ZNF248 antibody - N-terminal region (ARP35991_P050)
- Known as:
- ZNF248 (anti-) - N-terminal region (ARP35991_P050)
- Catalog number:
- arp35991_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF248 antibody - N-terminal region (ARP35991_P050)
Related genes to: ZNF248 antibody - N-terminal region (ARP35991_P050)
- Gene:
- ZNF248 NIH gene
- Name:
- zinc finger protein 248
- Previous symbol:
- -
- Synonyms:
- bA162G10.3
- Chromosome:
- 10p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-30
- Date modifiied:
- 2015-08-26
Related products to: ZNF248 antibody - N-terminal region (ARP35991_P050)
Related articles to: ZNF248 antibody - N-terminal region (ARP35991_P050)
- Despite recent advances in glioblastoma (GBM) therapies, patient survival remains dismal. Existing prognostic markers lack sufficient accuracy, and the resistance of GBM to chemotherapy underscores the need for both improved predictive models and new therapeutic targets. - Source: PubMed
Publication date: 2025/12/21
Wang ShaowenXing SongyuLi KunyuLiu SiyuYang YuluZhu XinzhouPoon Wai Sang - Liver hepatocellular carcinoma (LIHC) is a major contributor to cancer-related mortality worldwide, posing substantial diagnostic and therapeutic challenges. Although zinc finger proteins (ZNFs) are known to play a role in LIHC, the specific function of ZNF248 remains poorly understood. In this study, we analyzed genomic and clinical data from The Cancer Genome Atlas (TCGA) to elucidate the role of ZNF248 through differential expression analysis, bioenrichment, immune response correlation, and drug sensitivity evaluation. Machine learning was employed to identify prognostic signatures derived from ZNF248, which were further validated using Receiver Operating Characteristic (ROC) analysis. Functional assays, including Western blot and rescue experiments, were performed to assess the impact of ZNF248 on the PI3K/AKT signaling pathway. Our results demonstrate that ZNF248 is significantly overexpressed in LIHC patients and is associated with poor prognosis. Bioenrichment analysis revealed activation of oncogenic pathways, and elevated ZNF248 expression correlated with increased immune cell infiltration and enhanced immune scores, thereby influencing both immunotherapy response and drug sensitivity. Functional assays further confirmed that ZNF248 promotes LIHC progression and invasion, while silencing ZNF248 inhibited the PI3K/AKT pathway - a phenomenon reversible by the AKT activator SC79. These findings suggest that ZNF248 contributes to LIHC progression through the PI3K/AKT pathway and may represent a novel immunotherapeutic target and prognostic biomarker for LIHC. - Source: PubMed
Publication date: 2024/11/15
Weng LifangCheng ZhichengQiu ZhisongShi JinChen LibinHe ChunshengWang LijuanJin Feng - Colorectal cancer (CRC) is one of the most common malignant tumors globally, with metastasis emerging as the leading cause of mortality in CRC patients. Transcription factors play pivotal roles in the metastatic process. Using bioinformatics tools, we analyzed the TCGA-COAD and GES146587 datasets and identified ZNF248 participating in tumor progression. By analyzing 100 CRC patient tissues, it is found that ZNF248 is highly expressed in cancer tissue as well as in CRC cell lines identified by qRT-PCR. Our study discovered that ZNF248 enhances CRC cell migratory and invasive capabilities. A positive correlation was found between ZNF248 and epithelial-mesenchymal transition (EMT)-related markers (ZEB1, snail1), while E-cadherin exhibited a negative correlation with ZNF248. In addition, the analysis of the TCGA dataset demonstrated a strong correlation between the mRNA level of ZNF248 and ZEB1 expressions. Furthermore, it is found that the overexpression of ZEB1 could reverse CRC cell invasion and migration, along with the inhibition on EMT marker expressions induced by the RNA interference with ZNF248. Immunohistochemical analysis indicated a substantial association of ZNF248 expression with the lymph node metastasis, and with the liver metastasis (P =0.01, P =0.01), and a positive correlation between ZNF248 and ZEB1 expression (P =0.021) was also identified. Using Chip-PCR assay, it is found that ZNF248 bound to the ZEB1 promoter region. These findings showed that ZNF248 promotes CRC metastasis in vivo, revealed its role as an oncogene in CRC by targeting ZEB1 and activating the EMT pathway, which provided novel and promising biomarkers for CRC therapy through targeting ZEB1. - Source: PubMed
Publication date: 2024/08/19
Ren YanyingSun XiaoxuChen XinShao ShuaiTang JingTongXu ZhaohuiXu YangKang HaonanWang Liming - To defend against the invasion of transposons, hundreds of KRAB-zinc finger genes (ZNFs) evolved to recognize and silence various repeat families specifically. However, most repeat elements reside in the human genome with high copy numbers, making the ChIP-seq reads of ZNFs targeting these repeats predominantly multi-mapping reads. This complicates downstream data analysis and signal quantification. To better visualize and quantify the arms race between transposons and ZNFs, the R package TECookbook has been developed to lift ChIP-seq data into reference repeat coordinates with proper normalization and extract all putative ZNF binding sites from defined loci of reference repeats for downstream analysis. In conjunction with specificity profiles derived from Spec-seq data, human ZNF10 has been found to bind to a conserved ORF2 locus of selected LINE-1 subfamilies. This provides insight into how LINE-1 evaded capture at least twice and was subsequently recaptured by ZNF10 during evolutionary history. Through similar analyses, ZNF382 and ZNF248 were shown to be broad-spectrum LINE-1 binders. Overall, this work establishes a general analysis workflow to decipher the arms race between ZNFs and transposons through nucleotide substitutions rather than structural variations, particularly in the protein-coding region of transposons. - Source: PubMed
Publication date: 2023/09/06
Zuo Zheng - Treatment-resistant depression (TRD) is a severe form of major depressive disorder (MDD) with substantial public health impact and poor treatment outcome. Treatment outcome in MDD is significantly heritable, but genome-wide association studies have failed to identify replicable common marker alleles, suggesting a potential role for uncommon variants. Here we investigated the hypothesis that uncommon, putatively functional genetic variants are associated with TRD. Whole-exome sequencing data was obtained from 182 TRD cases and 2021 psychiatrically healthy controls. After quality control, the remaining 149 TRD cases and 1976 controls were analyzed with tests designed to detect excess burdens of uncommon variants. At the gene level, 5 genes, ZNF248, PRKRA, PYHIN1, SLC7A8, and STK19 each carried exome-wide significant excess burdens of variants in TRD cases (q < 0.05). Analysis of 41 pre-selected gene sets suggested an excess of uncommon, functional variants among genes involved in lithium response. Among the genes identified in previous TRD studies, ZDHHC3 was also significant in this sample after multiple test correction. ZNF248 and STK19 are involved in transcriptional regulation, PHYIN1 and PRKRA are involved in immune response, SLC7A8 is associated with thyroid hormone transporter activity, and ZDHHC3 regulates synaptic clustering of GABA and glutamate receptors. These results implicate uncommon, functional alleles in TRD and suggest promising novel targets for future research. - Source: PubMed
Publication date: 2023/08/01
Shah Shrey BPeddada Teja NSong ChristopherMensah MaameSung HeejongYavi ManiYuan PeixiongZarate Carlos AMickey Brian JBurmeister MargitAkula NirmalaMcMahon Francis J