TFAP2A antibody - C-terminal region (P100878_T100)
- Known as:
- TFAP2A (anti-) - C-terminal region (P100878_T100)
- Catalog number:
- p100878_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TFAP2A antibody - C-terminal region (P100878_T100)
Related genes to: TFAP2A antibody - C-terminal region (P100878_T100)
- 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 - C-terminal region (P100878_T100)
Related articles to: TFAP2A antibody - C-terminal region (P100878_T100)
- The skin serves as a barrier against environmental stresses. Melanocytes synthesize melanin to protect against ultraviolet (UV) radiation; however, excessive melanin can lead to hyperpigmentation disorders. Proper pigment distribution requires melanosome transport, mediated by a complex of Mlph, Myo Va, and Rab27a. Dysregulation of this transport machinery disrupts pigment homeostasis and contributes to various pigmentation disorders. The aryl hydrocarbon receptor and transcription factor TFAP2A are known regulators of melanocyte function, but their direct regulatory relationship remains unclear. Understanding how these pathways converge is essential for elucidating the molecular basis of environmentally induced pigmentation. Here, we identify a signaling axis in which AHR activation increases TFAP2A expression, leading to the upregulation of Myo Va and Mlph. Conversely, AHR inhibition caused melanosome aggregation and reduced their expression. Mechanistically, AHR binds to the intron 1 enhancer of TFAP2A, and TFAP2A directly targets intron 1 regions of Myo Va and Mlph. Collectively, these findings reveal that the AHR-TFAP2A axis orchestrates melanosome transport in response to environmental stimuli and may represent a potential therapeutic target for environmentally induced pigmentation disorders. - Source: PubMed
Publication date: 2026/09/17
Sung Hye YounJo Chan SongHairu ZhaoBaek Gyu CheolYou Chang MoHwang Jae Sung - Skin cell fate determination is a core issue in wound repair and regenerative medicine. The multistability of the PGTM gene regulatory network, comprising ΔNp63α, GRHL2, TFAP2A, and MYC, provides a structural basis for cell fate plasticity. However, the mechanism by which the key microenvironmental signal EDAR regulates the PGTM network remains unclear. - Source: PubMed
Publication date: 2026/08/31
Li ChunWang LuDeng WenjieLi YideZu LiZheng Xiaoqi - Radioresistance remains a major obstacle in the treatment of non-small cell lung cancer (NSCLC). Transcription factor AP-2α (TFAP2A) has been implicated in tumor progression, but its role in NSCLC radioresistance and translational therapeutic relevance remain unclear. - Source: PubMed
Publication date: 2026/07/30
Ma JiachunWang FeiZhang JingxinTian ChenBao ShunshunYuan JupengYu JinmingZhang XiaoChen Dawei - Cervical cancer (CC) remains a leading cause of cancer-related mortality among women, and advances in its therapeutic approaches are disappointing, in which novel therapies and precise experimental approaches are needed to be exploited. This study intends to explore the effects and involved molecular mechanism of Stichopus japonicus acidic mucopolysaccharide (SJAMP) on CC progression. CCK8 and EdU assays were utilized to test the ability of cell proliferation. Colony formation, transwell, flow cytometry assays were applied to detect cell colonies, migration, invasion, and apoptosis accordingly. RT-qPCR and western blot were used to quantify the expression levels of transcription factor AP-2 Alpha (TFAP2A) and centromere protein W (CENPW), respectively. JASPAR website, ChIP-qPCR, and dual-luciferase reporter assay were used to verify the binding loci of TFAP2A on the promoter region of CENPW. Xenograft tumor models were produced to confirm the effects of CENPW silence or SJAMP treatment in CC. SJAMP suppressed malignant phenotypes of CC cells in a dosage-dependent manner. Besides, SJAMP regulated the biological behaviors of CC cells via regulating TFAP2A expression, which further regulated CENPW expression as its transcription factor. The expression of CENPW was elevated in CC and positively correlated with TFAP2A, and the silence of CENPW hampered tumor growth in vivo. In addition, CENPW overexpression abolished the repressed cell malignant activities induced by TFAP2A silence. Xenograft tumor models proved that SJAMP curbed tumor growth in vivo via repressing TFAP2A-mediated CENPW expression. Our research revealed that SJAMP exerted its anti-tumor effects via decreasing TFAP2A-mediated CENPW expression in CC. - Source: PubMed
Publication date: 2026/07/24
Cai ZhengxiangLiu DachunHe YongpengFang ZhanglanYang HuguangLan XiaHe MiaoXian YiGong Juan - Combination targeted therapy with BRAF/MEK inhibitors and immune therapy show promising therapeutic outcomes in melanoma; however, the development of drug resistance still represents a formidable challenge. Remaining unexplored is the possibility that BRAF/MEK inhibitors themselves inadvertently compromise the tumor immune microenvironment, limiting the efficacy of immunotherapy when it is used in combination with targeted inhibitors. Herein, we profiled the landscape of the BRAF regulatome identifying a novel transcription factor, TFAP2A, newly linking BRAF/MEK drug resistance to antitumor immunity. Specifically, we found that BRAF/MEK inhibitors significantly upregulate TFAP2A. Further, genetic disruption of TFAP2A overcomes BRAF/MEK-inhibitor resistance, promotes stromal enrichment, and enhances intratumoral infiltration of macrophages in an immune-compromised mouse model. In a syngeneic mouse model, TFAP2a knockout not only suppresses tumor growth but also induces potent anti-tumor tertiary lymphoid structures (TLSs). Single cell transcriptomics revealed that the absence of TFAP2A shapes the antitumor microenvironment with an influx of M1-like macrophages, CD8+ T cells and mature dendritic cells. By identifying TFAP2A as a shared driver of both targeted therapy resistance and immunosuppression, our work offers a one-stone-two-bird strategy to overcome drug resistance and elicit antitumor immunity. - Source: PubMed
Publication date: 2026/07/10
Mou HaiweiYakovishina VeronikaDeRosa KristenChen YeqingXiao MinDunne MaggieShi NancyThomas MonzySmith Jordan LLiu QinHerlyn Meenhard