TFAP2D antibody - C-terminal region (ARP30084_T100)
- Known as:
- TFAP2D (anti-) - C-terminal region (ARP30084_T100)
- Catalog number:
- arp30084_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TFAP2D antibody - C-terminal region (ARP30084_T100)
Related genes to: TFAP2D antibody - C-terminal region (ARP30084_T100)
- Gene:
- TFAP2D NIH gene
- Name:
- transcription factor AP-2 delta
- Previous symbol:
- TFAP2BL1
- Synonyms:
- -
- Chromosome:
- 6p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-27
- Date modifiied:
- 2016-04-06
Related products to: TFAP2D antibody - C-terminal region (ARP30084_T100)
Related articles to: TFAP2D antibody - C-terminal region (ARP30084_T100)
- Neuroblastoma (NB) is recognized as the predominant extracranial malignant solid tumor in children and adolescent; the prognosis for high-risk patients remains poor. This limitation stems from its low mutational burden, an absence of antigen-presenting molecules, and vascular irregularities, which collectively impede immune cell infiltration, characterizing NB as a prototypical "cold tumor". Intriguingly, metabolic pathways, especially through a novel glucose-dependent cellular death mechanism termed disulfidptosis and fatty acid metabolism (FAM), are pivotal in modulating the tumor's energy dynamics and activating the tumor microenvironment (TME). Therefore, this study aims to explore the prognostic value and immunological implications of disulfidptosis-related fatty acid metabolism (DFAM) within the NB TME. - Source: PubMed
Publication date: 2026/02/12
Li XiaoyingGong BaochengQu TongyuanJin YanChen ChongZhao Qiang - Fertilization involves fusion between sperm and metaphase II (MII) oocyte, initiating a cascade of events including oocyte activation, resumption of meiosis, formation and interdigitation of male and female pronuclei, and zygote formation. Total Fertilization Failure (TFF), characterized by the disruption of any of these processes, occurs in 1-3% of intracytoplasmic sperm injection (ICSI) cycles. The genetic basis of TFF remains largely unexplored. TFF can occur in cases where no single genetic cause is apparent, suggesting a potential polygenic contribution. - Source: PubMed
Publication date: 2025/11/04
Ata ManarChoucair FadiDjekidel Mohamed NadhirSousa Esteves MariaAl Ali FatimaNawaz ShoaibEl Taha LinaSoloviov OleksandrSathappan AbbiramiAliyev ElbayFakhro KhalidAwwad JohnnyAvella Matteo A - Selective fibroblast growth factor receptor (FGFR) inhibitors are emerging and promising treatment options in oncology, currently approved for metastatic cholangiocarcinoma and urothelial carcinoma. These agents are associated with various adverse events, including a range of dermatologic toxicities. In rare cases, they can cause calcinosis cutis (calcium deposition in the skin and subcutaneous tissue) or calciphylaxis (calcium deposition in blood vessels). Hyperphosphatemia, a common side effect, is considered a predisposing factor for these conditions. We report a rare case of pemigatinib-induced calcinosis cutis in a 46-year-old woman with FGFR2-TFAP2D fusion-positive metastatic cholangiocarcinoma. Ten days into treatment with pemigatinib, she developed painful, pruritic, erythematous leg lesions. Labs showed hyperphosphatemia with normal calcium; biopsy confirmed calcinosis cutis. Discontinuation of pemigatinib, phosphate binder therapy (calcium acetate), and topical steroids (triamcinolone) led to symptom resolution. We also review 10 similar cases linked to selective FGFR inhibitors, highlighting clinical features, management, and outcomes. Although rare, these conditions can be serious and potentially debilitating. Early recognition, regular phosphate monitoring, prompt intervention, drug adjustment or discontinuation, electrolyte correction, and wound care are key to improving patient outcomes. - Source: PubMed
Publication date: 2025/05/09
Ghimire BipinGor DhairyaAbbas OmarDiab Maria - Retinal degeneration accompanied by abnormal neovascularization from the choroid in the macular area is a critical disease to cure. Retinal cell apoptosis or inflammation in the macula can lead to neovascularization in that area. Some environmental factors such as long-term light exposure, particularly the blue end of the light spectrum, can damage the retina, causing such a disease. Improved understanding of genetic molecules has indicated that certain genes may be potential biomarkers of neovascular macular degeneration. This study aimed to investigate the expression of transcription factor activator protein-2 δ (TFAP-2D) in the retina and explore its role in the pathogenesis of retinal degeneration. For this, a long-term light exposure animal model was used to evaluate TFAP-2D expression in the retina. In addition, two vectors overexpressing different genotypes of TFAP-2D were transfected into retinal pigment epithelial (RPE) cells, and the expression of angiogenesis molecules was investigated. It was found that TFAP-2D expression was observed in the RPE area of the retina in long-term light-exposed rats; however, no TFAP-2D expression was detected in the retina of control (normal) rats. Interleukins (ILs) 1B, IL8, vascular endothelial growth factor (VEGF)-C, and one VEGF receptor (kinase insert domain receptor) were significantly upregulated in RPE cells with TFAP-2D with a C allele at rs78648104 (TFAP-2D-C) overexpression. In conclusion, experiments with different TFAP-2D genotypes revealed that long-term light exposure upregulated TFAP-2D expression in the RPE cells of the retina. In addition, overexpression of TFAP-2D-C induced the release of IL1B, IL8, and VEGF-C, which may lead to neovascularization in the choroid and retina. - Source: PubMed
Publication date: 2025/05/21
Chin Chih-HuiChien Chih-ChengHuang Chi-JungKe Chia-YingLee Yih-Jing - The ventrolateral pallial (VLp) excitatory neurons in the claustro-amygdalar complex and piriform cortex (PIR; which forms part of the palaeocortex) form reciprocal connections with the prefrontal cortex (PFC), integrating cognitive and sensory information that results in adaptive behaviours. Early-life disruptions in these circuits are linked to neuropsychiatric disorders, highlighting the importance of understanding their development. Here we reveal that the transcription factors SOX4, SOX11 and TFAP2D have a pivotal role in the development, identity and PFC connectivity of these excitatory neurons. The absence of SOX4 and SOX11 in post-mitotic excitatory neurons results in a marked reduction in the size of the basolateral amygdala complex (BLC), claustrum (CLA) and PIR. These transcription factors control BLC formation through direct regulation of Tfap2d expression. Cross-species analyses, including in humans, identified conserved Tfap2d expression in developing excitatory neurons of BLC, CLA, PIR and the associated transitional areas of the frontal, insular and temporal cortex. Although the loss and haploinsufficiency of Tfap2d yield similar alterations in learned threat-response behaviours, differences emerge in the phenotypes at different Tfap2d dosages, particularly in terms of changes observed in BLC size and BLC-PFC connectivity. This underscores the importance of Tfap2d dosage in orchestrating developmental shifts in BLC-PFC connectivity and behavioural modifications that resemble symptoms of neuropsychiatric disorders. Together, these findings reveal key elements of a conserved gene regulatory network that shapes the development and function of crucial VLp excitatory neurons and their PFC connectivity and offer insights into their evolution and alterations in neuropsychiatric disorders. - Source: PubMed
Publication date: 2025/01/15
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