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<!-- The PBB_Controls template provides controls for Protein Box Bot, please see Template:PBB_Controls for details. -->
{{Infobox_gene}}
{{PBB_Controls
'''Zinc finger protein ZIC2''' is a [[protein]] that in humans is encoded by the ''ZIC2'' [[gene]].<ref name="pmid9771712">{{cite journal | vauthors = Brown SA, Warburton D, Brown LY, Yu CY, Roeder ER, Stengel-Rutkowski S, Hennekam RC, Muenke M | title = Holoprosencephaly due to mutations in ZIC2, a homologue of Drosophila odd-paired | journal = Nat Genet | volume = 20 | issue = 2 | pages = 180–3 | year = 1998 | pmid = 9771712 | pmc =  | doi = 10.1038/2484 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: ZIC2 Zic family member 2 (odd-paired homolog, Drosophila)| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=7546| accessdate = }}</ref> ZIC2 is a member of the ''Zi''nc finger of the ''c''erebellum (ZIC) [[protein]] family.<ref name="pmid22964024">{{cite journal | vauthors = Ali RG, Bellchambers HM, Arkell RM | title = Zinc finger of the cerebellum (Zic): Transcription factors and co-factors | journal = Int J Biochem Cell Biol | volume =  44| issue = 11 | pages = 2065–8 | date = November 2012 | pmid = 22964024 | pmc = | doi = 10.1016/j.biocel.2012.08.012 }}</ref>
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| update_protein_box = yes
| update_summary = yes
| update_citations = yes
}}


<!-- The GNF_Protein_box is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
== Function ==
{{GNF_Protein_box
| image =
| image_source =
| PDB =
| Name = Zic family member 2 (odd-paired homolog, Drosophila)
| HGNCid = 12873
| Symbol = ZIC2
| AltSymbols =; HPE5
| OMIM = 603073
| ECnumber = 
| Homologene = 5171
| MGIid = 106679
| GeneAtlas_image1 = PBB_GE_ZIC2_gnf1h00103_at_tn.png
| Function = {{GNF_GO|id=GO:0003677 |text = DNA binding}} {{GNF_GO|id=GO:0005249 |text = voltage-gated potassium channel activity}} {{GNF_GO|id=GO:0005515 |text = protein binding}} {{GNF_GO|id=GO:0008270 |text = zinc ion binding}} {{GNF_GO|id=GO:0046872 |text = metal ion binding}}
| Component = {{GNF_GO|id=GO:0005622 |text = intracellular}} {{GNF_GO|id=GO:0005634 |text = nucleus}} {{GNF_GO|id=GO:0008076 |text = voltage-gated potassium channel complex}}
| Process = {{GNF_GO|id=GO:0001843 |text = neural tube closure}} {{GNF_GO|id=GO:0006813 |text = potassium ion transport}} {{GNF_GO|id=GO:0007275 |text = multicellular organismal development}} {{GNF_GO|id=GO:0007420 |text = brain development}} {{GNF_GO|id=GO:0030154 |text = cell differentiation}} {{GNF_GO|id=GO:0048066 |text = pigmentation during development}}
| Orthologs = {{GNF_Ortholog_box
    | Hs_EntrezGene = 7546
    | Hs_Ensembl = ENSG00000043355
    | Hs_RefseqProtein = NP_009060
    | Hs_RefseqmRNA = NM_007129
    | Hs_GenLoc_db = 
    | Hs_GenLoc_chr = 13
    | Hs_GenLoc_start = 99432294
    | Hs_GenLoc_end = 99437019
    | Hs_Uniprot = O95409
    | Mm_EntrezGene = 22772
    | Mm_Ensembl = ENSMUSG00000061524
    | Mm_RefseqmRNA = XM_981175
    | Mm_RefseqProtein = XP_986269
    | Mm_GenLoc_db = 
    | Mm_GenLoc_chr = 14
    | Mm_GenLoc_start = 121610615
    | Mm_GenLoc_end = 121615032
    | Mm_Uniprot = Q8BQC1
  }}
}}
'''Zic family member 2 (odd-paired homolog, Drosophila)''', also known as '''ZIC2''', is a human [[gene]].<ref name="entrez">{{cite web | title = Entrez Gene: ZIC2 Zic family member 2 (odd-paired homolog, Drosophila)| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=7546| accessdate = }}</ref>


<!-- The PBB_Summary template is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
ZIC2 is classified as a ZIC protein due to conservation of the five C2H2 [[zinc finger]]s, which enables the protein to interact with DNA and proteins.<ref name="entrez"/>
{{PBB_Summary
 
| section_title =  
== Clinical significance ==
| summary_text = This gene encodes a member of the ZIC family of C2H2-type zinc finger proteins. This protein functions as a transcriptional repressor and may regulate tissue specific expression of dopamine receptor D1. Mutations in this gene cause holoprosencephaly type 5. Holoprosencephaly is the most common structural anomaly of the human brain. A polyhistidine tract polymorphism in this gene may be associated with increased risk of neural tube defects. This gene is closely linked to a gene encoding zinc finger protein of the cerebellum 5, a related family member on chromosome 13.<ref name="entrez">{{cite web | title = Entrez Gene: ZIC2 Zic family member 2 (odd-paired homolog, Drosophila)| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=7546| accessdate = }}</ref>
 
}}
Correct function of these proteins is critical for early development, and as such mutations of the genes encoding these proteins is known to result in various congenital defects. For example, mutation of ''ZIC2'' is known to result in [[holoprosencephaly]] due to defect in the function of the organizer region (node), which leads to a defective anterior notochord (ANC). The ANC provides a maintenance signal to the [[Prechordal plate]] (PCP), thus a defective ANC results in degradation of the PCP, which is normally responsible for sending a [[Sonic hedgehog|shh]] signal to the developing forebrain resulting in the formation of the two hemispheres.<ref name="pmid18617531">{{cite journal | vauthors = Warr N, Powles-Glover N, Chappell A, Robson J, Norris D, Arkell RM | title = Zic2-associated holoprosencephaly is caused by a transient defect in the organizer region during gastrulation | journal = Hum Mol Genet | volume = 17 | issue = 19 | pages = 2986–96 | date = October 2008 | pmid = 18617531 | pmc =  | doi = 10.1093/hmg/ddn197 }}</ref>  [[Holoprosencephaly]] is the most common structural anomaly of the human forebrain.
 
Recently ZIC2 has also been shown to be critical for establishment of the left-right axis, thus loss of ZIC2 function can result in defects in heart formation.<ref name="pmid24585447">{{cite journal | vauthors = Barratt KS, Glanville-Jones HC, Arkell RM | title = The Zic2 gene directs the formation and function of node cilia to control cardiac situs. | journal = Genesis | volume = 52 | issue = 6 | pages = 626–35 | date = Jun 2013 | pmid = 24585447 | pmc =  | doi = 10.1002/dvg.22767 }}</ref> Another member of the ZIC family, [[ZIC3]], has previously been linked to establishment of the left-right axis.
 
A polyhistidine tract polymorphism in this gene may be associated with increased risk of neural tube defects ([[spina bifida]]). This gene is closely linked to a gene encoding ZIC5, a related family member on chromosome 13.<ref name="entrez"/>
 
== Interactions ==
 
ZIC2 has recently been found to interact with TCF7L2, enabling it to act as a Wnt/β-catenin  signalling inhibitor.<ref name=pmid21908606>{{cite journal | vauthors = Pourebrahim R, Houtmeyers R, Ghogomu S, Janssens S, Thelie A, Tran HT, Langenberg T, Vleminckx K, Bellefroid E, Cassiman JJ, Tejpar S | title = Transcription factor Zic2 inhibits Wnt/β-catenin protein signaling. | journal = J Biol Chem | volume = 286 | issue = 43 | pages = 37732–40 | date = October 2011 | pmid = 21908606 | pmc = 3199516 | doi = 10.1074/jbc.M111.242826 }}</ref> Such a role is of critical importance, as not only is correct Wnt signalling critical for early development,<ref name=pmid21228006 >{{cite journal | vauthors = Fossat N, Jones V, Khoo PL, Bogani D, Hardy A, Steiner K, Mukhopadhyay M, Westphal H, Nolan PM, Arkell R, Tam PP | title = Stringent requirement of a proper level of canonical WNT signalling activity for head formation in mouse embryo. | journal = Development | volume = 138 | issue = 4 | pages = 667–76 | date = February 2011 | pmid = 21228006 | pmc =  | doi = 10.1242/dev.052803 }}</ref> Wnt signalling has also been found to be upregulated to several cancers. ZIC2 has also been shown to [[Protein-protein interaction|interact]] with [[GLI3]].<ref name=pmid11238441>{{cite journal | vauthors = Koyabu Y, Nakata K, Mizugishi K, Aruga J, Mikoshiba K | title = Physical and functional interactions between Zic and Gli proteins | journal = J. Biol. Chem. | volume = 276 | issue = 10 | pages = 6889–92 | date = March 2001 | pmid = 11238441 | doi = 10.1074/jbc.C000773200 }}</ref>
 
== References ==
{{Reflist}}


==References==
{{reflist|2}}
==Further reading==
==Further reading==
{{refbegin | 2}}
{{Refbegin | 2}}
{{PBB_Further_reading
*{{cite journal | vauthors = Houtmeyers R, Souopgui J, Tejpar S, Arkell R | title = The ZIC gene family encodes multi-functional proteins essential for patterning and morphogenesis. | journal = Cell Mol Life Sci | volume = 70 | issue = 20 | pages = 3791–811 | year = 2013 | pmid = 23443491 | doi = 10.1007/s00018-013-1285-5 }}
| citations =  
*{{cite journal | vauthors = Brown S, Gersen S, Anyane-Yeboa K, Warburton D | title = Preliminary definition of a "critical region" of chromosome 13 in q32: report of 14 cases with 13q deletions and review of the literature. | journal = Am. J. Med. Genet. | volume = 45 | issue = 1 | pages = 52–9 | year = 1993 | pmid = 8418661 | doi = 10.1002/ajmg.1320450115 }}
*{{cite journal | author=Brown S, Gersen S, Anyane-Yeboa K, Warburton D |title=Preliminary definition of a "critical region" of chromosome 13 in q32: report of 14 cases with 13q deletions and review of the literature. |journal=Am. J. Med. Genet. |volume=45 |issue= 1 |pages= 52-9 |year= 1993 |pmid= 8418661 |doi= 10.1002/ajmg.1320450115 }}
*{{cite journal | vauthors = Brown LY, Odent S, David V, Blayau M, Dubourg C, Apacik C, Delgado MA, Hall BD, Reynolds JF, Sommer A, Wieczorek D, Brown SA, Muenke M | title = Holoprosencephaly due to mutations in ZIC2: alanine tract expansion mutations may be caused by parental somatic recombination | journal = Hum. Mol. Genet. | volume = 10 | issue = 8 | pages = 791–6 | year = 2001 | pmid = 11285244 | doi = 10.1093/hmg/10.8.791 }}
*{{cite journal | author=Aruga J, Nagai T, Tokuyama T, ''et al.'' |title=The mouse zic gene family. Homologues of the Drosophila pair-rule gene odd-paired. |journal=J. Biol. Chem. |volume=271 |issue= 2 |pages= 1043-7 |year= 1996 |pmid= 8557628 |doi=  }}
*{{cite journal | vauthors = Dubourg C, Lazaro L, Pasquier L, Bendavid C, Blayau M, Le Duff F, Durou MR, Odent S, David V | title = Molecular screening of SHH, ZIC2, SIX3, and TGIF genes in patients with features of holoprosencephaly spectrum: Mutation review and genotype-phenotype correlations | journal = Hum. Mutat. | volume = 24 | issue = 1 | pages = 43–51 | year = 2004 | pmid = 15221788 | doi = 10.1002/humu.20056 }}
*{{cite journal  | author=Brown SA, Warburton D, Brown LY, ''et al.'' |title=Holoprosencephaly due to mutations in ZIC2, a homologue of Drosophila odd-paired. |journal=Nat. Genet. |volume=20 |issue= 2 |pages= 180-3 |year= 1998 |pmid= 9771712 |doi= 10.1038/2484 }}
*{{cite journal | vauthors = Brown L, Paraso M, Arkell R, Brown S | title = In vitro analysis of partial loss-of-function ZIC2 mutations in holoprosencephaly: alanine tract expansion modulates DNA binding and transactivation | journal = Hum. Mol. Genet. | volume = 14 | issue = 3 | pages = 411–20 | year = 2005 | pmid = 15590697 | doi = 10.1093/hmg/ddi037 }}
*{{cite journal  | author=Yang Y, Hwang CK, Junn E, ''et al.'' |title=ZIC2 and Sp3 repress Sp1-induced activation of the human D1A dopamine receptor gene. |journal=J. Biol. Chem. |volume=275 |issue= 49 |pages= 38863-9 |year= 2001 |pmid= 10984499 |doi= 10.1074/jbc.M007906200 }}
*{{cite journal | vauthors = Ishiguro A, Ideta M, Mikoshiba K, Chen DJ, Aruga J | title = ZIC2-dependent transcriptional regulation is mediated by DNA-dependent protein kinase, poly(ADP-ribose) polymerase, and RNA helicase A | journal = J. Biol. Chem. | volume = 282 | issue = 13 | pages = 9983–95 | year = 2007 | pmid = 17251188 | doi = 10.1074/jbc.M610821200 }}
*{{cite journal  | author=Salero E, Pérez-Sen R, Aruga J, ''et al.'' |title=Transcription factors Zic1 and Zic2 bind and transactivate the apolipoprotein E gene promoter. |journal=J. Biol. Chem. |volume=276 |issue= 3 |pages= 1881-8 |year= 2001 |pmid= 11038359 |doi= 10.1074/jbc.M007008200 }}
{{Refend}}
*{{cite journal  | author=Koyabu Y, Nakata K, Mizugishi K, ''et al.'' |title=Physical and functional interactions between Zic and Gli proteins. |journal=J. Biol. Chem. |volume=276 |issue= 10 |pages= 6889-92 |year= 2001 |pmid= 11238441 |doi= 10.1074/jbc.C000773200 }}
 
*{{cite journal  | author=Brown LY, Odent S, David V, ''et al.'' |title=Holoprosencephaly due to mutations in ZIC2: alanine tract expansion mutations may be caused by parental somatic recombination. |journal=Hum. Mol. Genet. |volume=10 |issue= 8 |pages= 791-6 |year= 2001 |pmid= 11285244 |doi=  }}
*{{cite journal  | author=Brown LY, Hodge SE, Johnson WG, ''et al.'' |title=Possible association of NTDs with a polyhistidine tract polymorphism in the ZIC2 gene. |journal=Am. J. Med. Genet. |volume=108 |issue= 2 |pages= 128-31 |year= 2002 |pmid= 11857562 |doi=  }}
*{{cite journal  | author=Marcorelles P, Loget P, Fallet-Bianco C, ''et al.'' |title=Unusual variant of holoprosencephaly in monosomy 13q. |journal=Pediatr. Dev. Pathol. |volume=5 |issue= 2 |pages= 170-8 |year= 2002 |pmid= 11910512 |doi= 10.1007/s10024-001-0200-5 }}
*{{cite journal  | author=Herrera E, Brown L, Aruga J, ''et al.'' |title=Zic2 patterns binocular vision by specifying the uncrossed retinal projection. |journal=Cell |volume=114 |issue= 5 |pages= 545-57 |year= 2003 |pmid= 13678579 |doi=  }}
*{{cite journal  | author=Dunham A, Matthews LH, Burton J, ''et al.'' |title=The DNA sequence and analysis of human chromosome 13. |journal=Nature |volume=428 |issue= 6982 |pages= 522-8 |year= 2004 |pmid= 15057823 |doi= 10.1038/nature02379 }}
*{{cite journal | author=Dubourg C, Lazaro L, Pasquier L, ''et al.'' |title=Molecular screening of SHH, ZIC2, SIX3, and TGIF genes in patients with features of holoprosencephaly spectrum: Mutation review and genotype-phenotype correlations. |journal=Hum. Mutat. |volume=24 |issue= 1 |pages= 43-51 |year= 2004 |pmid= 15221788 |doi= 10.1002/humu.20056 }}
*{{cite journal | author=Brown L, Paraso M, Arkell R, Brown S |title=In vitro analysis of partial loss-of-function ZIC2 mutations in holoprosencephaly: alanine tract expansion modulates DNA binding and transactivation. |journal=Hum. Mol. Genet. |volume=14 |issue= 3 |pages= 411-20 |year= 2005 |pmid= 15590697 |doi= 10.1093/hmg/ddi037 }}
*{{cite journal | author=Ishiguro A, Ideta M, Mikoshiba K, ''et al.'' |title=ZIC2-dependent transcriptional regulation is mediated by DNA-dependent protein kinase, poly(ADP-ribose) polymerase, and RNA helicase A. |journal=J. Biol. Chem. |volume=282 |issue= 13 |pages= 9983-95 |year= 2007 |pmid= 17251188 |doi= 10.1074/jbc.M610821200 }}
}}
{{refend}}


{{protein-stub}}
{{Gene-13-stub}}
{{WikiDoc Sources}}

Latest revision as of 11:33, 9 January 2019

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez

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Ensembl

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UniProt

n/a

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RefSeq (mRNA)

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RefSeq (protein)

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Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

Zinc finger protein ZIC2 is a protein that in humans is encoded by the ZIC2 gene.[1][2] ZIC2 is a member of the Zinc finger of the cerebellum (ZIC) protein family.[3]

Function

ZIC2 is classified as a ZIC protein due to conservation of the five C2H2 zinc fingers, which enables the protein to interact with DNA and proteins.[2]

Clinical significance

Correct function of these proteins is critical for early development, and as such mutations of the genes encoding these proteins is known to result in various congenital defects. For example, mutation of ZIC2 is known to result in holoprosencephaly due to defect in the function of the organizer region (node), which leads to a defective anterior notochord (ANC). The ANC provides a maintenance signal to the Prechordal plate (PCP), thus a defective ANC results in degradation of the PCP, which is normally responsible for sending a shh signal to the developing forebrain resulting in the formation of the two hemispheres.[4] Holoprosencephaly is the most common structural anomaly of the human forebrain.

Recently ZIC2 has also been shown to be critical for establishment of the left-right axis, thus loss of ZIC2 function can result in defects in heart formation.[5] Another member of the ZIC family, ZIC3, has previously been linked to establishment of the left-right axis.

A polyhistidine tract polymorphism in this gene may be associated with increased risk of neural tube defects (spina bifida). This gene is closely linked to a gene encoding ZIC5, a related family member on chromosome 13.[2]

Interactions

ZIC2 has recently been found to interact with TCF7L2, enabling it to act as a Wnt/β-catenin signalling inhibitor.[6] Such a role is of critical importance, as not only is correct Wnt signalling critical for early development,[7] Wnt signalling has also been found to be upregulated to several cancers. ZIC2 has also been shown to interact with GLI3.[8]

References

  1. ↑ Brown SA, Warburton D, Brown LY, Yu CY, Roeder ER, Stengel-Rutkowski S, Hennekam RC, Muenke M (1998). "Holoprosencephaly due to mutations in ZIC2, a homologue of Drosophila odd-paired". Nat Genet. 20 (2): 180–3. doi:10.1038/2484. PMID 9771712.
  2. ↑ 2.0 2.1 2.2 "Entrez Gene: ZIC2 Zic family member 2 (odd-paired homolog, Drosophila)".
  3. ↑ Ali RG, Bellchambers HM, Arkell RM (November 2012). "Zinc finger of the cerebellum (Zic): Transcription factors and co-factors". Int J Biochem Cell Biol. 44 (11): 2065–8. doi:10.1016/j.biocel.2012.08.012. PMID 22964024.
  4. ↑ Warr N, Powles-Glover N, Chappell A, Robson J, Norris D, Arkell RM (October 2008). "Zic2-associated holoprosencephaly is caused by a transient defect in the organizer region during gastrulation". Hum Mol Genet. 17 (19): 2986–96. doi:10.1093/hmg/ddn197. PMID 18617531.
  5. ↑ Barratt KS, Glanville-Jones HC, Arkell RM (Jun 2013). "The Zic2 gene directs the formation and function of node cilia to control cardiac situs". Genesis. 52 (6): 626–35. doi:10.1002/dvg.22767. PMID 24585447.
  6. ↑ Pourebrahim R, Houtmeyers R, Ghogomu S, Janssens S, Thelie A, Tran HT, Langenberg T, Vleminckx K, Bellefroid E, Cassiman JJ, Tejpar S (October 2011). "Transcription factor Zic2 inhibits Wnt/β-catenin protein signaling". J Biol Chem. 286 (43): 37732–40. doi:10.1074/jbc.M111.242826. PMC 3199516. PMID 21908606.
  7. ↑ Fossat N, Jones V, Khoo PL, Bogani D, Hardy A, Steiner K, Mukhopadhyay M, Westphal H, Nolan PM, Arkell R, Tam PP (February 2011). "Stringent requirement of a proper level of canonical WNT signalling activity for head formation in mouse embryo". Development. 138 (4): 667–76. doi:10.1242/dev.052803. PMID 21228006.
  8. ↑ Koyabu Y, Nakata K, Mizugishi K, Aruga J, Mikoshiba K (March 2001). "Physical and functional interactions between Zic and Gli proteins". J. Biol. Chem. 276 (10): 6889–92. doi:10.1074/jbc.C000773200. PMID 11238441.

Further reading

  • Houtmeyers R, Souopgui J, Tejpar S, Arkell R (2013). "The ZIC gene family encodes multi-functional proteins essential for patterning and morphogenesis". Cell Mol Life Sci. 70 (20): 3791–811. doi:10.1007/s00018-013-1285-5. PMID 23443491.
  • Brown S, Gersen S, Anyane-Yeboa K, Warburton D (1993). "Preliminary definition of a "critical region" of chromosome 13 in q32: report of 14 cases with 13q deletions and review of the literature". Am. J. Med. Genet. 45 (1): 52–9. doi:10.1002/ajmg.1320450115. PMID 8418661.
  • Brown LY, Odent S, David V, Blayau M, Dubourg C, Apacik C, Delgado MA, Hall BD, Reynolds JF, Sommer A, Wieczorek D, Brown SA, Muenke M (2001). "Holoprosencephaly due to mutations in ZIC2: alanine tract expansion mutations may be caused by parental somatic recombination". Hum. Mol. Genet. 10 (8): 791–6. doi:10.1093/hmg/10.8.791. PMID 11285244.
  • Dubourg C, Lazaro L, Pasquier L, Bendavid C, Blayau M, Le Duff F, Durou MR, Odent S, David V (2004). "Molecular screening of SHH, ZIC2, SIX3, and TGIF genes in patients with features of holoprosencephaly spectrum: Mutation review and genotype-phenotype correlations". Hum. Mutat. 24 (1): 43–51. doi:10.1002/humu.20056. PMID 15221788.
  • Brown L, Paraso M, Arkell R, Brown S (2005). "In vitro analysis of partial loss-of-function ZIC2 mutations in holoprosencephaly: alanine tract expansion modulates DNA binding and transactivation". Hum. Mol. Genet. 14 (3): 411–20. doi:10.1093/hmg/ddi037. PMID 15590697.
  • Ishiguro A, Ideta M, Mikoshiba K, Chen DJ, Aruga J (2007). "ZIC2-dependent transcriptional regulation is mediated by DNA-dependent protein kinase, poly(ADP-ribose) polymerase, and RNA helicase A". J. Biol. Chem. 282 (13): 9983–95. doi:10.1074/jbc.M610821200. PMID 17251188.


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