ZNF263 antibody - N-terminal region (ARP31457_P050)
- Known as:
- ZNF263 (anti-) - N-terminal region (ARP31457_P050)
- Catalog number:
- arp31457_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF263 antibody - N-terminal region (ARP31457_P050)
Related genes to: ZNF263 antibody - N-terminal region (ARP31457_P050)
- Gene:
- ZNF263 NIH gene
- Name:
- zinc finger protein 263
- Previous symbol:
- -
- Synonyms:
- FPM315, ZKSCAN12, ZSCAN44
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-11
- Date modifiied:
- 2015-08-26
Related products to: ZNF263 antibody - N-terminal region (ARP31457_P050)
Related articles to: ZNF263 antibody - N-terminal region (ARP31457_P050)
- Pancreatic cancer is one of the most lethal malignancies. Genome-wide association studies (GWAS) identify multiple susceptibility loci, but most map to noncoding regions, leaving variant-to-gene links unresolved. In this study, a genome-wide regulatory map is constructed using expression quantitative trait loci (eQTL) analysis of 482 pancreatic tissues, and integrated with a GWAS meta-analysis to prioritize causal variants. A total of 82 significant variants and 15 target genes for pancreatic cancer risk are identified, with enrichment in cancer-related pathways. The variant rs11102484 is validated in an independent cohort of 569 cases and 2691 controls. The combined analysis of 5699 cases and 8467 controls confirms that the G allele of rs11102484 significantly reduces pancreatic cancer risk (odds ratio = 0.85, 95% confidence interval = 0.80-0.90, P = 4.83 × 10). Functional assays demonstrate that the G allele impairs ZNF263 binding at rs11102484, thereby weakening a long-range silencer-promoter interaction and increasing ST7L expression. Elevated ST7L dampens AKT/β-catenin signaling and suppresses pancreatic cancer cell proliferation, consistent with the protective association. Overall, this study implicates functional genes in pancreatic cancer risk and characterizes a regulatory variant that modulates ST7L expression, advancing the interpretation of GWAS findings and understanding of pancreatic cancer biology. - Source: PubMed
Publication date: 2026/03/13
Wang XiaoyangGeng HuiYao ZhengyanJiang YuanChen CanLu ZequnTian ShuangshuangZhang MingLiu RuiyanFeng ChenxiLi BinMiao XiaopingTian JianboZhang ShaokaiZhu Ying - Colorectal cancer (CRC) is one of the most prevalent and lethal cancers worldwide and is characterized by uncontrolled cell invasion, migration, and proliferation. The progression of CRC is driven by genetic mutations and alterations in key signaling pathways. This study investigates the role of and implicated in CRC progression. The gene, which regulates G protein signaling pathways, plays a vital role in cell movement and growth, contributing to the metastatic potential of cancer cells. The gene, a zinc finger protein involved in gene expression regulation, is also linked to CRC progression, with its dysregulation affecting the cell cycle, apoptosis, and migration. In particular, this study explores how ZNF263 acts as a transcription factor, modulating the expression of GPSM2 to increase CRC cell invasion, migration, and proliferation. This study confirms that ZNF263 activates the cell cycle pathway in a GPSM2-dependent manner, driving the aggressive behavior of CRC cells. Bioinformatics analysis using the GEO database further supports these findings, identifying key genetic alterations in CRC. These insights provide a deeper understanding of the molecular mechanisms underlying CRC progression and highlight the potential of ZNF263 and GPSM2 as therapeutic targets for intervention. This study underscores the importance of early detection and exploration of targeted therapies to improve CRC patient outcomes. - Source: PubMed
Publication date: 2026/03/03
Shi YouquanBaral ShantanuZhang YouleiJiang YongjunLi RuiqiZhang YueWang WeiWang Daorong - Conventional human embryonic stem cells (hESCs) are capable of self-renewal and simultaneously poised for differentiation. But the mechanisms underlying this primed pluripotent state, which endows them with elevated responsiveness to differentiation cues, remain largely underexplored. Especially, little is known about the pivotal transcription factors (TFs) that orchestrate hESCs towards primed pluripotency. Here, we report a function of TF ZNF263 in pluripotency priming. Genetic and functional assays reveal that ZNF263 directly initiates the incipient expression of early differentiation genes and concurrently dampens the core pluripotency circuitry in hESCs, greatly tilting the balance from pluripotency maintenance to lineage priming. Importantly, ZNF263 deficiency markedly impairs pluripotency dissolution and multi-lineage differentiation in hESCs, particularly toward ectoderm. Moreover, single-cell transcriptomic profiling reveals that ZNF263 promotes the priming of cell fate commitment in hESCs, suggesting its indispensable requirement for pluripotency priming and lineage commitment continuum. Together, we demonstrate the role of ZNF263 in establishing the primed pluripotent state in hESCs and facilitating their differentiation into primary germ layer lineages. - Source: PubMed
Publication date: 2025/11/05
Yin QianqianHuang JingSun HongduoZhou ShuhanRuan LinjieZeng YiLi YanaGong ZhaohuiChen PeiyuYuan XinboWan JiafangWang QingzhongWang YuangaoLi HaipengJing NaiheLiu XinShao Zhen - Pulmonary hypertension (PH) represents a significant cardiovascular disorder marked by both functional and structural alterations within the pulmonary vasculature. Long noncoding RNAs have been closely associated with PH pathogenesis and progression, particularly in vascular remodeling and cell proliferation. Nonetheless, how long noncoding RNAs interact with downstream targets to modulate PH remains unclear. - Source: PubMed
Publication date: 2025/07/22
Wang YingqiYin LuluZheng ShuangLiu AijingLiu ChunmiaoBao ZhituZhu HeZhao XiaoxuZhao ZiruPan YuZhu DalingYu Hang - Metastasis is the leading cause of gastric cancer (GC)-related death. However, the molecular mechanisms underlying GC metastasis are not well understood. In this study, we focused on dopamine receptor 5 pseudogene 2 (DRD5P2), a novel long non-coding RNA, in GC metastasis. - Source: PubMed
Publication date: 2025/04/23
Yu ZhenjiaPan TaoWang XiaofengJin ZhijianLu YifanWu XiongyanHou JunyiWu AirongLi ZhenChang XinyuZhou QuanLi JianfangLiu WentaoNi ZhentianYang ZhongyinLi ChenYan MinLiu BingyaYan ChaoZhu ZhenggangSu Liping