OLIG2

OLIG2
Identifikatori
Aliasi	OLIG2
Vanjski ID-jevi	OMIM: 606386 MGI: 1355331 HomoloGene: 4241 GeneCards: OLIG2
Lokacija gena (čovjek)
Hrom.	Hromosom 21 (čovjek)
Kraj	33,029,196 bp
Lokacija gena (miš)
Hrom.	Hromosom 16 (miš)
Kraj	91,025,565 bp
Obrazac RNK ekspresije
	; ;
	Više referentnih podataka o ekspresiji
Ontologija gena
Molekularna funkcija	• vezivanje sa DNK; • protein dimerization activity; • protein homodimerization activity; • GO:0001131, GO:0001151, GO:0001130, GO:0001204 DNA-binding transcription factor activity; • HMG box domain binding; • transcription factor activity, RNA polymerase II distal enhancer sequence-specific binding; • GO:0001200, GO:0001133, GO:0001201 DNA-binding transcription factor activity, RNA polymerase II-specific;
Ćelijska komponenta	• citoplazma; • jedro;
Biološki proces	• positive regulation of oligodendrocyte differentiation; • GO:0009373 regulation of transcription, DNA-templated; • negative regulation of neuron differentiation; • thalamus development; • spinal cord oligodendrocyte cell fate specification; • oligodendrocyte differentiation; • GO:1901227 negative regulation of transcription by RNA polymerase II; • transcription, DNA-templated; • nervous system development; • multicellular organism development; • oligodendrocyte cell fate specification; • neuron differentiation; • myelination; • neuron fate commitment; • spinal cord motor neuron differentiation; • spinal cord oligodendrocyte cell differentiation;
	Izvori:Amigo / QuickGO
Ortolozi
	10215
	50913
	ENSG00000205927
	ENSMUSG00000039830
	Q13516
	Q9EQW6
	NM_005806
	NM_016967
	NP_005797
	NP_058663
	Wikipodaci
Pogledaj/uredi – čovjek	Pogledaj/uredi – miš

Oligodendrocitni transkripcijski faktor (OLIG2) jest bazni heliks-prtla-heliks (bHLH) transkripcijski faktor, protein koji je kod ljudi kodiran genom Olig2 sa hromosoma 21. Protein je dug 329 aminokiselina, veličine 32 kDa i sadrži jednan bazmi domeni koji veže DNK heliks-petlja-heliks.^[5] Jedan je od tri člana porodice bHLH. Druga dva člana su OLIG1 i OLIG3. Ekspresija OLIG2 je uglavnom ograničena u centralni nervni sistem, gdje djeluje i kao antineurigeni i neurigeni faktor u različitim fazama razvoja. OLIG2 je dobro poznat po određivanju diferencijacije motornih neurona i oligodendrocita, kao i po njegovoj ulozi u održavanju replikacije u ranom razvoju. Uglavnom je uključen u bolesti kao što su tumor na mozgu i Downov sindrom.

Aminokiselinska sekvenca

Dužina polipeptidnog lanca je 323 aminokiseline, a molekulska težina 32.385 Da.

C: Cistein

D: Asparaginska kiselina

E: Glutaminska kiselina

F: Fenilalanin

G: Glicin

H: Histidin

I: Izoleucin

K: Lizin

L: Leucin

M: Metionin

N: Asparagin

P: Prolin

Q: Glutamin

R: Arginin

S: Serin

T: Treonin

V: Valin

W: Triptofan

Y: Tirozin

10	20	30	40	50
MDSDASLVSS	RPSSPEPDDL	FLPARSKGSS	GSAFTGGTVS	SSTPSDCPPE
LSAELRGAMG	SAGAHPGDKL	GGSGFKSSSS	STSSSTSSAA	ASSTKKDKKQ
MTEPELQQLR	LKINSRERKR	MHDLNIAMDG	LREVMPYAHG	PSVRKLSKIA
TLLLARNYIL	MLTNSLEEMK	RLVSEIYGGH	HAGFHPSACG	GLAHSAPLPA
ATAHPAAAAH	AAHHPAVHHP	ILPPAAAAAA	AAAAAAAVSS	ASLPGSGLPS
VGSIRPPHGL	LKSPSAAAAA	PLGGGGGGSG	ASGGFQHWGG	MPCPCSMCQV
PPPHHHVSAM	GAGSLPRLTS	DAK

Funkcija

OLIG2 je uglavnom eksprimiran u ograničenim domenima mozga i komorske zone kičmene moždine, koji stvaraju oligodendrocite i specifične tipove neurona. U kičmenoj moždini, regija pMN sekvencijijski stvara motorne neurone i oligodendrocite. Tokom embriogeneze, OLIG2 prvo usmjerava sudbinu motornih neurona, uspostavljanjem ventralnog domena progenitora motornih neurona i podstcanjem neuronske diferencijacije. OLIG2 zatim prelazi na stimuliranje formiranja prekursora oligodendrocita i diferencijacije oligodendrocita u kasnijim fazama razvoja. Osim što funkcionira kao neurogeni faktor u specifikaciji i diferencijaciji motornih neurona i oligodendrocita, OLIG2 također funkcionira kao antineurogeni faktor u ranim vremenskim razdobljima u pMN progenitorima, kako bi održao ciklički pul progenitora. Ova strana antineurogenosti OLIG2 kasnije ima veću ulogu kod malignostima poput glioma.^[6]

Uloga fosforilacije je nedavno istaknuta kako bi se objasnile višestruke funkcije OLIG2 u diferencijaciji i proliferaciji. Studije su pokazale da stanje fosforilacije OLIG2 u Ser30 određuje sudbinu korteksnih progenitorskih ćelija, u kojima će se ove progenitorske ćelije ili diferencirati u astrocite ili ostati kao neuronski progenitori.^[7] S druge strane, pokazalo se da fosforilacija na trostrukom serinskom motivu (Ser10, Ser13 i Ser14) regulira proliferativnu funkciju OLIG2.^[8] Utvrđeno je da još jedno fosforilacijsko mjesto Ser147 predviđeno bioinformatičkom analizom reguliše razvoj motornih neurona, regulacijom vezivanja između OLIG2 i NGN2.^[9] Nadalje, OLIG2 sadrži ST-kutiju, sastavljenu sekvenc sa 12 susjednih ostataka serina i treonina na poziciji Ser77-Ser88. Vjeruje se da je fosforilacija u ST-kutiji biološki funkcionalna,^[10] ali njena uloga tek treba da se razjasni i in vivo.^[11]

OLIG2 je također uključen u ontogenezu goveđih rogova. Bio je to jedini gen u lokusu goveda koji je pokazao različitu ekspresiju između navodnog pupoljka roga i prednjeg dijela čeone kože.^[12]

Klinički značaj

OLIG2 u raku

OLIG2 je dobro poznat po svojoj važnosti u istraživanju raka, posebno tumora mozga i leukemija. OLIG2 je univerzalno eksprimiran u glioblastomu i drugim difuznim gliomima (astrocitomi, oligodendrogliomi i oligoastrocitomi), a koristan je pozitivni dijagnostički marker ovih tumora mozga.^[13] Konkretno, OLIG2 se selektivno eksprimira u podgrupi ćelija glioma koje su visoko tumorigene,^[14] i pokazalo se da je potreban za proliferaciju ljudskih ćelija glioma implantiranih u mozak sa teškom kombinovanom imunodeficijencijom (SCID) kod miševa.^[15]

Iako molekulski mehanizam koji stoji iza ove tumorigeneze nije sasvim jasan, nedavno je objavljeno više studija koje ukazuju na različite dokaze i potencijalnu ulogu OLIG2 u progresiji glioma. Vjeruje se da OLIG2 promovira proliferaciju nervnih matičnih i progenitornih ćelija, suprotstavljenim p53 putu, što potencijalno doprinosi progresiji glioma. Pokazalo se da OLIG2 direktno potiskuje efektor p53 tumor-supresorskog puta p21^WAF1/CIP1,^[16] potiskujući acetilaciju p53 i ometajući vezivanje p53 za nekoliko pojačivačkih mjesta.^[17] Nadalje je pronađeno da je fosforilacija motiva trostrukog serina u OLIG2 prisutna u nekoliko linija glioma i da je tumorogenija nego nefosforilirani status.^[18] U studiji koja koristi ćelijsku liniju U12-1 za kontroliranu ekspresiju OLIG2, pokazano je da OLIG2 može potisnuti proliferaciju U12-1, transaktivacijom gena p27^Kip1 ^[19] i može inhibirati pokretljivost ćelije, aktivacijom RhoA.^[20]

Osim glioma, OLIG2 je također uključen u leukemogenezu. Gen Olig2 je zapravo prvi put identifikovan u studiji na T-ćelijama akutne limfoblastne leukemije, u kojoj je otkriveno da je ekspresija OLIG2 povišena nakon translokacije t(14;21)(q11.2;q22).^[21] Prekomjerna ekspresija OLIG2 pokazala se kasnije I kod malignosti izvan glioma i leukemije, kao što su rak dojke, melanom i ćelijske linije plućnog karcinoma nemalih ćelija.^[22] Također je pokazano da nadregulacija OLIG2 zajedno sa LMO1 i Notch1 pomaže da se obezbede proliferacijski signali.

OLIG2 u nervnim bolestima

OLIG2 je također povezan s Downovim sindromom, jer se nalazi na hromosomu 21, unutar ili blizu kritične regije Downovog sindroma na istom kraku. Vjeruje se da ova regija doprinosi kognitivnim defektima Downovog sindroma. Značajno povećanje broja inhibicijskih neurona [[[prednji mozak|prednjeg mozga]] koje se često opaža kod Ts65dn miša (mišji model trisomije 21) može dovesti do neravnoteže između ekscitacije i inhibicije i abnormalnosti u ponašanju. Međutim, genetičko smanjenje OLIG2 i OLIG1, sa tri kopije na dvije, spasilo je prekomjernu proizvodnju interneurona, što ukazuje na ključnu ulogu nivoa ekspresije OLIG2 u Downovom sindromu.^[23] Povezanost između OLIG2 i nervnih bolesti (tj. shizofrenija i Alzheimerova bolest) je pod nadzorom, jer je nekoliko jednognukleotidnih polimorfizama (SNP) povezanih s ovim bolestima u OLIG2 identificirano analizom asocijacija širom genoma.^[24]^[25]

OLIG2 također ima funkcionalnu ulogu u popravci živaca. Studije su pokazale da se broj ćelija koje eksprimiraju OLIG2 povećao u leziji nakon korteksne ubodne rane, podržavajući ulogu OLIG2 u reaktivnoj gliozi.^[26] OLIG2 je također bio umiješan u stvaranje reaktivnih astrocita, vjerovatno na prolazan način ponovne ekspresije, ali mehanizmi nisu jasni.^[27]

Reference

^ ^a ^b ^c GRCh38: Ensembl release 89: ENSG00000205927 - Ensembl, maj 2017
^ ^a ^b ^c GRCm38: Ensembl release 89: ENSMUSG00000039830 - Ensembl, maj 2017
^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^ "OLIG2". Atlas of Genetics and Cytogenetics in Oncology and Hematology.
^ 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. S2CID 18323261.
^ 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.
^ 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.
^ 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.
^ 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.
^ 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.
^ 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. Bibcode:2013PLoSO...863512A. doi:10.1371/journal.pone.0063512. PMC 3661542. PMID 23717440.
^ 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.
^ 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.
^ 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.
^ 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.
^ 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.
^ 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.
^ 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.
^ 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.
^ 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. Bibcode:1977RSPSB.196..251B. doi:10.1098/rspb.1977.0040. PMID 16268. S2CID 1651311.
^ 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.
^ 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.
^ 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. Bibcode:2006PNAS..10312469G. doi:10.1073/pnas.0603029103. PMC 1567903. PMID 16891421.
^ 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. S2CID 9038729.
^ 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. Bibcode:2005PNAS..10218183B. doi:10.1073/pnas.0506535102. PMC 1312388. PMID 16330768.
^ 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. Bibcode:2008PNAS..105.3581B. doi:10.1073/pnas.0709002105. PMC 2265175. PMID 18299565.

Dopunska literatura

Sun T, Dong H, Wu L, Kane M, Rowitch DH, Stiles CD (Oct 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. 23 (29): 9547–56. doi:10.1523/JNEUROSCI.23-29-09547.2003. PMC 6740479. PMID 14573534.
Fukuda S, Kondo T, Takebayashi H, Taga T (Feb 2004). "Negative regulatory effect of an oligodendrocytic bHLH factor OLIG2 on the astrocytic differentiation pathway". Cell Death and Differentiation. 11 (2): 196–202. doi:10.1038/sj.cdd.4401332. PMID 14576772.
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.
Hori Y, Gu X, Xie X, Kim SK (Apr 2005). "Differentiation of insulin-producing cells from human neural progenitor cells". PLOS Medicine. 2 (4): e103. doi:10.1371/journal.pmed.0020103. PMC 1087208. PMID 15839736.
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.
Jakovcevski I, Zecevic N (Nov 2005). "Olig transcription factors are expressed in oligodendrocyte and neuronal cells in human fetal CNS". The Journal of Neuroscience. 25 (44): 10064–73. doi:10.1523/JNEUROSCI.2324-05.2005. PMC 6725798. PMID 16267213.
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 (Jan 2006). "Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes". Genome Research. 16 (1): 55–65. doi:10.1101/gr.4039406. PMC 1356129. PMID 16344560.
Sun T, Hafler BP, Kaing S, Kitada M, Ligon KL, Widlund HR, Yuk DI, Stiles CD, Rowitch DH (Apr 2006). "Evidence for motoneuron lineage-specific regulation of Olig2 in the vertebrate neural tube". Developmental Biology. 292 (1): 152–64. doi:10.1016/j.ydbio.2005.12.047. PMID 16469306.
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.
Wissmüller S, Kosian T, Wolf M, Finzsch M, Wegner M (2006). "The high-mobility-group domain of Sox proteins interacts with DNA-binding domains of many transcription factors". Nucleic Acids Research. 34 (6): 1735–44. doi:10.1093/nar/gkl105. PMC 1421504. PMID 16582099.
Ligon KL, Kesari S, Kitada M, Sun T, Arnett HA, Alberta JA, Anderson DJ, Stiles CD, Rowitch DH (May 2006). "Development of NG2 neural progenitor cells requires Olig gene function". Proceedings of the National Academy of Sciences of the United States of America. 103 (20): 7853–8. Bibcode:2006PNAS..103.7853L. doi:10.1073/pnas.0511001103. PMC 1472534. PMID 16682644.
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. Bibcode:2006PNAS..10312469G. doi:10.1073/pnas.0603029103. PMC 1567903. PMID 16891421.
Ruf N, Martelli M, Weschke B, Uhlenberg B (Apr 2007). "Oligodendroglial transcription factor (OLIG1 and OLIG2) mutations are not associated with Pelizaeus-Merzbacher-like leukodystrophy". American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics. 144B (3): 365–6. doi:10.1002/ajmg.b.30434. PMID 17171653. S2CID 25663863.

Vanjski linkovi

OLIG2 protein, human na US National Library of Medicine Medical Subject Headings (MeSH)
OLIG2 lokacija ljudskog genoma UCSC Genome Browser.

OLIG2 detalji ljudskog genoma u UCSC Genome Browser.

Ovaj članak uključuje tekst iz Nacionalne medicinske biblioteke Sjedinjenih Država, koji je u javnom vlasništvu.

[refGRCh38Ensembl-1] GRCh38: Ensembl release 89: ENSG00000205927 - Ensembl, maj 2017

[refGRCm38Ensembl-2] GRCm38: Ensembl release 89: ENSMUSG00000039830 - Ensembl, maj 2017

[3] "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[4] "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[5] "OLIG2". Atlas of Genetics and Cytogenetics in Oncology and Hematology.

[6] 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. S2CID 18323261.

[7] 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.

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