ZNF124 Antibody
- Known as:
- ZNF124 Antibody
- Catalog number:
- GWB-E0F0AB
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- ZNF124 Antibody
Related genes to: ZNF124 Antibody
- Gene:
- ZNF124 NIH gene
- Name:
- zinc finger protein 124
- Previous symbol:
- -
- Synonyms:
- HZF16, HZF-16
- Chromosome:
- 1q44
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-24
- Date modifiied:
- 2015-08-26
Related products to: ZNF124 Antibody
Related articles to: ZNF124 Antibody
- Retinitis pigmentosa (RP), affecting more than 20 million people worldwide, refers to a group of inherited retinal dystrophies characterized by progressive photoreceptor degeneration and vision loss. However, the underlying genetic causes of substantial RP cases remain unidentified. In this report, we identified a novel homozygous splicing variant, c.219-1delG, which introduced skipping of exon 4 of the ZNF124 gene in a large RP pedigree by whole-exome sequencing analysis. To elucidate the pathogenesis of the mutation, we generated a retina-specific knockout mouse model of ZNF124 murine homologous gene Gm20541, which manifested RP-like phenotypes characterized by reduced electroretinogram response and progressive retinal degeneration. Integrated analysis using CUT&Tag, ChIP-exo, and RNA-seq data further revealed that ZNF124 regulated MSX2 expression through binding its promoter region. Moreover, deletion of Msx2in the retina led to thinning of retina owing to progressive degeneration of rod cells. Integrated analysis of RNA-seq data from both Gm20541 and Msx2 mutant retinas indicated that ZNF124 is essential for maintaining normal retinal function by regulating Msx2 transcription, which in turn controls the expression of murine homologues of retinal dystrophy genes Rs1, Pde6g, and Pdc. Taken together, our study identified a novel mechanism of transcriptional regulation for retinal homeostasis via ZNF124-MSX2 axis and ZNF124 as a novel candidate gene for RP. - Source: PubMed
Publication date: 2026/02/19
Yang YemingJiang XiaoyanLi ShujinSun KuanxiangZou RongChen CanShi YiLiu WenjingSundaresan PeriasamyHuang LulinZhang LinYang ZhenglinZhu Xianjun - Evidence increasingly indicates that HPV infection plays a pivotal role in the initiation and progression of bladder cancer (BC). Yet, determining the predictive value of HPV-associated genes in BC remains challenging. We identified differentially expressed HPV-associated genes of BC patients from the TCGA and GEO databases. We screened prognostic genes using COX and LASSO regression, subsequently establishing a risk prediction model. The model's precision and clinical relevance were gauged using Kaplan-Meier survival analyses and ROC curves. Functional enrichment, immune cell infiltration, and drug sensitivity analyses were performed across both high-risk and low-risk sets. PCR assays were utilized to measure the expression levels of genes. We identified 13 HPV-associated genes for our risk model. Among these, FLRT2, HOXC5, LDLR, SCD, GRM7, DSC1, EMP1, and HMGA1 were identified as risk contributors, while LPA, SERPINA6, ZNF124, ETV7, and SCO2 were deemed protective. Cox regression analysis verified that our model provides an independent prediction of overall survival (OS) in bladder cancer (BC) patients. Gene Ontology (GO) analysis revealed predominant gene enrichment in wound healing, extracellular matrix composition, and collagen-rich extracellular matrices. KEGG pathway analysis highlighted primary enrichment areas, including focal adhesion, the PI3K-Akt signalling pathway, and ECM-receptor interaction. Risk scores were correlated with tumor microenvironment (TME) scores, immune cell infiltration, and sensitivities to both chemotherapy and immunotherapy. We have formulated a risk-assessment model pinpointing 13 central HPV-associated genes in BC. These genes present potential as prognostic indicators and therapeutic targets, emphasizing the intertwined relationship between HPV-induced BC progression and the immune landscape. - Source: PubMed
Publication date: 2025/01/01
Tang ZhichengQian YuxinWang NiChen YinqiuHuang HaojunZhang JiahaoLuo HongchengLu ZechaoLi ZhibiaoHe ZhaohuiTang Fucai - Myelodysplastic syndromes (MDS) consist of a group of hematological malignancies characterized by ineffective hematopoiesis, cytogenetic abnormalities, and often a high risk of transformation to acute myeloid leukemia (AML). So far, there have been only a very limited number of studies assessing the epigenetics component contributing to the pathophysiology of these disorders, but not a single study assessing this at a genome-wide level. Here, we implemented a generic high throughput epigenomics approach, using methylated DNA sequencing (MeD-seq) of LpnPI digested fragments to identify potential epigenomic targets associated with MDS subtypes. Our results highlighted that PCDHG and ZNF gene families harbor potential epigenomic targets, which have been shown to be differentially methylated in a variety of comparisons between different MDS subtypes. Specifically, CpG islands, transcription start sites and post-transcriptional start sites within ZNF124, ZNF497 and PCDHG family are differentially methylated with fold change above 3,5. Overall, these findings highlight important aspects of the epigenomic component of MDS syndromes pathogenesis and the pharmacoepigenomic basis to the hypomethylating agents drug treatment response, while this generic high throughput whole epigenome sequencing approach could be readily implemented to other genetic diseases with a strong epigenetic component. - Source: PubMed
Publication date: 2023/04/25
Siamoglou StavroulaBoers RubenKoromina MariaBoers JoachimTsironi AnnaChatzilygeroudi TheodoraLazaris VasileiosVerigou EvgeniaKourakli Alexandravan IJcken Wilfred F JGribnau JoostSymeonidis ArgirisPatrinos George P - Tick-borne encephalitis virus (TBEV), the most medically relevant tick-transmitted flavivirus in Eurasia, targets the host central nervous system and frequently causes severe encephalitis. The severity of TBEV-induced neuropathogenesis is highly cell-type specific and the exact mechanism responsible for such differences has not been fully described yet. Thus, we performed a comprehensive analysis of alterations in host poly-(A)/miRNA/lncRNA expression upon TBEV infection in human primary neurons (high cytopathic effect) and astrocytes (low cytopathic effect). Infection with severe but not mild TBEV strain resulted in a high neuronal death rate. In comparison, infection with either of TBEV strains in human astrocytes did not. Differential expression and splicing analyses with an prediction of miRNA/mRNA/lncRNA/vd-sRNA networks found significant changes in inflammatory and immune response pathways, nervous system development and regulation of mitosis in TBEV Hypr-infected neurons. Candidate mechanisms responsible for the aforementioned phenomena include specific regulation of host mRNA levels via differentially expressed miRNAs/lncRNAs or vd-sRNAs mimicking endogenous miRNAs and virus-driven modulation of host pre-mRNA splicing. We suggest that these factors are responsible for the observed differences in the virulence manifestation of both TBEV strains in different cell lines. This work brings the first complex overview of alterations in the transcriptome of human astrocytes and neurons during the infection by two TBEV strains of different virulence. The resulting data could serve as a starting point for further studies dealing with the mechanism of TBEV-host interactions and the related processes of TBEV pathogenesis. - Source: PubMed
Publication date: 2022/05/30
Selinger MartinVěchtová PavlínaTykalová HanaOšlejšková PetraRumlová MichaelaŠtěrba JánGrubhoffer Libor - Medulloblastoma (MB) is the most common malignant pediatric brain tumor, however, the mechanisms underlying tumorigenesis in different MB subgroups remain incompletely understood. Although previous studies of MB predisposition have been conducted in tertiary referral centers primarily in Caucasian cohorts, it is not unclear clear whether there exist population-specific genetic alterations in MBs. In this study, we investigated the contribution of genomic and transcriptomic alterations to the risk of malignant MB in the Chinese population (designated as the Asian cohort). We analyze the genomic and transcriptomic alterations of the Asian MB cohort by using a combination of whole-exome sequencing (WES) and RNA-deep-sequencing. In addition, we integrate publicly available data with the Asian MB cohort and identify a subset of potential MB-driving genes specifically enriched in each of the MB subgroups. We further characterize a newly identified group-3-enriched transcriptional regulator, ZNF124, and demonstrate that ZNF124 is critical for the growth of the most aggressive group-3 MB cells. Together, our analyses indicate conserved yet distinct genetic alterations and gene expression patterns of MBs between different ethnic groups. Our studies further provide an important resource for identifying potential tumor-driving factors in MBs, enhancing our understanding of the disease process for developing ethnically targeted therapies in patients with MB. - Source: PubMed
Publication date: 2021/02/18
Luo ZailiDong XinranYu JianzhongXia YongBerry Kalen PRao RohitXu LingliXue PingChen TongLin YifengYu JiyangHuang GuoyingLi HaoZhou WenhaoLu Q Richard