Ask about this productRelated genes to: ZNF488 antibody
- Gene:
- ZNF488 NIH gene
- Name:
- zinc finger protein 488
- Previous symbol:
- -
- Synonyms:
- FLJ32104
- Chromosome:
- 10q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-21
- Date modifiied:
- 2015-08-26
Related products to: ZNF488 antibody
Related articles to: ZNF488 antibody
- MicroRNAs (miRNAs) are evolutionarily conserved post-transcriptional regulators that play critical roles in cellular development and differentiation across species. Although the importance of miRNAs in oligodendrocyte lineage cell (OLLC) differentiation has been extensively studied in rodent models, their roles in human OL development remain less understood. To address this gap, we used a human embryonic stem cell (hESC) reporter system designed to study human OLs and OL progenitor cells (OPCs). Using an optimized differentiation protocol, we used the reporter hESCs to generate and isolate well-characterized OLLCs at specific developmental stages and performed next-generation sequencing-based miRNA profiling to identify stage-specific miRNAs enriched during OL lineage specification and maturation. In addition to canonical miRNAs known to be enriched at various stages of OL development, our study identified several lesser-known miRNAs with distinct stage-specific enrichment patterns that may serve as useful molecular markers for classifying human CNS cell types in future studies. Target analysis of OPC- and OL-enriched miRNAs revealed key genes, including transcription factors ZNF488 and DLX1, cytoskeletal regulator CSNK2B, and potassium channel gene KCNJ1, along with key signaling pathways such as AKT, SMAD2/3, estrogen receptor, and insulin signaling, which regulate OPC and OL lineage function. These findings advance our understanding of the OLLC-specific miRNAs, and miRNA-mediated regulatory networks governing human OL differentiation and maturation and provide promising therapeutic targets for future studies aimed at restoring myelin integrity and improving outcomes in demyelinating diseases. - Source: PubMed
Publication date: 2025/12/26
Barzegar MansourehDhukhwa AsmitaPatel Vaidehi NileshVelasquez Fernanda CDas SamarjitPatil Arun HHalushka Marc KZack Donald JChamling Xitiz - In the United States, African Americans (AA) have higher Pancreatic ductal adenocarcinoma (PDAC) incidence and mortality rates than Caucasian Americans (CA). This study aimed to identify distinct gene expression signatures and differentially regulated pathways in AA and CA PDACs. - Source: PubMed
Publication date: 2025/07/04
Bajpai PrachiPaluri RaviDiffalha Sameer AlChandrashekar Darshan SAfaq FarrukhOtali DennisElkholy AmrMiller C RyanPeter ShajanManne AshishNagaraju Ganji PurnachandraSaddala Madhu SudhanaKhushman Moh'dVarambally SooryanarayanaManne Upender - Tumor treating fields (TTFields) use low-intensity, alternating electric fields to exert antitumor activity and have demonstrated efficacy against multiple cancers, including glioblastoma (GBM). Unfortunately, cancer cells inevitably develop resistance to TTFields, highlighting the need to elucidate the underlying mechanisms to develop approaches to induce durable responses. Using a gene network-based machine learning algorithm, we interrogated TTFields-resistant GBM cells and uncovered a regulatory axis anchored by the prostaglandin E2 receptor 3 (EP3) and the transcription factor zinc finger 488 (ZNF488). Mechanistically, TTFields induced EP3 upregulation and nuclear envelope localization, where it formed a complex with ZNF488 to induce resistance to TTFields by promoting self-renewal of glioma stem-like cells (GSC). Overexpression of EP3 and/or ZNF488 in TTFields-sensitive GSC conferred resistance and enhanced self-renewal, whereas expression of noninteracting mutants of these proteins abrogated the formation of the nuclear complex and prevented resistance. Inhibition of either partner in this protein complex in resistant GSC, including those freshly isolated from TTFields-resistant GBM tumors, resensitized cells to the cytotoxic effects of TTFields, concomitant with reduced self-renewal and in vivo tumorigenicity. Importantly, inhibition of EP3 in TTFields-sensitive GSC preemptively halted the development of resistance. The EP3-ZNF488 axis was significantly upregulated in TTFields-resistant GBM tumors, and coexpression of EP3 and ZNF488 in other cancers correlated with lower survival rates. Collectively, these results indicate that the nuclear EP3-ZNF488 axis is necessary and sufficient to establish TTFields resistance, underscoring the potential to target this axis to prevent or reverse resistance in GBM and possibly other cancers. Significance: The EP3-ZNF488 master regulatory axis in cancer stem-like cells drives resistance to treatments like tumor treating fields, opening avenues for developing strategies to enhance therapeutic efficacy. - Source: PubMed
Chen DongjiangLe Son BManektalia HarshitLiu TianyiHutchinson Tarun EO'Dell AdamSalhia BodourTran David D - CSF1R-related disorder (CSF1R-RD) is a neurodegenerative condition that predominantly affects white matter due to genetic alterations in the CSF1R gene, which is expressed by microglia. We studied an elderly man with a hereditary, progressive dementing disorder of unclear etiology. Standard genetic testing for leukodystrophy and other neurodegenerative conditions was negative. Brain autopsy revealed classic features of adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP), including confluent white matter degeneration with axonal spheroids and pigmented glial cells in the affected white matter, consistent with CSF1R-RD. Subsequent long-read sequencing identified a novel deletion in CSF1R that was not detectable with short-read exome sequencing. To gain insight into potential mechanisms underlying white matter degeneration in CSF1R-RD, we studied multiple brain regions exhibiting varying degrees of white matter pathology. We found decreased CSF1R transcript and protein across brain regions, including intact white matter. Single nuclear RNA sequencing (snRNAseq) identified two disease-associated microglial cell states: lipid-laden microglia (expressing GPNMB, ATG7, LGALS1, LGALS3) and inflammatory microglia (expressing IL2RA, ATP2C1, FCGBP, VSIR, SESN3), along with a small population of CD44 peripheral monocyte-derived macrophages exhibiting migratory and phagocytic signatures. GPNMB lipid-laden microglia with ameboid morphology represented the end-stage disease microglia state. Disease-associated oligodendrocytes exhibited cell stress signatures and dysregulated apoptosis-related genes. Disease-associated oligodendrocyte precursor cells (OPCs) displayed a failure in their differentiation into mature myelin-forming oligodendrocytes, as evidenced by upregulated LRP1, PDGFRA, SOX5, NFIA, and downregulated NKX2-2, NKX6.2, SOX4, SOX8, TCF7L2, YY1, ZNF488. Overall, our findings highlight microglia-oligodendroglia crosstalk in demyelination, with CSF1R dysfunction promoting phagocytic and inflammatory microglia states, an arrest in OPC differentiation, and oligodendrocyte depletion. - Source: PubMed
Publication date: 2024/08/28
Pan JieFores-Martos JaumeDelpirou Nouh ClaireJensen Tanner DVallejo KristenCayrol RomainAhmadian SamanAshley Euan AGreicius Michael DCobos Inma - Pancreatic cancer is a malignancy with high mortality. Once diagnosed, effective treatment strategies are limited and the five-year survival is extremely poor. Recent studies have shown that zinc finger proteins play important roles in tumorigenesis, including pancreatic cancer. However, it remains unknown on the clinical significance, function and underlying mechanisms of zinc finger protein 488 (ZNF488) during the development of pancreatic cancer. - Source: PubMed
Publication date: 2023/11/20
Xiao QifengLan ZhongminZhang ShuishengRen HuWang ShundaWang PengFeng LinLi DanWang ChengfengBai XiaofengZhang Jianwei