TFAP4 antibody - C-terminal region (ARP33435_T100)
- Known as:
- TFAP4 (anti-) - C-terminal region (ARP33435_T100)
- Catalog number:
- arp33435_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TFAP4 antibody - C-terminal region (ARP33435_T100)
Ask about this productRelated genes to: TFAP4 antibody - C-terminal region (ARP33435_T100)
- Gene:
- TFAP4 NIH gene
- Name:
- transcription factor AP-4
- Previous symbol:
- -
- Synonyms:
- AP-4, bHLHc41
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-01
- Date modifiied:
- 2016-10-05
Related products to: TFAP4 antibody - C-terminal region (ARP33435_T100)
Related articles to: TFAP4 antibody - C-terminal region (ARP33435_T100)
- Breast cancer exhibits marked clinical heterogeneity and dynamic epigenetic reprogramming during tumor progression, yet current subtyping approaches fail to capture molecular changes associated with metastasis. Here, we establish a comprehensive biobank of patient-derived organoids (PDOs) from matched primary tumors, adjacent normal tissues, and lymph node metastases. Integrated genomic, transcriptomic, and epigenetic analyses demonstrate that these PDOs preserve tumor-specific molecular signatures and recapitulate epigenetic remodeling during disease evolution. Epigenetic profiling defines four distinct clusters, characterized by unique transcription factor (TF) networks, pathway activities, and therapeutic vulnerabilities not fully represented by conventional classifications. The lymph node metastasis cluster, predominantly comprising metastatic PDOs, displays extensive chromatin remodeling driven by metastasis-enriched TFs, whose depletion markedly impairs spontaneous metastasis in vivo. Together, these findings establish PDO-based epigenetic characterization as a platform for elucidating regulatory mechanisms underlying breast cancer progression and for advancing precision therapeutic strategies. - Source: PubMed
Publication date: 2026/03/16
Rao XinxinWang JingwenQiao ZhibinHong LeiQiao MengxueNi LiangweiSong AixiaDeng YunZhao XuMeng JinChen XingxingZhou YifanXue JingyanChi YayunWang XinruiYu ZhaoweiChen QianqianXu ConglingTang ShuangHu JingXu MidieXu WeiZhang ZhenZhang YongXu YanhuiJiang Yi-ZhouWu JiongShen MinhongGuo XiaomaoYu XiaoliChen Fei Xavier - Black Americans face a high burden of cardiovascular disease (CVD), with more than 60% of Black adult women affected. However, sex-specific molecular mechanisms underlying poor cardiovascular health (CVH) in this population remain largely unknown. In this study, we examined sex-specific transcriptomics signatures associated with CVH among Black adult men and women. - Source: PubMed
Publication date: 2026/01/19
Blankson Harriet NaDelmer CeciliaVerma RashiGuven EmineRooney KimberlyPearson AndreaBaltrus PeterQuyumi Arshed APemu PriscillaJordan I KingHerman TaylorMeller RobertSearles Charles D - Mitochondrial failure is a cornerstone of diabetic organ damage. While it is well understood that shattered mitochondria (excessive fission) and aggressive cleanup (mitophagy) drive this deterioration, the upstream genetic "switches" that trigger these processes remain unclear. This study investigates whether a specific regulatory chain the TFAP4-UBC9-SUMO1 axis orchestrates this mitochondrial breakdown in diabetic tissues. - Source: PubMed
Publication date: 2026/01/28
Jin ZhiyuJiang YingTao DayunLi ZunyanHe XiulingZhou HaoZhu HangRen Lina - Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are clinically heterogeneous malignancies whose biology and microenvironmental organization remain poorly understood. Here, we integrated single-nucleus multiomic (snRNA-seq and snATAC-seq) and spatial transcriptomic profiling across 38 well-differentiated pancreatic (pNET) and small-intestinal (siNET) tumors to define conserved malignant programs, their regulatory circuits, and spatial niches. We observed two conserved malignant cell programs spanning a continuous transcriptional spectrum: a neuronal-like program (si-cNMF1/p-cNMF1), and a secretory neuroendocrine program (si-cNMF2/p-cNMF2). Matched chromatin accessibility profiles uncovered distinct, tissue-specific regulatory networks, including and transcription factor binding motifs in siNETs versus and in pNETs, indicating organ-specific epigenetic control. Spatial transcriptomic analyses revealed that si/p-cNMF1-high regions localized to high cell density, immune-rich tumor areas, whereas si/p-cNMF2-high regions occupied stromal and vascularized niches and co-occured with fibroblast and endothelial compartments enriched for , , and signaling. Across both tumor types, the cNMF2 program was enriched in metastatic lesions and was enrichedfor pro-fibrotic and pro-angiogenic gene signatures. Thus, GEP-NETs are organized along a conserved neuronal-to-secretory axis defined by distinct epigenetic programs and spatially coupled to specific microenvironmental niches. This framework unifies NET heterogeneity across organ sites and identifies pathway-specific, microenvironment-linked vulnerabilities for therapeutic targeting. - Source: PubMed
Publication date: 2025/12/29
Karam JulieHoffman Samantha EGarza AmandaGui DanHoffman Hannah ITitchen Breanna MTanaka YutaroPimenta EricaPappa TheodoraValderrabano LauraBi KevinGillani RiazBrais LaurenShannon ErinHornick Jason LPark JihyeChan JenniferVan Allen Eliezer M - To investigate auditory acclimatization to high-altitude hypobaric hypoxia, we conducted longitudinal transcriptomic analyses in Wistar rats rapidly transported from 500 m to 3,700 m. Auditory brainstem response (ABR) testing and hematoxylin and eosin staining revealed progressive changes, with hearing impairment at 30 days (D30) followed by acclimatization at 60 days (D60). RNA-seq of cochlear tissues identified 1,329 differentially expressed genes (DEGs) during impairment and 1,441 DEGs during acclimatization. STEM analysis linked these temporal patterns to specific biological processes: peripheral nervous system development (acclimatization) and myotube differentiation (impairment), as annotated by GO/KEGG and Metascape. STEM analysis revealed gene expression profiles that significantly correlated with ABR threshold shifts, encompassing biological processes such as sensory organ morphogenesis and gravity-sensing pathways. Subsequent validation through RT-PCR and immunofluorescence staining confirmed the involvement of key candidate genes, including morphogenesis-associated factors (Aqp1, Rbp4), the mechanosensitive hormone Bglap, and critical transcriptional regulators (Maz, Tfap4, Nf1) in the acclimatization response. This study elucidates key transcriptional mechanisms governing both the initial hearing impairment and subsequent acclimatization processes during high-altitude adaptation. - Source: PubMed
Publication date: 2026/01/05
Awang DanzengDanzeng KanziRen HailongDa ZhenGesang QuzhenDeji QuzongXie HongjunLiu XinzhuZhao BinghanGongga Lanzi