TFAP2A: Difference between revisions

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{{Infobox_gene}}
{{PBB_Controls
'''Transcription factor AP-2 alpha''' (<u>A</u>ctivating enhancer binding <u>P</u>rotein <u>2</u> <u>alpha</u>), also known as '''TFAP2A''', is a [[protein]] that in humans is encoded by the ''TFAP2A'' [[gene]].<ref name="entrez">{{cite web | title = Entrez Gene: TFAP2A transcription factor AP-2 alpha (activating enhancer binding protein 2 alpha)| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=7020| accessdate = }}</ref>
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| update_protein_box = yes
| update_summary = yes
| update_citations = yes
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<!-- 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 = Transcription factor AP-2 alpha (activating enhancer binding protein 2 alpha)
| HGNCid = 11742
| Symbol = TFAP2A
| AltSymbols =; AP-2; AP-2alpha; AP2TF; TFAP2
| OMIM = 107580
| ECnumber = 
| Homologene = 2421
| MGIid = 104671
| GeneAtlas_image1 = PBB_GE_TFAP2A_204653_at_tn.png
| GeneAtlas_image2 = PBB_GE_TFAP2A_204654_s_at_tn.png
| GeneAtlas_image3 = PBB_GE_TFAP2A_210669_at_tn.png
| Function = {{GNF_GO|id=GO:0003700 |text = transcription factor activity}} {{GNF_GO|id=GO:0003705 |text = RNA polymerase II transcription factor activity, enhancer binding}} {{GNF_GO|id=GO:0003713 |text = transcription coactivator activity}} {{GNF_GO|id=GO:0046983 |text = protein dimerization activity}}
| Component = {{GNF_GO|id=GO:0005634 |text = nucleus}}
| Process = {{GNF_GO|id=GO:0006350 |text = transcription}} {{GNF_GO|id=GO:0006355 |text = regulation of transcription, DNA-dependent}} {{GNF_GO|id=GO:0006357 |text = regulation of transcription from RNA polymerase II promoter}} {{GNF_GO|id=GO:0007165 |text = signal transduction}} {{GNF_GO|id=GO:0007398 |text = ectoderm development}}
| Orthologs = {{GNF_Ortholog_box
    | Hs_EntrezGene = 7020
    | Hs_Ensembl = ENSG00000137203
    | Hs_RefseqProtein = NP_001027451
    | Hs_RefseqmRNA = NM_001032280
    | Hs_GenLoc_db = 
    | Hs_GenLoc_chr = 6
    | Hs_GenLoc_start = 10504906
    | Hs_GenLoc_end = 10527824
    | Hs_Uniprot = P05549
    | Mm_EntrezGene = 21418
    | Mm_Ensembl = ENSMUSG00000021359
    | Mm_RefseqmRNA = NM_011547
    | Mm_RefseqProtein = NP_035677
    | Mm_GenLoc_db = 
    | Mm_GenLoc_chr = 13
    | Mm_GenLoc_start = 40726649
    | Mm_GenLoc_end = 40745894
    | Mm_Uniprot = Q3UL09
  }}
}}
'''Transcription factor AP-2 alpha (activating enhancer binding protein 2 alpha)''', also known as '''TFAP2A''', is a human [[gene]].<ref name="entrez">{{cite web | title = Entrez Gene: TFAP2A transcription factor AP-2 alpha (activating enhancer binding protein 2 alpha)| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=7020| accessdate = }}</ref>


<!-- The PBB_Summary template is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
The AP-2 alpha protein acts as a sequence-specific DNA-binding [[transcription factor]] recognizing and binding to the specific DNA sequence and recruiting transcription machinery. Its binding site is a GC-rich sequence that is present in the [[cis-regulatory element|cis-regulatory]] regions of several viral and cellular genes.<ref name="pmid2010091"/> AP2-alpha is a 52-kD [[retinoic acid]]-inducible and developmentally regulated activator of transcription that binds to a consensus DNA-binding sequence GCCNNNGGC in the [[SV40]] and [[metallothionein]] promoters.<ref name="entrez" />
{{PBB_Summary
| section_title =
| summary_text = AP2-alpha is a 52-kD retinoic acid-inducible and developmentally regulated activator of transcription that binds to a consensus DNA-binding sequence CCCCAGGC in the SV40 and metallothionein (MIM 156350) promoters.[supplied by OMIM]<ref name="entrez">{{cite web | title = Entrez Gene: TFAP2A transcription factor AP-2 alpha (activating enhancer binding protein 2 alpha)| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=7020| accessdate = }}</ref>
}}


==See also==
AP-2 alpha is expressed in [[neural crest]] cell lineages with the highest levels of expression corresponding to early neural crest cells, suggesting that AP-2 alpha plays a role in their differentiation and development. Transcription factor AP-2 alpha is expressed in [[ectoderm]] and in neural-crest cells migrating from the cranial folds during closure of the neural tube in the mouse. Cranial neural crest cell provides [[regional specification|patterning]] information for [[craniofacial]] [[morphogenesis]] and  generate most of the skull bones and the [[cranial nerve ganglia|cranial ganglia]].<ref name="pmid2010091">{{cite journal | vauthors = Williams T, Tjian R | title = Analysis of the DNA-binding and activation properties of the human transcription factor AP-2 | journal = Genes & Development | volume = 5 | issue = 4 | pages = 670–82 | date = Apr 1991 | pmid = 2010091 | doi = 10.1101/gad.5.4.670 }}</ref><ref name="pmid3040262">{{cite journal | vauthors = Mitchell PJ, Wang C, Tjian R | title = Positive and negative regulation of transcription in vitro: enhancer-binding protein AP-2 is inhibited by SV40 T antigen | journal = Cell | volume = 50 | issue = 6 | pages = 847–61 | date = Sep 1987 | pmid = 3040262 | doi = 10.1016/0092-8674(87)90512-5 }}</ref><ref name="pmid3063603">{{cite journal | vauthors = Williams T, Admon A, Lüscher B, Tjian R | title = Cloning and expression of AP-2, a cell-type-specific transcription factor that activates inducible enhancer elements | journal = Genes & Development | volume = 2 | issue = 12A | pages = 1557–69 | date = Dec 1988 | pmid = 3063603 | doi = 10.1101/gad.2.12a.1557 }}</ref><ref name="pmid8365563">{{cite journal | vauthors = Le Douarin NM, Ziller C, Couly GF | title = Patterning of neural crest derivatives in the avian embryo: in vivo and in vitro studies | journal = Developmental Biology | volume = 159 | issue = 1 | pages = 24–49 | date = Sep 1993 | pmid = 8365563 | doi = 10.1006/dbio.1993.1219 }}</ref>
 
AP-2 alpha [[knockout mouse|knockout mice]] die [[Pregnancy#Perinatal period|perinatally]] with cranio-[[gastroschisis|abdominoschisis]] and severe dysmorphogenesis of the face, skull, sensory organs, and cranial ganglia.<ref name="pmid8622765">{{cite journal | vauthors = Schorle H, Meier P, Buchert M, Jaenisch R, Mitchell PJ | title = Transcription factor AP-2 essential for cranial closure and craniofacial development | journal = Nature | volume = 381 | issue = 6579 | pages = 235–8 | date = May 1996 | pmid = 8622765 | doi = 10.1038/381235a0 }}</ref>  [[Zygosity#Homozygous|Homozygous]] knockout mice also have neural tube defects followed by craniofacial and body wall abnormalities.<ref name="pmid8622766">{{cite journal | vauthors = Zhang J, Hagopian-Donaldson S, Serbedzija G, Elsemore J, Plehn-Dujowich D, McMahon AP, Flavell RA, Williams T | title = Neural tube, skeletal and body wall defects in mice lacking transcription factor AP-2 | journal = Nature | volume = 381 | issue = 6579 | pages = 238–41 | date = May 1996 | pmid = 8622766 | doi = 10.1038/381238a0 }}</ref> In vivo gene delivery of AP-2 alpha suppressed spontaneous intestinal polyps in the Apc(Min/+) mouse.<ref name="pmid19376641">{{cite journal | vauthors = Li Q, Löhr CV, Dashwood RH | title = Activator protein 2alpha suppresses intestinal tumorigenesis in the Apc(min) mouse | journal = Cancer Letters | volume = 283 | issue = 1 | pages = 36–42 | date = Sep 2009 | pmid = 19376641 | pmc = 2713803 | doi = 10.1016/j.canlet.2009.03.026 }}</ref> AP-2 alpha also functions as a master regulator of multiple transcription factors in the mouse liver.<ref name="pmid21682828">{{cite journal | vauthors = Li Q, Luo C, Löhr CV, Dashwood RH | title = Activator protein-2α functions as a master regulator of multiple transcription factors in the mouse liver | journal = Hepatology Research | volume = 41 | issue = 8 | pages = 776–83 | date = Aug 2011 | pmid = 21682828 | doi = 10.1111/j.1872-034X.2011.00827.x }}</ref>
 
In [[melanocytes|melanocytic]] cells TFAP2A gene expression may be regulated by [[Microphthalmia-associated transcription factor|MITF]].<ref name="pmid19067971">{{cite journal | vauthors = Hoek KS, Schlegel NC, Eichhoff OM, Widmer DS, Praetorius C, Einarsson SO, Valgeirsdottir S, Bergsteinsdottir K, Schepsky A, Dummer R, Steingrimsson E | title = Novel MITF targets identified using a two-step DNA microarray strategy | journal = Pigment Cell & Melanoma Research | volume = 21 | issue = 6 | pages = 665–76 | date = Dec 2008 | pmid = 19067971 | doi = 10.1111/j.1755-148X.2008.00505.x }}</ref>
 
== Clinical significance ==
 
Mutations in the TFAP2A gene cause Branchio-oculo-facial syndrome often with a midline [[cleft lip]].<ref>Dixon MJ, Marazita ML, Beaty TH, Murray JC (2011). "Cleft lip and palate: understanding genetic and environmental influences". Nature Reviews Genetics (12): 167-178.</ref> In a family with branchio-oculo-facial syndrome (BOFS),<ref name="OMIM113620">{{OMIM|113620}}</ref> a 3.2-Mb deletion at chromosome 6p24.3 was detected.<ref name="pmid18423521">{{cite journal | vauthors = Milunsky JM, Maher TA, Zhao G, Roberts AE, Stalker HJ, Zori RT, Burch MN, Clemens M, Mulliken JB, Smith R, Lin AE | title = TFAP2A mutations result in branchio-oculo-facial syndrome | journal = American Journal of Human Genetics | volume = 82 | issue = 5 | pages = 1171–7 | date = May 2008 | pmid = 18423521 | pmc = 2427243 | doi = 10.1016/j.ajhg.2008.03.005 }}</ref> Sequencing of candidate genes in that region in 4 additional unrelated BOFS patients revealed 4 different de novo missense mutations in the exons 4 and 5 of the TFAP2A gene.
 
A disruption of an AP-2 alpha binding site in an [[IRF6]] enhancer is associated with [[cleft lip]].<ref name="pmid18836445">{{cite journal | vauthors = Rahimov F, Marazita ML, Visel A, Cooper ME, Hitchler MJ, Rubini M, Domann FE, Govil M, Christensen K, Bille C, Melbye M, Jugessur A, Lie RT, Wilcox AJ, Fitzpatrick DR, Green ED, Mossey PA, Little J, Steegers-Theunissen RP, Pennacchio LA, Schutte BC, Murray JC | title = Disruption of an AP-2alpha binding site in an IRF6 enhancer is associated with cleft lip | journal = Nature Genetics | volume = 40 | issue = 11 | pages = 1341–7 | date = Nov 2008 | pmid = 18836445 | pmc = 2691688 | doi = 10.1038/ng.242 }}</ref>  Mutations in IRF6 gene cause [[Van der Woude syndrome]] (VWS)<ref name="OMIM119300">{{OMIM|119300}}</ref> that is a rare mendelian clefting autossomal dominant disorder with lower lip pits in 85% of affected individuals.<ref name="pmid12219090">{{cite journal | vauthors = Kondo S, Schutte BC, Richardson RJ, Bjork BC, Knight AS, Watanabe Y, Howard E, de Lima RL, Daack-Hirsch S, Sander A, McDonald-McGinn DM, Zackai EH, Lammer EJ, Aylsworth AS, Ardinger HH, Lidral AC, Pober BR, Moreno L, Arcos-Burgos M, Valencia C, Houdayer C, Bahuau M, Moretti-Ferreira D, Richieri-Costa A, Dixon MJ, Murray JC | title = Mutations in IRF6 cause Van der Woude and popliteal pterygium syndromes | journal = Nature Genetics | volume = 32 | issue = 2 | pages = 285–9 | date = Oct 2002 | pmid = 12219090 | pmc = 3169431 | doi = 10.1038/ng985 }}</ref> The remaining 15% of individuals with Van der Woude syndrome show only [[cleft lip]] and/or [[cleft palate]] (CL/P) and are clinically indistinguishable from the common non syndromic CL/P. NSCL/P occur in approximately 1/700 live births and is one of the most common form of congenital abnormalities. A previous association study between SNPs in and around IRF6 and NSCL/P have shown significant results in different populations<ref name="pmid15317890">{{cite journal | vauthors = Zucchero TM, Cooper ME, Maher BS, Daack-Hirsch S, Nepomuceno B, Ribeiro L, Caprau D, Christensen K, Suzuki Y, Machida J, Natsume N, Yoshiura K, Vieira AR, Orioli IM, Castilla EE, Moreno L, Arcos-Burgos M, Lidral AC, Field LL, Liu YE, Ray A, Goldstein TH, Schultz RE, Shi M, Johnson MK, Kondo S, Schutte BC, Marazita ML, Murray JC | title = Interferon regulatory factor 6 (IRF6) gene variants and the risk of isolated cleft lip or palate | journal = The New England Journal of Medicine | volume = 351 | issue = 8 | pages = 769–80 | date = Aug 2004 | pmid = 15317890 | doi = 10.1056/NEJMoa032909 }}</ref> and was independently replicated.<ref name="pmid15558496">{{cite journal | vauthors = Scapoli L, Palmieri A, Martinelli M, Pezzetti F, Carinci P, Tognon M, Carinci F | title = Strong evidence of linkage disequilibrium between polymorphisms at the IRF6 locus and nonsyndromic cleft lip with or without cleft palate, in an Italian population | journal = American Journal of Human Genetics | volume = 76 | issue = 1 | pages = 180–3 | date = Jan 2005 | pmid = 15558496 | pmc = 1196422 | doi = 10.1086/427344 }}</ref><ref name="pmid16096995">{{cite journal | vauthors = Blanton SH, Cortez A, Stal S, Mulliken JB, Finnell RH, Hecht JT | title = Variation in IRF6 contributes to nonsyndromic cleft lip and palate | journal = American Journal of Medical Genetics Part A | volume = 137A | issue = 3 | pages = 259–62 | date = Sep 2005 | pmid = 16096995 | doi = 10.1002/ajmg.a.30887 }}</ref><ref name="pmid16132054">{{cite journal | vauthors = Ghassibé M, Bayet B, Revencu N, Verellen-Dumoulin C, Gillerot Y, Vanwijck R, Vikkula M | title = Interferon regulatory factor-6: a gene predisposing to isolated cleft lip with or without cleft palate in the Belgian population | journal = European Journal of Human Genetics | volume = 13 | issue = 11 | pages = 1239–42 | date = Nov 2005 | pmid = 16132054 | doi = 10.1038/sj.ejhg.5201486 }}</ref><ref name="pmid17438386">{{cite journal | vauthors = Park JW, McIntosh I, Hetmanski JB, Jabs EW, Vander Kolk CA, Wu-Chou YH, Chen PK, Chong SS, Yeow V, Jee SH, Park BY, Fallin MD, Ingersoll R, Scott AF, Beaty TH | title = Association between IRF6 and nonsyndromic cleft lip with or without cleft palate in four populations | journal = Genetics in Medicine | volume = 9 | issue = 4 | pages = 219–27 | date = Apr 2007 | pmid = 17438386 | pmc = 2846512 | doi = 10.1097/GIM.0b013e3180423cca }}</ref>
 
A search of NSCL/P cases for potential regulatory elements for IRF6 gene was made aligning genomic sequences to a 500 Kb region encompassing IRF6 from 17 vertebrate species. Human sequence as reference and searched for multispecies conserved sequences (MCSs). Regions contained in introns 5’ and 3’ flanking IRF6 were screened by direct sequencing for potential causative variants in 184 NSCL/P cases.  The rare allele of the SNP rs642961 showed a significant association with cleft lip cases. Analysis of transcription factor binding site analysis showed that the risk allele disrupt a binding site for AP-2 alpha.<ref name="pmid18836445" />
 
Mutations in the AP-2 alpha gene also cause branchio-oculo-facial syndrome,<ref name="pmid18423521" /> which has overlapping features with Van der Woude syndrome such as orofacial clefting and occasional lip pits what make rs642961 a good candidate for an etiological variant. These findings show that IRF6 and AP-2 alpha are in the same developmental pathway and identify a variant in a regulatory region that contributes substantially to a common complex disorder.
 
== Interactions ==
 
TFAP2A has been shown to [[Protein-protein interaction|interact]] with:
* [[APC (gene)|APC]]<ref name="pmid15331612">{{cite journal | vauthors = Li Q, Dashwood RH | title = Activator protein 2alpha associates with adenomatous polyposis coli/beta-catenin and Inhibits beta-catenin/T-cell factor transcriptional activity in colorectal cancer cells | journal = The Journal of Biological Chemistry | volume = 279 | issue = 44 | pages = 45669–75 | date = Oct 2004 | pmid = 15331612 | pmc = 2276578 | doi = 10.1074/jbc.M405025200 }}</ref>
* [[CITED2]]<ref name=pmid12586840/><ref name="pmid11744733">{{cite journal | vauthors = Bragança J, Swingler T, Marques FI, Jones T, Eloranta JJ, Hurst HC, Shioda T, Bhattacharya S | title = Human CREB-binding protein/p300-interacting transactivator with ED-rich tail (CITED) 4, a new member of the CITED family, functions as a co-activator for transcription factor AP-2 | journal = The Journal of Biological Chemistry | volume = 277 | issue = 10 | pages = 8559–65 | date = Mar 2002 | pmid = 11744733 | doi = 10.1074/jbc.M110850200 }}</ref>
* [[DEK (gene)|DEK]]<ref name="pmid12595566">{{cite journal | vauthors = Campillos M, García MA, Valdivieso F, Vázquez J | title = Transcriptional activation by AP-2alpha is modulated by the oncogene DEK | journal = Nucleic Acids Research | volume = 31 | issue = 5 | pages = 1571–5 | date = Mar 2003 | pmid = 12595566 | pmc = 149840 | doi = 10.1093/nar/gkg247 }}</ref>
* [[EP300]]<ref name="pmid12586840">{{cite journal | vauthors = Bragança J, Eloranta JJ, Bamforth SD, Ibbitt JC, Hurst HC, Bhattacharya S | title = Physical and functional interactions among AP-2 transcription factors, p300/CREB-binding protein, and CITED2 | journal = The Journal of Biological Chemistry | volume = 278 | issue = 18 | pages = 16021–9 | date = May 2003 | pmid = 12586840 | doi = 10.1074/jbc.M208144200 }}</ref>
* [[Myc]]<ref name="pmid7729426">{{cite journal | vauthors = Gaubatz S, Imhof A, Dosch R, Werner O, Mitchell P, Buettner R, Eilers M | title = Transcriptional activation by Myc is under negative control by the transcription factor AP-2 | journal = The EMBO Journal | volume = 14 | issue = 7 | pages = 1508–19 | date = Apr 1995 | pmid = 7729426 | pmc = 398238 | doi =  }}</ref> and
* [[P53]].<ref name="pmid12226108">{{cite journal | vauthors = McPherson LA, Loktev AV, Weigel RJ | title = Tumor suppressor activity of AP2alpha mediated through a direct interaction with p53 | journal = The Journal of Biological Chemistry | volume = 277 | issue = 47 | pages = 45028–33 | date = Nov 2002 | pmid = 12226108 | doi = 10.1074/jbc.M208924200 }}</ref>
 
== See also ==
* [[Activating protein 2]]
* [[Activating protein 2]]
* [[Branchio-oculo-facial syndrome]]


==References==
== References ==
{{reflist|2}}
{{reflist|33em}}


==Further reading==
== Further reading ==
{{refbegin | 2}}
{{refbegin|33em}}
{{PBB_Further_reading
* {{cite journal | vauthors = Murphy JE, Keen JH | title = Recognition sites for clathrin-associated proteins AP-2 and AP-3 on clathrin triskelia | journal = The Journal of Biological Chemistry | volume = 267 | issue = 15 | pages = 10850–5 | date = May 1992 | pmid = 1587861 | doi =  }}
| citations =
* {{cite journal | vauthors = Gaynor RB, Muchardt C, Xia YR, Klisak I, Mohandas T, Sparkes RS, Lusis AJ | title = Localization of the gene for the DNA-binding protein AP-2 to human chromosome 6p22.3-pter | journal = Genomics | volume = 10 | issue = 4 | pages = 1100–2 | date = Aug 1991 | pmid = 1916817 | doi = 10.1016/0888-7543(91)90209-W }}
*{{cite journal | author=Murphy JE, Keen JH |title=Recognition sites for clathrin-associated proteins AP-2 and AP-3 on clathrin triskelia. |journal=J. Biol. Chem. |volume=267 |issue= 15 |pages= 10850-5 |year= 1992 |pmid= 1587861 |doi=  }}
* {{cite journal | vauthors = Williams T, Tjian R | title = Characterization of a dimerization motif in AP-2 and its function in heterologous DNA-binding proteins | journal = Science | volume = 251 | issue = 4997 | pages = 1067–71 | date = Mar 1991 | pmid = 1998122 | doi = 10.1126/science.1998122 }}
*{{cite journal | author=Gaynor RB, Muchardt C, Xia YR, ''et al.'' |title=Localization of the gene for the DNA-binding protein AP-2 to human chromosome 6p22.3-pter. |journal=Genomics |volume=10 |issue= 4 |pages= 1100-2 |year= 1991 |pmid= 1916817 |doi= }}
* {{cite journal | vauthors = Williams T, Tjian R | title = Analysis of the DNA-binding and activation properties of the human transcription factor AP-2 | journal = Genes & Development | volume = 5 | issue = 4 | pages = 670–82 | date = Apr 1991 | pmid = 2010091 | doi = 10.1101/gad.5.4.670 }}
*{{cite journal | author=Williams T, Tjian R |title=Characterization of a dimerization motif in AP-2 and its function in heterologous DNA-binding proteins. |journal=Science |volume=251 |issue= 4997 |pages= 1067-71 |year= 1991 |pmid= 1998122 |doi= }}
* {{cite journal | vauthors = Williams T, Admon A, Lüscher B, Tjian R | title = Cloning and expression of AP-2, a cell-type-specific transcription factor that activates inducible enhancer elements | journal = Genes & Development | volume = 2 | issue = 12A | pages = 1557–69 | date = Dec 1988 | pmid = 3063603 | doi = 10.1101/gad.2.12a.1557 }}
*{{cite journal | author=Williams T, Tjian R |title=Analysis of the DNA-binding and activation properties of the human transcription factor AP-2. |journal=Genes Dev. |volume=5 |issue= 4 |pages= 670-82 |year= 1991 |pmid= 2010091 |doi= }}
* {{cite journal | vauthors = Bauer R, Imhof A, Pscherer A, Kopp H, Moser M, Seegers S, Kerscher M, Tainsky MA, Hofstaedter F, Buettner R | title = The genomic structure of the human AP-2 transcription factor | journal = Nucleic Acids Research | volume = 22 | issue = 8 | pages = 1413–20 | date = Apr 1994 | pmid = 8190633 | pmc = 307999 | doi = 10.1093/nar/22.8.1413 }}
*{{cite journal | author=Williams T, Admon A, Lüscher B, Tjian R |title=Cloning and expression of AP-2, a cell-type-specific transcription factor that activates inducible enhancer elements. |journal=Genes Dev. |volume=2 |issue= 12A |pages= 1557-69 |year= 1989 |pmid= 3063603 |doi= }}
* {{cite journal | vauthors = Buettner R, Kannan P, Imhof A, Bauer R, Yim SO, Glockshuber R, Van Dyke MW, Tainsky MA | title = An alternatively spliced mRNA from the AP-2 gene encodes a negative regulator of transcriptional activation by AP-2 | journal = Molecular and Cellular Biology | volume = 13 | issue = 7 | pages = 4174–85 | date = Jul 1993 | pmid = 8321221 | pmc = 359967 | doi =  10.1128/mcb.13.7.4174}}
*{{cite journal | author=Bauer R, Imhof A, Pscherer A, ''et al.'' |title=The genomic structure of the human AP-2 transcription factor. |journal=Nucleic Acids Res. |volume=22 |issue= 8 |pages= 1413-20 |year= 1994 |pmid= 8190633 |doi= }}
* {{cite journal | vauthors = Williamson JA, Bosher JM, Skinner A, Sheer D, Williams T, Hurst HC | title = Chromosomal mapping of the human and mouse homologues of two new members of the AP-2 family of transcription factors | journal = Genomics | volume = 35 | issue = 1 | pages = 262–4 | date = Jul 1996 | pmid = 8661133 | doi = 10.1006/geno.1996.0351 }}
*{{cite journal | author=Buettner R, Kannan P, Imhof A, ''et al.'' |title=An alternatively spliced mRNA from the AP-2 gene encodes a negative regulator of transcriptional activation by AP-2. |journal=Mol. Cell. Biol. |volume=13 |issue= 7 |pages= 4174-85 |year= 1993 |pmid= 8321221 |doi=  }}
* {{cite journal | vauthors = Pirozzi G, McConnell SJ, Uveges AJ, Carter JM, Sparks AB, Kay BK, Fowlkes DM | title = Identification of novel human WW domain-containing proteins by cloning of ligand targets | journal = The Journal of Biological Chemistry | volume = 272 | issue = 23 | pages = 14611–6 | date = Jun 1997 | pmid = 9169421 | doi = 10.1074/jbc.272.23.14611 }}
*{{cite journal | author=Williamson JA, Bosher JM, Skinner A, ''et al.'' |title=Chromosomal mapping of the human and mouse homologues of two new members of the AP-2 family of transcription factors. |journal=Genomics |volume=35 |issue= 1 |pages= 262-4 |year= 1996 |pmid= 8661133 |doi= 10.1006/geno.1996.0351 }}
* {{cite journal | vauthors = Batsché E, Muchardt C, Behrens J, Hurst HC, Crémisi C | title = RB and c-Myc activate expression of the E-cadherin gene in epithelial cells through interaction with transcription factor AP-2 | journal = Molecular and Cellular Biology | volume = 18 | issue = 7 | pages = 3647–58 | date = Jul 1998 | pmid = 9632747 | pmc = 108947 | doi =  10.1128/mcb.18.7.3647}}
*{{cite journal | author=Pirozzi G, McConnell SJ, Uveges AJ, ''et al.'' |title=Identification of novel human WW domain-containing proteins by cloning of ligand targets. |journal=J. Biol. Chem. |volume=272 |issue= 23 |pages= 14611-6 |year= 1997 |pmid= 9169421 |doi= }}
* {{cite journal | vauthors = Mertens PR, Alfonso-Jaume MA, Steinmann K, Lovett DH | title = A synergistic interaction of transcription factors AP2 and YB-1 regulates gelatinase A enhancer-dependent transcription | journal = The Journal of Biological Chemistry | volume = 273 | issue = 49 | pages = 32957–65 | date = Dec 1998 | pmid = 9830047 | doi = 10.1074/jbc.273.49.32957 }}
*{{cite journal | author=Batsché E, Muchardt C, Behrens J, ''et al.'' |title=RB and c-Myc activate expression of the E-cadherin gene in epithelial cells through interaction with transcription factor AP-2. |journal=Mol. Cell. Biol. |volume=18 |issue= 7 |pages= 3647-58 |year= 1998 |pmid= 9632747 |doi=  }}
* {{cite journal | vauthors = García MA, Campillos M, Marina A, Valdivieso F, Vázquez J | title = Transcription factor AP-2 activity is modulated by protein kinase A-mediated phosphorylation | journal = FEBS Letters | volume = 444 | issue = 1 | pages = 27–31 | date = Feb 1999 | pmid = 10037142 | doi = 10.1016/S0014-5793(99)00021-6 }}
*{{cite journal | author=Mertens PR, Alfonso-Jaume MA, Steinmann K, Lovett DH |title=A synergistic interaction of transcription factors AP2 and YB-1 regulates gelatinase A enhancer-dependent transcription. |journal=J. Biol. Chem. |volume=273 |issue= 49 |pages= 32957-65 |year= 1999 |pmid= 9830047 |doi= }}
* {{cite journal | vauthors = Rosenthal JA, Chen H, Slepnev VI, Pellegrini L, Salcini AE, Di Fiore PP, De Camilli P | title = The epsins define a family of proteins that interact with components of the clathrin coat and contain a new protein module | journal = The Journal of Biological Chemistry | volume = 274 | issue = 48 | pages = 33959–65 | date = Nov 1999 | pmid = 10567358 | doi = 10.1074/jbc.274.48.33959 }}
*{{cite journal | author=García MA, Campillos M, Marina A, ''et al.'' |title=Transcription factor AP-2 activity is modulated by protein kinase A-mediated phosphorylation. |journal=FEBS Lett. |volume=444 |issue= 1 |pages= 27-31 |year= 1999 |pmid= 10037142 |doi= }}
* {{cite journal | vauthors = Heicklen-Klein A, Ginzburg I | title = Tau promoter confers neuronal specificity and binds Sp1 and AP-2 | journal = Journal of Neurochemistry | volume = 75 | issue = 4 | pages = 1408–18 | date = Oct 2000 | pmid = 10987820 | doi = 10.1046/j.1471-4159.2000.0751408.x }}
*{{cite journal | author=Rosenthal JA, Chen H, Slepnev VI, ''et al.'' |title=The epsins define a family of proteins that interact with components of the clathrin coat and contain a new protein module. |journal=J. Biol. Chem. |volume=274 |issue= 48 |pages= 33959-65 |year= 1999 |pmid= 10567358 |doi= }}
* {{cite journal | vauthors = Nyormoi O, Wang Z, Doan D, Ruiz M, McConkey D, Bar-Eli M | title = Transcription factor AP-2alpha is preferentially cleaved by caspase 6 and degraded by proteasome during tumor necrosis factor alpha-induced apoptosis in breast cancer cells | journal = Molecular and Cellular Biology | volume = 21 | issue = 15 | pages = 4856–67 | date = Aug 2001 | pmid = 11438643 | pmc = 87191 | doi = 10.1128/MCB.21.15.4856-4867.2001 }}
*{{cite journal | author=Heicklen-Klein A, Ginzburg I |title=Tau promoter confers neuronal specificity and binds Sp1 and AP-2. |journal=J. Neurochem. |volume=75 |issue= 4 |pages= 1408-18 |year= 2000 |pmid= 10987820 |doi= }}
* {{cite journal | vauthors = Rao DS, Chang JC, Kumar PD, Mizukami I, Smithson GM, Bradley SV, Parlow AF, Ross TS | title = Huntingtin interacting protein 1 Is a clathrin coat binding protein required for differentiation of late spermatogenic progenitors | journal = Molecular and Cellular Biology | volume = 21 | issue = 22 | pages = 7796–806 | date = Nov 2001 | pmid = 11604514 | pmc = 99949 | doi = 10.1128/MCB.21.22.7796-7806.2001 }}
*{{cite journal | author=Nyormoi O, Wang Z, Doan D, ''et al.'' |title=Transcription factor AP-2alpha is preferentially cleaved by caspase 6 and degraded by proteasome during tumor necrosis factor alpha-induced apoptosis in breast cancer cells. |journal=Mol. Cell. Biol. |volume=21 |issue= 15 |pages= 4856-67 |year= 2001 |pmid= 11438643 |doi= 10.1128/MCB.21.15.4856-4867.2001 }}
* {{cite journal | vauthors = Bragança J, Swingler T, Marques FI, Jones T, Eloranta JJ, Hurst HC, Shioda T, Bhattacharya S | title = Human CREB-binding protein/p300-interacting transactivator with ED-rich tail (CITED) 4, a new member of the CITED family, functions as a co-activator for transcription factor AP-2 | journal = The Journal of Biological Chemistry | volume = 277 | issue = 10 | pages = 8559–65 | date = Mar 2002 | pmid = 11744733 | doi = 10.1074/jbc.M110850200 }}
*{{cite journal | author=Rao DS, Chang JC, Kumar PD, ''et al.'' |title=Huntingtin interacting protein 1 Is a clathrin coat binding protein required for differentiation of late spermatogenic progenitors. |journal=Mol. Cell. Biol. |volume=21 |issue= 22 |pages= 7796-806 |year= 2001 |pmid= 11604514 |doi= 10.1128/MCB.21.22.7796-7806.2001 }}
* {{cite journal | vauthors = Mertens PR, Steinmann K, Alfonso-Jaume MA, En-Nia A, Sun Y, Lovett DH | title = Combinatorial interactions of p53, activating protein-2, and YB-1 with a single enhancer element regulate gelatinase A expression in neoplastic cells | journal = The Journal of Biological Chemistry | volume = 277 | issue = 28 | pages = 24875–82 | date = Jul 2002 | pmid = 11973333 | doi = 10.1074/jbc.M200445200 }}
*{{cite journal | author=Bragança J, Swingler T, Marques FI, ''et al.'' |title=Human CREB-binding protein/p300-interacting transactivator with ED-rich tail (CITED) 4, a new member of the CITED family, functions as a co-activator for transcription factor AP-2. |journal=J. Biol. Chem. |volume=277 |issue= 10 |pages= 8559-65 |year= 2002 |pmid= 11744733 |doi= 10.1074/jbc.M110850200 }}
* {{cite journal | vauthors = Eloranta JJ, Hurst HC | title = Transcription factor AP-2 interacts with the SUMO-conjugating enzyme UBC9 and is sumolated in vivo | journal = The Journal of Biological Chemistry | volume = 277 | issue = 34 | pages = 30798–804 | date = Aug 2002 | pmid = 12072434 | doi = 10.1074/jbc.M202780200 }}
*{{cite journal | author=Mertens PR, Steinmann K, Alfonso-Jaume MA, ''et al.'' |title=Combinatorial interactions of p53, activating protein-2, and YB-1 with a single enhancer element regulate gelatinase A expression in neoplastic cells. |journal=J. Biol. Chem. |volume=277 |issue= 28 |pages= 24875-82 |year= 2002 |pmid= 11973333 |doi= 10.1074/jbc.M200445200 }}
* {{cite journal | vauthors = Ben-Zimra M, Koler M, Orly J | title = Transcription of cholesterol side-chain cleavage cytochrome P450 in the placenta: activating protein-2 assumes the role of steroidogenic factor-1 by binding to an overlapping promoter element | journal = Molecular Endocrinology | volume = 16 | issue = 8 | pages = 1864–80 | date = Aug 2002 | pmid = 12145340 | doi = 10.1210/me.2002-0056 }}
*{{cite journal | author=Eloranta JJ, Hurst HC |title=Transcription factor AP-2 interacts with the SUMO-conjugating enzyme UBC9 and is sumolated in vivo. |journal=J. Biol. Chem. |volume=277 |issue= 34 |pages= 30798-804 |year= 2002 |pmid= 12072434 |doi= 10.1074/jbc.M202780200 }}
*{{cite journal | author=Ben-Zimra M, Koler M, Orly J |title=Transcription of cholesterol side-chain cleavage cytochrome P450 in the placenta: activating protein-2 assumes the role of steroidogenic factor-1 by binding to an overlapping promoter element. |journal=Mol. Endocrinol. |volume=16 |issue= 8 |pages= 1864-80 |year= 2003 |pmid= 12145340 |doi= }}
}}
{{refend}}
{{refend}}


== External links ==
== External links ==
* [https://www.ncbi.nlm.nih.gov/books/NBK55063/  GeneReviews/NCBI/NIH/UW entry on Branchiooculofacial Syndrome]
* {{MeshName|TFAP2A+protein,+human}}
* {{MeshName|TFAP2A+protein,+human}}
* {{FactorBook|AP-2alpha}}
* {{UCSC genome browser|TFAP2A}}
* {{UCSC gene details|TFAP2A}}
{{NLM content}}
{{Transcription factors|g1}}


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

Revision as of 11:46, 15 September 2017

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Orthologs
SpeciesHumanMouse
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Transcription factor AP-2 alpha (Activating enhancer binding Protein 2 alpha), also known as TFAP2A, is a protein that in humans is encoded by the TFAP2A gene.[1]

Function

The AP-2 alpha protein acts as a sequence-specific DNA-binding transcription factor recognizing and binding to the specific DNA sequence and recruiting transcription machinery. Its binding site is a GC-rich sequence that is present in the cis-regulatory regions of several viral and cellular genes.[2] AP2-alpha is a 52-kD retinoic acid-inducible and developmentally regulated activator of transcription that binds to a consensus DNA-binding sequence GCCNNNGGC in the SV40 and metallothionein promoters.[1]

AP-2 alpha is expressed in neural crest cell lineages with the highest levels of expression corresponding to early neural crest cells, suggesting that AP-2 alpha plays a role in their differentiation and development. Transcription factor AP-2 alpha is expressed in ectoderm and in neural-crest cells migrating from the cranial folds during closure of the neural tube in the mouse. Cranial neural crest cell provides patterning information for craniofacial morphogenesis and generate most of the skull bones and the cranial ganglia.[2][3][4][5]

AP-2 alpha knockout mice die perinatally with cranio-abdominoschisis and severe dysmorphogenesis of the face, skull, sensory organs, and cranial ganglia.[6] Homozygous knockout mice also have neural tube defects followed by craniofacial and body wall abnormalities.[7] In vivo gene delivery of AP-2 alpha suppressed spontaneous intestinal polyps in the Apc(Min/+) mouse.[8] AP-2 alpha also functions as a master regulator of multiple transcription factors in the mouse liver.[9]

In melanocytic cells TFAP2A gene expression may be regulated by MITF.[10]

Clinical significance

Mutations in the TFAP2A gene cause Branchio-oculo-facial syndrome often with a midline cleft lip.[11] In a family with branchio-oculo-facial syndrome (BOFS),[12] a 3.2-Mb deletion at chromosome 6p24.3 was detected.[13] Sequencing of candidate genes in that region in 4 additional unrelated BOFS patients revealed 4 different de novo missense mutations in the exons 4 and 5 of the TFAP2A gene.

A disruption of an AP-2 alpha binding site in an IRF6 enhancer is associated with cleft lip.[14] Mutations in IRF6 gene cause Van der Woude syndrome (VWS)[15] that is a rare mendelian clefting autossomal dominant disorder with lower lip pits in 85% of affected individuals.[16] The remaining 15% of individuals with Van der Woude syndrome show only cleft lip and/or cleft palate (CL/P) and are clinically indistinguishable from the common non syndromic CL/P. NSCL/P occur in approximately 1/700 live births and is one of the most common form of congenital abnormalities. A previous association study between SNPs in and around IRF6 and NSCL/P have shown significant results in different populations[17] and was independently replicated.[18][19][20][21]

A search of NSCL/P cases for potential regulatory elements for IRF6 gene was made aligning genomic sequences to a 500 Kb region encompassing IRF6 from 17 vertebrate species. Human sequence as reference and searched for multispecies conserved sequences (MCSs). Regions contained in introns 5’ and 3’ flanking IRF6 were screened by direct sequencing for potential causative variants in 184 NSCL/P cases. The rare allele of the SNP rs642961 showed a significant association with cleft lip cases. Analysis of transcription factor binding site analysis showed that the risk allele disrupt a binding site for AP-2 alpha.[14]

Mutations in the AP-2 alpha gene also cause branchio-oculo-facial syndrome,[13] which has overlapping features with Van der Woude syndrome such as orofacial clefting and occasional lip pits what make rs642961 a good candidate for an etiological variant. These findings show that IRF6 and AP-2 alpha are in the same developmental pathway and identify a variant in a regulatory region that contributes substantially to a common complex disorder.

Interactions

TFAP2A has been shown to interact with:

See also

References

  1. ↑ 1.0 1.1 "Entrez Gene: TFAP2A transcription factor AP-2 alpha (activating enhancer binding protein 2 alpha)".
  2. ↑ 2.0 2.1 Williams T, Tjian R (Apr 1991). "Analysis of the DNA-binding and activation properties of the human transcription factor AP-2". Genes & Development. 5 (4): 670–82. doi:10.1101/gad.5.4.670. PMID 2010091.
  3. ↑ Mitchell PJ, Wang C, Tjian R (Sep 1987). "Positive and negative regulation of transcription in vitro: enhancer-binding protein AP-2 is inhibited by SV40 T antigen". Cell. 50 (6): 847–61. doi:10.1016/0092-8674(87)90512-5. PMID 3040262.
  4. ↑ Williams T, Admon A, Lüscher B, Tjian R (Dec 1988). "Cloning and expression of AP-2, a cell-type-specific transcription factor that activates inducible enhancer elements". Genes & Development. 2 (12A): 1557–69. doi:10.1101/gad.2.12a.1557. PMID 3063603.
  5. ↑ Le Douarin NM, Ziller C, Couly GF (Sep 1993). "Patterning of neural crest derivatives in the avian embryo: in vivo and in vitro studies". Developmental Biology. 159 (1): 24–49. doi:10.1006/dbio.1993.1219. PMID 8365563.
  6. ↑ Schorle H, Meier P, Buchert M, Jaenisch R, Mitchell PJ (May 1996). "Transcription factor AP-2 essential for cranial closure and craniofacial development". Nature. 381 (6579): 235–8. doi:10.1038/381235a0. PMID 8622765.
  7. ↑ Zhang J, Hagopian-Donaldson S, Serbedzija G, Elsemore J, Plehn-Dujowich D, McMahon AP, Flavell RA, Williams T (May 1996). "Neural tube, skeletal and body wall defects in mice lacking transcription factor AP-2". Nature. 381 (6579): 238–41. doi:10.1038/381238a0. PMID 8622766.
  8. ↑ Li Q, Löhr CV, Dashwood RH (Sep 2009). "Activator protein 2alpha suppresses intestinal tumorigenesis in the Apc(min) mouse". Cancer Letters. 283 (1): 36–42. doi:10.1016/j.canlet.2009.03.026. PMC 2713803. PMID 19376641.
  9. ↑ Li Q, Luo C, Löhr CV, Dashwood RH (Aug 2011). "Activator protein-2α functions as a master regulator of multiple transcription factors in the mouse liver". Hepatology Research. 41 (8): 776–83. doi:10.1111/j.1872-034X.2011.00827.x. PMID 21682828.
  10. ↑ Hoek KS, Schlegel NC, Eichhoff OM, Widmer DS, Praetorius C, Einarsson SO, Valgeirsdottir S, Bergsteinsdottir K, Schepsky A, Dummer R, Steingrimsson E (Dec 2008). "Novel MITF targets identified using a two-step DNA microarray strategy". Pigment Cell & Melanoma Research. 21 (6): 665–76. doi:10.1111/j.1755-148X.2008.00505.x. PMID 19067971.
  11. ↑ Dixon MJ, Marazita ML, Beaty TH, Murray JC (2011). "Cleft lip and palate: understanding genetic and environmental influences". Nature Reviews Genetics (12): 167-178.
  12. ↑ Online Mendelian Inheritance in Man (OMIM) 113620
  13. ↑ 13.0 13.1 Milunsky JM, Maher TA, Zhao G, Roberts AE, Stalker HJ, Zori RT, Burch MN, Clemens M, Mulliken JB, Smith R, Lin AE (May 2008). "TFAP2A mutations result in branchio-oculo-facial syndrome". American Journal of Human Genetics. 82 (5): 1171–7. doi:10.1016/j.ajhg.2008.03.005. PMC 2427243. PMID 18423521.
  14. ↑ 14.0 14.1 Rahimov F, Marazita ML, Visel A, Cooper ME, Hitchler MJ, Rubini M, Domann FE, Govil M, Christensen K, Bille C, Melbye M, Jugessur A, Lie RT, Wilcox AJ, Fitzpatrick DR, Green ED, Mossey PA, Little J, Steegers-Theunissen RP, Pennacchio LA, Schutte BC, Murray JC (Nov 2008). "Disruption of an AP-2alpha binding site in an IRF6 enhancer is associated with cleft lip". Nature Genetics. 40 (11): 1341–7. doi:10.1038/ng.242. PMC 2691688. PMID 18836445.
  15. ↑ Online Mendelian Inheritance in Man (OMIM) 119300
  16. ↑ Kondo S, Schutte BC, Richardson RJ, Bjork BC, Knight AS, Watanabe Y, Howard E, de Lima RL, Daack-Hirsch S, Sander A, McDonald-McGinn DM, Zackai EH, Lammer EJ, Aylsworth AS, Ardinger HH, Lidral AC, Pober BR, Moreno L, Arcos-Burgos M, Valencia C, Houdayer C, Bahuau M, Moretti-Ferreira D, Richieri-Costa A, Dixon MJ, Murray JC (Oct 2002). "Mutations in IRF6 cause Van der Woude and popliteal pterygium syndromes". Nature Genetics. 32 (2): 285–9. doi:10.1038/ng985. PMC 3169431. PMID 12219090.
  17. ↑ Zucchero TM, Cooper ME, Maher BS, Daack-Hirsch S, Nepomuceno B, Ribeiro L, Caprau D, Christensen K, Suzuki Y, Machida J, Natsume N, Yoshiura K, Vieira AR, Orioli IM, Castilla EE, Moreno L, Arcos-Burgos M, Lidral AC, Field LL, Liu YE, Ray A, Goldstein TH, Schultz RE, Shi M, Johnson MK, Kondo S, Schutte BC, Marazita ML, Murray JC (Aug 2004). "Interferon regulatory factor 6 (IRF6) gene variants and the risk of isolated cleft lip or palate". The New England Journal of Medicine. 351 (8): 769–80. doi:10.1056/NEJMoa032909. PMID 15317890.
  18. ↑ Scapoli L, Palmieri A, Martinelli M, Pezzetti F, Carinci P, Tognon M, Carinci F (Jan 2005). "Strong evidence of linkage disequilibrium between polymorphisms at the IRF6 locus and nonsyndromic cleft lip with or without cleft palate, in an Italian population". American Journal of Human Genetics. 76 (1): 180–3. doi:10.1086/427344. PMC 1196422. PMID 15558496.
  19. ↑ Blanton SH, Cortez A, Stal S, Mulliken JB, Finnell RH, Hecht JT (Sep 2005). "Variation in IRF6 contributes to nonsyndromic cleft lip and palate". American Journal of Medical Genetics Part A. 137A (3): 259–62. doi:10.1002/ajmg.a.30887. PMID 16096995.
  20. ↑ Ghassibé M, Bayet B, Revencu N, Verellen-Dumoulin C, Gillerot Y, Vanwijck R, Vikkula M (Nov 2005). "Interferon regulatory factor-6: a gene predisposing to isolated cleft lip with or without cleft palate in the Belgian population". European Journal of Human Genetics. 13 (11): 1239–42. doi:10.1038/sj.ejhg.5201486. PMID 16132054.
  21. ↑ Park JW, McIntosh I, Hetmanski JB, Jabs EW, Vander Kolk CA, Wu-Chou YH, Chen PK, Chong SS, Yeow V, Jee SH, Park BY, Fallin MD, Ingersoll R, Scott AF, Beaty TH (Apr 2007). "Association between IRF6 and nonsyndromic cleft lip with or without cleft palate in four populations". Genetics in Medicine. 9 (4): 219–27. doi:10.1097/GIM.0b013e3180423cca. PMC 2846512. PMID 17438386.
  22. ↑ Li Q, Dashwood RH (Oct 2004). "Activator protein 2alpha associates with adenomatous polyposis coli/beta-catenin and Inhibits beta-catenin/T-cell factor transcriptional activity in colorectal cancer cells". The Journal of Biological Chemistry. 279 (44): 45669–75. doi:10.1074/jbc.M405025200. PMC 2276578. PMID 15331612.
  23. ↑ 23.0 23.1 Bragança J, Eloranta JJ, Bamforth SD, Ibbitt JC, Hurst HC, Bhattacharya S (May 2003). "Physical and functional interactions among AP-2 transcription factors, p300/CREB-binding protein, and CITED2". The Journal of Biological Chemistry. 278 (18): 16021–9. doi:10.1074/jbc.M208144200. PMID 12586840.
  24. ↑ Bragança J, Swingler T, Marques FI, Jones T, Eloranta JJ, Hurst HC, Shioda T, Bhattacharya S (Mar 2002). "Human CREB-binding protein/p300-interacting transactivator with ED-rich tail (CITED) 4, a new member of the CITED family, functions as a co-activator for transcription factor AP-2". The Journal of Biological Chemistry. 277 (10): 8559–65. doi:10.1074/jbc.M110850200. PMID 11744733.
  25. ↑ Campillos M, García MA, Valdivieso F, Vázquez J (Mar 2003). "Transcriptional activation by AP-2alpha is modulated by the oncogene DEK". Nucleic Acids Research. 31 (5): 1571–5. doi:10.1093/nar/gkg247. PMC 149840. PMID 12595566.
  26. ↑ Gaubatz S, Imhof A, Dosch R, Werner O, Mitchell P, Buettner R, Eilers M (Apr 1995). "Transcriptional activation by Myc is under negative control by the transcription factor AP-2". The EMBO Journal. 14 (7): 1508–19. PMC 398238. PMID 7729426.
  27. ↑ McPherson LA, Loktev AV, Weigel RJ (Nov 2002). "Tumor suppressor activity of AP2alpha mediated through a direct interaction with p53". The Journal of Biological Chemistry. 277 (47): 45028–33. doi:10.1074/jbc.M208924200. PMID 12226108.

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

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