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Transcription factor AP-2 beta

AP-2beta, TFAP2B, transcription factor AP-2beta, AP-2B
This gene encodes a member of the AP-2 family of transcription factors. AP-2 proteins form homo- or hetero-dimers with other AP-2 family members and bind specific DNA sequences. They are thought to stimulate cell proliferation and suppress terminal differentiation of specific cell types during embryonic development. Specific AP-2 family members differ in their expression patterns and binding affinity for different promoters. This protein functions as both a transcriptional activator and repressor. Mutations in this gene result in autosomal dominant Char syndrome, suggesting that this gene functions in the differentiation of neural crest cell derivatives. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: p15, fibrillin-1, CAN, FTO, AGE
Papers on AP-2beta
Genome-wide association analysis identifies three new susceptibility loci for childhood body mass index.
Bone Mineral Density in Childhood Study BMDCS et al., Copenhagen, Denmark. In Hum Mol Genet, Feb 2016
In total, 15 loci reached genome-wide significance (P-value < 5 × 10(-8)) in the joint discovery and replication analysis, of which 12 are previously identified loci in or close to ADCY3, GNPDA2, TMEM18, SEC16B, FAIM2, FTO, TFAP2B, TNNI3K, MC4R, GPR61, LMX1B and OLFM4 associated with adult body mass index or childhood obesity.
Single nucleotide polymorphisms in AGTR1, TFAP2B, and TRAF1 are not associated with the incidence of patent ductus arteriosus in Japanese preterm infants.
Saitoh et al., Nagoya, Japan. In Pediatr Int, Dec 2015
Single nucleotide polymorphisms (SNPs) in several genes, including angiotensin II receptor, type 1 (AGTR1), transcription factor AP-2 beta (TFAP2B) and TNF receptor-associated factor 1 (TRAF1), have been reported to be associated with the incidence of patent ductus arteriosus in preterm infants.
Transcription factor activating protein 2 beta (TFAP2B) mediates noradrenergic neuronal differentiation in neuroblastoma.
Fischer et al., Köln, Germany. In Mol Oncol, Dec 2015
We here investigated the role of transcription factor activating protein 2 beta (TFAP2B), a key factor in sympathetic nervous system development, in neuroblastoma pathogenesis and differentiation.
A transcriptome-based classifier to identify developmental toxicants by stem cell testing: design, validation and optimization for histone deacetylase inhibitors.
Leist et al., Dortmund, Germany. In Arch Toxicol, Sep 2015
Finally, optimization of the classifier based on 100 probe sets showed that eight genes (F2RL2, TFAP2B, EDNRA, FOXD3, SIX3, MT1E, ETS1 and LHX2) are sufficient to separate HDACi from mercurials.
Transcriptional analysis of human cranial compartments with different embryonic origins.
Cunningham et al., Seattle, United States. In Arch Oral Biol, Sep 2015
TFAP2A, TFAP2B, ICAM1, SULF1, TNC and FOXF2 were among differentially expressed genes.
Redon et al., Valencia, Spain. In J Hypertens, Jun 2015
The combined analysis of metabolomics and SNP data revealed an association between the metabolic profile of MS and genes polymorphism involved in the adiposity regulation and fatty acids metabolism: rs2272903_TT (TFAP2B), rs3803_TT (GATA2), rs174589_CC (FADS2) and rs174577_AA (FADS2).
Core promoter short tandem repeats as evolutionary switch codes for primate speciation.
Kazeminasab et al., Tehrān, Iran. In Am J Primatol, 2015
The identified genes are involved in important evolutionary and developmental processes, such as normal craniofacial development (TFAP2B), regulation of cell shape (PALMD), learning and long-term memory (RGS14), nervous system development (GFRA2), embryonic limb morphogenesis (PBX2), and forebrain development (APAF1).
Obesity susceptibility loci in Qataris, a highly consanguineous Arabian population.
Chouchane et al., Doha, Qatar. In J Transl Med, 2014
RESULTS: Two loci significantly associated with obesity in Qataris: the TFAP2B variation (rs987237) (A allele versus G allele: chi-square = 10.3;
What model organisms and interactomics can reveal about the genetics of human obesity.
Schiöth et al., Uppsala, Sweden. In Cell Mol Life Sci, 2012
Here, we searched biological databases and discovered 33 additional genes associated with human obesity (CADM2, GIPR, GPCR5B, LRP1B, NEGR1, NRXN3, SH2B1, FANCL, GNPDA2, HMGCR, MAP2K5, NUDT3, PRKD1, QPCTL, TNNI3K, MTCH2, DNAJC27, SLC39A8, MTIF3, RPL27A, SEC16B, ETV5, HMGA1, TFAP2B, TUB, ZNF608, FAIM2, KCTD15, LINGO2, POC5, PTBP2, TMEM18, TMEM160).
Meta-analysis identifies common variants associated with body mass index in east Asians.
Shu et al., Nashville, United States. In Nat Genet, 2012
Three additional loci nearly reached the genome-wide significance threshold, including two previously identified loci in the GNPDA2 and TFAP2B genes and a newly identified signal near PAX6, all of which were associated with BMI with P < 5.0 × 10(-7).
Mutations of TFAP2B in congenital heart disease patients in Mysore, South India.
Nallur et al., Mysore, India. In Indian J Med Res, 2011
The findings suggest the lack of involvement of known mutations of TFAP2B with syndromic or nonsyndromic CHDs in Mysore patients
Familial nonsyndromic patent ductus arteriosus caused by mutations in TFAP2B.
Li et al., Shanghai, China. In Pediatr Cardiol, 2011
TFAP2B mutation should be considered a risk factor for isolated PDA. However, the detailed genetic mechanism underlying nonsyndromic the PDA-causing TFAP2B mutation is yet to be elucidated.
[Role of TFAP2B and WntSB in adipose tissue].
Maeda et al., Japan. In Nihon Rinsho, 2011
It causes accumulation of neutral fats and causes insulin resistance through exaggerated glucose uptake independent of insulin and induces abnormal adipokine secretion, fat cell enlargement and insulin resistance.
Implications of central obesity-related variants in LYPLAL1, NRXN3, MSRA, and TFAP2B on quantitative metabolic traits in adult Danes.
Pedersen et al., Copenhagen, Denmark. In Plos One, 2010
central obesity-associated variants in LYPLAL1, NRXN3, MSRA, and TFAP2B
A heart-hand syndrome gene: Tfap2b plays a critical role in the development and remodeling of mouse ductus arteriosus and limb patterning.
Moser et al., New York City, United States. In Plos One, 2010
Tfap2b is associated with the development and remodeling of mouse ductus arteriosus and limb patterning.
[Dual role of transcription factor AP-2 in carcinogenesis].
Deng et al., Hangzhou, China. In Zhejiang Da Xue Xue Bao Yi Xue Ban, 2010
Five isoforms of AP-2 have been discovered, they are AP-2alpha, AP-2beta, AP-2gamma, AP-2delta and AP-2epsilon.
Insights into the pathogenesis and genetic background of patency of the ductus arteriosus.
Gittenberger-de Groot et al., Leiden, Netherlands. In Neonatology, 2010
Genetic research has identified the cause of syndromic forms of PDA, such as the TFAP2B mutations in Char syndrome.
Roles of AP-2 transcription factors in the regulation of cartilage and skeletal development.
Bosserhoff et al., Regensburg, Germany. In Febs J, 2010
This review gives an overview of AP-2s, and discusses the recent findings on the AP-2 family, in particular AP-2alpha, AP-2beta, and AP-2epsilon, as regulators of cartilage and skeletal development.
Char Syndrome
Gelb, Seattle, United States. In Unknown Journal, 2003
TFAP2B is the only gene in which mutations are known to cause Char syndrome.
Mutations in TFAP2B cause Char syndrome, a familial form of patent ductus arteriosus.
Gelb et al., New York City, United States. In Nat Genet, 2000
Using a positional candidacy strategy, we mapped TFAP2B, encoding a transcription factor expressed in neural crest cells, to the Char syndrome critical region and identified missense mutations altering conserved residues in two affected families.
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