Ask about this productRelated genes to: TFAP2A antibody
- Gene:
- TFAP2A NIH gene
- Name:
- transcription factor AP-2 alpha
- Previous symbol:
- TFAP2, AP2TF
- Synonyms:
- AP-2
- Chromosome:
- 6p24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-12
- Date modifiied:
- 2016-04-06
Related products to: TFAP2A antibody
Related articles to: TFAP2A antibody
- Long-term exposure to low-dose food contact materials (FCMs) has raised concerns regarding developmental toxicity. In the present study, we prioritized FCMs with potential developmental toxicity using a weight-of-evidence computational model, which predicted 127 chemicals to be of high concern. From these, we selected 7 chemicals-representing both high and low concern categories-and evaluated their potential embryotoxicity using the mouse embryonic stem cell test (mEST). Among the selected chemicals, thiram most strongly inhibited cardiac differentiation in mEST. We further examined the effects of thiram on morphology and expression of differentiation-related genes in mouse embryonic stem cells (mESCs). Treatment with thiram inhibited 50% early differentiation in mESCs, suppressed the expression of markers associated with the three-germ layers, but increased the expression of neurectoderm markers during early embryogenesis. Additionally, treatment with 20 ng/mL thiram, which was the lowest-observed-effect concentration of cytotoxicity, disrupted neuronal differentiation in both mESCs and human pluripotent embryonal carcinoma NT2 cells. Finally, based on transcriptome analysis, 20 and 30 ng/mL thiram disrupted the neural crest differentiation pathway, altering the expression of genes including homeobox A1 (HOXA1), homeobox B1 (HOXB1), Heart And Neural Crest Derivatives Expressed 1 (HAND1), Distal-Less Homeobox 5 (DLX5), and transcription factor AP-2 alpha (TFAP2A) in NT2 cells. Therefore, disruption of neural crest differentiation is one of the potential mechanisms underlying thiram-induced embryotoxicity. The integrated alternative approach adopted in the present study to identify mechanism-based biomarkers for thiram-induced embryotoxicity in a human-relevant model could facilitate safety assessment for data-poor chemicals in future. - Source: PubMed
Publication date: 2026/04/21
Ho Chia-ChiTung Chun-WeiYen B LinjuWeng Chen-YiHsu Ju-HsinTsai Ming-HsienArrokhman SalimLin Pinpin - Understanding the factors that shape population genetic structure is crucial for advancing evolutionary studies and developing effective management and conservation strategies. The northern pike (Esox lucius L.) is a top teleost predator that inhabits fresh and brackish water environments in the northern hemisphere. Pike populations in the brackish Baltic Sea typically display strong genetic structuring, with coastal sympatric populations that separate during spring for spawning in either shallow, sheltered brackish bays or in freshwater tributaries and wetlands. In contrast to the Baltic Sea, genomic structuring in freshwater environments, particularly in large lacustrine systems, remains poorly understood. To address this gap, we used restriction site-associated DNA-sequencing to assess the genetic structure and diversity of northern pike in two ecologically contrasting habitats: freshwater Vänern Lake, Sweden (8932 single nucleotide polimorphisms [SNPs]), and the brackish Baltic Sea around Saaremaa, Estonia (6899 SNPs). The results show strong genetic structuring and lower genetic diversity in brackish environment compared to the higher genetic diversity and extremely low genetic structuring observed in freshwater habitat. We found no evidence of divergent selection within environments. However, we identified 187 outlier SNPs and 62 outlier genes distinguishing the brackish and freshwater environments, potentially reflecting adaptation to salinity. Notably, several of these genes are associated with key biological processes, including osmotic stress regulation (akap13), early development (tfap2a) and pathogens response (tlr18). From a fisheries management perspective, our results indicate that the freshwater system can be managed as a single stock, while strong population structuring among Baltic coastal pike likely requires either large-scale solutions and/or population-specific fine-scale management efforts to maintain the genetic and life-history diversity among brackish coastal pike populations. - Source: PubMed
Publication date: 2026/03/30
Diaz-Suarez AlfonsoLópez María-EugeniaSundblad GöranVasemägi Anti - To explore the role of ferroptosis in the process of corneal epithelial repair and to elucidate the underlying molecular regulatory mechanisms. - Source: PubMed
Publication date: 2026/03/23
Jiang HanyiChen ZhiweiLuan WenkangLi JiaYin Ningbei - Both short and long sleep duration have been associated with poor glycemic control and an increased risk of developing type 2 diabetes mellitus. Although sleep duration may differentially modify the effects of genetic risk factors for type 2 diabetes, this has not been systematically investigated. In the present study, we conducted genome-wide gene by sleep duration meta-analyses, separately assessing interactions of short and long sleep, for fasting glucose, fasting insulin, and hemoglobin A1c in up to 489,309 individuals without diabetes from seven different population groups. In total, 16 loci were identified to interact with sleep duration - six with short sleep and ten with long sleep. Of these, four loci were identified through cross-population meta-analysis. Mapped genes exhibit pathway connections to pericyte apoptosis, NMDA receptor activity, the GLUT1 receptor, neurological health, and sleep architecture. Eleven loci () have not been reported in previous glycemic trait genome-wide association studies. Interaction loci identify divergent biological mechanisms for short and long sleep duration influencing glycemic control, suggesting specific pathways of intervention for precision medicine approaches to diabetes prevention and management. - Source: PubMed
Publication date: 2026/03/03
Wang HemingNagarajan PavithraMiller Clint LBentley Amy RNoordam RaymondWesterman Kenneth EBrown Michael RKraja Aldi TO'Connell Jeffrey RSchwander KarenLi ChangweiSanghvi Mihir MSong YipeiBartz Traci MBraunack-Mayer VincentChen LingDu JiawenDunca DianaFeitosa Mary FGudmundsdottir ValborgGuo XiuqingHarris Sarah EHighland Heather MHuang ZhijieKang ChanghoonLakka Timo ALefevre ChristopheLuan Jian'anLyytikäinen Leo-PekkaMissikpode CelestinMorrison John LPalmer Nicholette DRichmond AnneShahisavandi MinaTang Jingxianvan der Most Peter JWeiss StefanYu ChenglongZhu WanyingAnsari Md Abu YusufAnugu PramodAschard HuguesAshok KaavyaAttia John RBazzano Lydia ACade Brian ECampbell ArchieDimitrov Latchezar MDo AnhFaquih TariqFinesilverSmith Sandy LFisher-Hoch Susan PFretts Amanda MGharib Sina AGoodarzi Mark OGraff MariaelisaGu CharlesHanson PaulHe JiangHeikkinen SamiHixson JamesHsu SarahKähönen MikaKho MinjungKim HyunjuKomulainen PirjoLauner Lenore JLemaitre Rozenn N McNeil John JMcCormick Joseph BNolte Ilja MRaffield Laura MRaitakari Olli TRamírez JuliaRiha Renata LRisch MartinRisch LorenzRuss Tom CSarnowski ChloéSchram Miranda TScott Rodney JSofer TamarSun QuanVölker UweVölzke HenryWang Yujievan Dijk Ko WillemsWood Alexis CYoung Kristin LZhang RuiyuanZhu XiaofengBelow Jennifer EConen DavidCox Simon RFox Ervin RFranceschini NoraGhanbari MohsenGrabe Hans JörgenGudnason VilmundurHayward CarolineHolliday Elizabeth GJaquish Cashell ELacaze PaulLee SeunggeunLehtimäki TerhoLiu Ching-TiMorrison Alanna CNorth Kari EPeyser Patricia AProvince Michael APsaty Bruce MRauramaa RainerRosendaal Frits RRotter Jerome ISnieder HaroldWagenknecht Lynne EWareham Nicholas JGiri AyushKelly Tanika NMunroe Patricia BGauderman JamesWinkler Thomas Wde Vries Paul SRao Dabeeru CManning Alisa KChen Hande Las Fuentes LisaRedline SusanMeigs James B - Ferroptosis is an iron-dependent programmed cell death (PCD) implicated in cancer therapy response, yet its transcriptional control remains unevenly characterized and often centered on a limited subset of transcription factors (TFs) rather than systematically addressing TF families. The Activating enhancer-binding Protein-2 (AP-2) family of TFs is a plausible but understudied regulatory node linking oncogenic programs to ferroptosis, with prior research limited to AP-2α and AP-2γ, suggesting anti-ferroptotic and pro-tumorigenic roles. Thus, the present study aimed to provide a family-wide analysis of the relationships between AP-2 and ferroptosis across tumors in which this PCD type is considered biologically and clinically relevant. The research integrates ferroptosis gene modules with AP-2 targetomes, tumor-normal expression comparisons, survival stratification, ferroptosis scoring, cross-cohort functional analyses, and signaling pathway projection extending canonical ferroptosis circuits with AP-2-associated non-canonical elements. Consistent associations between AP-2 expression, prognosis, and ferroptosis score were observed in five tumor cohorts: cervical squamous cell carcinoma, glioblastoma, ovarian serous cystadenocarcinoma, pancreatic adenocarcinoma, and thyroid carcinoma. In addition, cross-cohort clustering highlighted genes enriched in redox- and lipid-metabolism programs linked to apoptosis and autophagy-dependent death. Among the candidates emerging from these analyses, ferroptotic markers (, , and ) and AP-2-linked nodes such as , , , , , , and warrant targeted functional and binding validation to infer whether these associations reflect direct AP-2 regulatory mechanisms. Most importantly, AP-2-centered research appears to be a valuable area for guiding studies of tumor-specific ferroptosis vulnerability or resistance. - Source: PubMed
Publication date: 2026/02/28
Kołat DamianGromek PiotrKciuk MateuszZhao Lin-YongKałuzińska-Kołat ŻanetaKontek RenataPłuciennik Elżbieta