmg.b.30434 }}
{{refend}}
{{refend}}


== External links ==
== External links ==
* {{MeshName|OLIG2+protein,+human}}
* {{MeshName|OLIG2+protein,+human}}
* {{UCSC genome browser|OLIG2}}
* {{UCSC gene details|OLIG2}}


{{NLM content}}
{{Transcription factors|g1}}


{{gene-21-stub}}
{{NLM content}}
{{Transcription factors}}
[[Category:Transcription factors]]
[[Category:Transcription factors]]
{{WikiDoc Sources}}

Latest revision as of 06:52, 20 May 2016

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Oligodendrocyte transcription factor (OLIG2) is a basic helix-loop-helix (bHLH) transcription factor encoded by the Olig2 gene. The protein is of 329 amino acids in length, 32kDa in size and contains 1 basic helix-loop-helix DNA-binding domain.[1] It is one of the three members of the bHLH family. The other two members are OLIG1 and OLIG3. The expression of OLIG2 is mostly restricted in central nervous system, where it acts as both an anti-neurigenic and a neurigenic factor at different stages of development. OLIG2 is well known for determining motor neuron and oligodendrocyte differentiation, as well as its role in sustaining replication in early development. It is mainly involved in diseases such as brain tumor and Down syndrome.

Function

OLIG2 is mostly expressed in restricted domains of the brain and spinal cord ventricular zone which give rise to oligodendrocytes and specific types of neurons. In the spinal cord, the pMN region sequentially generates motor neurons and oligodendrocytes. During embryogenesis, OLIG2 first directs motor neuron fate by establishing a ventral domain of motor neuron progenitors and promoting neuronal differentiation. OLIG2 then switches to promoting the formation of oligodendrocyte precursors and oligodendrocyte differentiation at later stages of development. Apart from functioning as a neurogenic factor in specification and the differentiation of motor neurons and oligodendrocytes, OLIG2 also functions as an anti-neurogenic factor at early time points in pMN progenitors to sustain the cycling progenitor pool. This side of anti-neurogenicity of OLIG2 later plays a bigger role in malignancies like glioma.[2]

The role of phosphorylation has been highlighted recently to account for the multifaceted functions of OLIG2 in differentiation and proliferation. Studies showed that the phosphorylation state of OLIG2 at Ser30 determines the fate of cortical progenitor cells, in which cortical progenitor cells will either differentiate into astrocytes or remain as neuronal progenitors.[3] Phosphorylation at a triple serine motif (Ser10, Ser13 and Ser14) on the other hand was shown to regulate the proliferative function of OLIG2.[4] Another phosphorylation site Ser147 predicted by bioinformatics was found to regulate motor neuron development by regulating the binding between OLIG2 and NGN2.[5] Further, OLIG2 contains a ST box composed of a string of 12 contiguous serine and threonine residues at position Ser77-Ser88. It is believed that phosphorylation at ST box is biologically functional,[6] yet the role of it still remains to be elucidated in vivo.[7]

OLIG2 has also been implicated in bovine horn ontogenesis. It was the only gene in the bovine polled locus to show differential expression between the putative horn bud and the frontal forehead skin.[8]

Clinical Significance

OLIG2 in Cancer

OLIG2 is well recognized for its importance in cancer research, particularly in brain tumors and leukemia. OLIG2 is universally expressed in glioblastoma and other diffuse gliomas (astrocytomas, oligodendrogliomas and oligoastrocytomas), and is a useful positive diagnostic marker of these brain tumors.[9] In particular, OLIG2 is selectively expressed in a subgroup of glioma cells that are highly tumorigenic,[10] and is shown to be required for proliferation of human glioma cells implanted in the brain of severe combined immunodeficiency (SCID) mice.[11]

Though the molecular mechanism behind this tumorigenesis is not entirely clear, more studies have recently been published pinpointing diverse evidence and potential roles for OLIG2 in glioma progression. It is believed that OLIG2 promotes neural stem cell and progenitor cell proliferation by opposing p53 pathway, which potentially contributes to glioma progression. OLIG2 has been shown to directly repress the p53 tumor-suppressor pathway effector p21WAF1/CIP1,[12] suppress p53 acetylation and impede the binding of p53 to several enhancer sites.[13] It is further found that the phosphorylation of triple-serine motif in OLIG2 is present in several glioma lines and is more tumorigenic than the unphosphorylated status.[14] In a study using the U12-1 cell line for controlled expression of OLIG2, researchers showed that OLIG2 can suppress the proliferation of U12-1 by transactivating the p27Kip1 gene[15] and can inhibit the motility of the cell by activating RhoA.[16]

Besides glioma, OLIG2 is also involved in leukemogenesis. The Olig2 gene was actually first identified in a study in T-cell acute lymphoblastic leukemia, in which the expression of OLIG2 was found elevated after t(14;21)(q11.2;q22) chromosomal translocation.[17] The overexpression of OLIG2 was later shown present in malignancies beyond glioma and leukemia, such as breast cancer, melanoma and non-small cell lung carcinoma cell lines.[18] It also has been shown that up-regulation of OLIG2 together with LMO1 and Notch1 helps to provide proliferation signals.

OLIG2 in Neural Diseases

OLIG2 is also associated with Down syndrome, as it locates at chromosome 21 within or near the Down syndrome critical region on the long arm. This region is believed to contribute to the cognitive defects of Down syndrome. The substantial increase in the number of forebrain inhibitory neurons often observed in Ts65dn mouse (a murine model of trisomy 21) could lead to imbalance between excitation and inhibition and behavioral abnormalities. However, genetic reduction of OLIG2 and OLIG1 from three copies to two rescued the overproduction of interneurons, indicating the pivotal role of OLIG2 expression level in Down syndrome.[19] The association between OLIG2 and neural diseases (i.e. schizophrenia and Alzheimer’s disease) are under scrutiny, as several single nucleotide polymorphisms (SNPs) associated with these diseases in OLIG2 were identified by genome-wide association work.[20][21]

OLIG2 also plays a functional role in neural repair. Studies showed that the number of OLIG2-expressing cells increased in the lesion after cortical stab-wound injury, supporting the role for OLIG2 in reactive gliosis.[22] OLIG2 was also implicated in generating reactive astrocytes possibly in a transient re-expression manner, but the mechanisms are unclear.[23]

References

  1. ↑ "OLIG2". Atlas of Genetics and Cytogenetics in Oncology and Hematology.
  2. ↑ Gaber ZB, Novitch BG (Mar 2011). "All the embryo's a stage, and Olig2 in its time plays many parts". Neuron. 69 (5): 833–5. doi:10.1016/j.neuron.2011.02.037. PMID 21382543.
  3. ↑ Setoguchi T, Kondo T (Sep 2004). "Nuclear export of OLIG2 in neural stem cells is essential for ciliary neurotrophic factor-induced astrocyte differentiation". The Journal of Cell Biology. 166 (7): 963–8. doi:10.1083/jcb.200404104. PMC 2172021. PMID 15452140.
  4. ↑ Sun Y, Meijer DH, Alberta JA, Mehta S, Kane MF, Tien AC, Fu H, Petryniak MA, Potter GB, Liu Z, Powers JF, Runquist IS, Rowitch DH, Stiles CD (Mar 2011). "Phosphorylation state of Olig2 regulates proliferation of neural progenitors". Neuron. 69 (5): 906–17. doi:10.1016/j.neuron.2011.02.005. PMC 3065213. PMID 21382551.
  5. ↑ Li H, de Faria JP, Andrew P, Nitarska J, Richardson WD (Mar 2011). "Phosphorylation regulates OLIG2 cofactor choice and the motor neuron-oligodendrocyte fate switch". Neuron. 69 (5): 918–29. doi:10.1016/j.neuron.2011.01.030. PMC 3093612. PMID 21382552.
  6. ↑ Huillard E, Ziercher L, Blond O, Wong M, Deloulme JC, Souchelnytskyi S, Baudier J, Cochet C, Buchou T (Jun 2010). "Disruption of CK2beta in embryonic neural stem cells compromises proliferation and oligodendrogenesis in the mouse telencephalon". Molecular and Cellular Biology. 30 (11): 2737–49. doi:10.1128/MCB.01566-09. PMC 2876519. PMID 20368359.
  7. ↑ Sun Y, Meijer DH, Alberta JA, Mehta S, Kane MF, Tien AC, Fu H, Petryniak MA, Potter GB, Liu Z, Powers JF, Runquist IS, Rowitch DH, Stiles CD (Mar 2011). "Phosphorylation state of Olig2 regulates proliferation of neural progenitors". Neuron. 69 (5): 906–17. doi:10.1016/j.neuron.2011.02.005. PMC 3065213. PMID 21382551.
  8. ↑ Allais-Bonnet A, Grohs C, Medugorac I, Krebs S, Djari A, Graf A, Fritz S, Seichter D, Baur A, Russ I, Bouet S, Rothammer S, Wahlberg P, Esquerré D, Hoze C, Boussaha M, Weiss B, Thépot D, Fouilloux MN, Rossignol MN, van Marle-Köster E, Hreiðarsdóttir GE, Barbey S, Dozias D, Cobo E, Reversé P, Catros O, Marchand JL, Soulas P, Roy P, Marquant-Leguienne B, Le Bourhis D, Clément L, Salas-Cortes L, Venot E, Pannetier M, Phocas F, Klopp C, Rocha D, Fouchet M, Journaux L, Bernard-Capel C, Ponsart C, Eggen A, Blum H, Gallard Y, Boichard D, Pailhoux E, Capitan A (2013). "Novel insights into the bovine polled phenotype and horn ontogenesis in Bovidae". PLOS ONE. 8 (5): e63512. doi:10.1371/journal.pone.0063512. PMC 3661542. PMID 23717440.
  9. ↑ Ligon KL, Alberta JA, Kho AT, Weiss J, Kwaan MR, Nutt CL, Louis DN, Stiles CD, Rowitch DH (May 2004). "The oligodendroglial lineage marker OLIG2 is universally expressed in diffuse gliomas". Journal of Neuropathology and Experimental Neurology. 63 (5): 499–509. doi:10.1093/jnen/63.5.499. PMID 15198128.
  10. ↑ Ligon KL, Huillard E, Mehta S, Kesari S, Liu H, Alberta JA, Bachoo RM, Kane M, Louis DN, Depinho RA, Anderson DJ, Stiles CD, Rowitch DH (Feb 2007). "Olig2-regulated lineage-restricted pathway controls replication competence in neural stem cells and malignant glioma". Neuron. 53 (4): 503–17. doi:10.1016/j.neuron.2007.01.009. PMC 1810344. PMID 17296553.
  11. ↑ Mehta S, Huillard E, Kesari S, Maire CL, Golebiowski D, Harrington EP, Alberta JA, Kane MF, Theisen M, Ligon KL, Rowitch DH, Stiles CD (Mar 2011). "The central nervous system-restricted transcription factor Olig2 opposes p53 responses to genotoxic damage in neural progenitors and malignant glioma". Cancer Cell. 19 (3): 359–71. doi:10.1016/j.ccr.2011.01.035. PMC 3070398. PMID 21397859.
  12. ↑ Ligon KL, Huillard E, Mehta S, Kesari S, Liu H, Alberta JA, Bachoo RM, Kane M, Louis DN, Depinho RA, Anderson DJ, Stiles CD, Rowitch DH (Feb 2007). "Olig2-regulated lineage-restricted pathway controls replication competence in neural stem cells and malignant glioma". Neuron. 53 (4): 503–17. doi:10.1016/j.neuron.2007.01.009. PMC 1810344. PMID 17296553.
  13. ↑ Mehta S, Huillard E, Kesari S, Maire CL, Golebiowski D, Harrington EP, Alberta JA, Kane MF, Theisen M, Ligon KL, Rowitch DH, Stiles CD (Mar 2011). "The central nervous system-restricted transcription factor Olig2 opposes p53 responses to genotoxic damage in neural progenitors and malignant glioma". Cancer Cell. 19 (3): 359–71. doi:10.1016/j.ccr.2011.01.035. PMC 3070398. PMID 21397859.
  14. ↑ Sun Y, Meijer DH, Alberta JA, Mehta S, Kane MF, Tien AC, Fu H, Petryniak MA, Potter GB, Liu Z, Powers JF, Runquist IS, Rowitch DH, Stiles CD (Mar 2011). "Phosphorylation state of Olig2 regulates proliferation of neural progenitors". Neuron. 69 (5): 906–17. doi:10.1016/j.neuron.2011.02.005. PMC 3065213. PMID 21382551.
  15. ↑ Tabu K, Ohnishi A, Sunden Y, Suzuki T, Tsuda M, Tanaka S, Sakai T, Nagashima K, Sawa H (Apr 2006). "A novel function of OLIG2 to suppress human glial tumor cell growth via p27Kip1 transactivation". Journal of Cell Science. 119 (Pt 7): 1433–41. doi:10.1242/jcs.02854. PMID 16554441.
  16. ↑ Tabu K, Ohba Y, Suzuki T, Makino Y, Kimura T, Ohnishi A, Sakai M, Watanabe T, Tanaka S, Sawa H (Oct 2007). "Oligodendrocyte lineage transcription factor 2 inhibits the motility of a human glial tumor cell line by activating RhoA". Molecular Cancer Research. 5 (10): 1099–109. doi:10.1158/1541-7786.MCR-07-0096. PMID 17951409.
  17. ↑ Birdsall B, Griffiths DV, Roberts GC, Feeney J, Burgen A (Mar 1977). "1H nuclear magnetic resonance studies of Lactobacillus casei dihydrofolate reductase: effects of substrate and inhibitor binding on the histidine residues". Proceedings of the Royal Society of London. Series B, Biological Sciences. 196 (1124): 251–65. doi:10.1098/rspb.1977.0040. PMID 16268.
  18. ↑ Lin YW, Deveney R, Barbara M, Iscove NN, Nimer SD, Slape C, Aplan PD (Aug 2005). "OLIG2 (BHLHB1), a bHLH transcription factor, contributes to leukemogenesis in concert with LMO1". Cancer Research. 65 (16): 7151–8. doi:10.1158/0008-5472.CAN-05-1400. PMC 1681523. PMID 16103065.
  19. ↑ Chakrabarti L, Best TK, Cramer NP, Carney RS, Isaac JT, Galdzicki Z, Haydar TF (Aug 2010). "Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome". Nature Neuroscience. 13 (8): 927–34. doi:10.1038/nn.2600. PMC 3249618. PMID 20639873.
  20. ↑ Georgieva L, Moskvina V, Peirce T, Norton N, Bray NJ, Jones L, Holmans P, Macgregor S, Zammit S, Wilkinson J, Williams H, Nikolov I, Williams N, Ivanov D, Davis KL, Haroutunian V, Buxbaum JD, Craddock N, Kirov G, Owen MJ, O'Donovan MC (Aug 2006). "Convergent evidence that oligodendrocyte lineage transcription factor 2 (OLIG2) and interacting genes influence susceptibility to schizophrenia". Proceedings of the National Academy of Sciences of the United States of America. 103 (33): 12469–74. doi:10.1073/pnas.0603029103. PMC 1567903. PMID 16891421.
  21. ↑ Sims R, Hollingworth P, Moskvina V, Dowzell K, O'Donovan MC, Powell J, Lovestone S, Brayne C, Rubinsztein D, Owen MJ, Williams J, Abraham R (Sep 2009). "Evidence that variation in the oligodendrocyte lineage transcription factor 2 (OLIG2) gene is associated with psychosis in Alzheimer's disease". Neuroscience Letters. 461 (1): 54–9. doi:10.1016/j.neulet.2009.05.051. PMID 19477230.
  22. ↑ Buffo A, Vosko MR, Ertürk D, Hamann GF, Jucker M, Rowitch D, Götz M (Dec 2005). "Expression pattern of the transcription factor Olig2 in response to brain injuries: implications for neuronal repair". Proceedings of the National Academy of Sciences of the United States of America. 102 (50): 18183–8. doi:10.1073/pnas.0506535102. PMC 1312388. PMID 16330768.
  23. ↑ Buffo A, Rite I, Tripathi P, Lepier A, Colak D, Horn AP, Mori T, Götz M (Mar 2008). "Origin and progeny of reactive gliosis: A source of multipotent cells in the injured brain". Proceedings of the National Academy of Sciences of the United States of America. 105 (9): 3581–6. doi:10.1073/pnas.0709002105. PMC 2265175. PMID 18299565.

Further reading

External links

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