Ask about this productRelated genes to: WDR89 antibody
- Gene:
- WDR89 NIH gene
- Name:
- WD repeat domain 89
- Previous symbol:
- C14orf150
- Synonyms:
- MGC9907
- Chromosome:
- 14q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-11
- Date modifiied:
- 2014-11-18
Related products to: WDR89 antibody
Related articles to: WDR89 antibody
- While Wilms tumor (WT) is primarily associated with mutations in and genes, these alterations account for only ~30% of cases, suggesting a broader, unexplored genetic landscape. - Source: PubMed
Publication date: 2026/05/05
Kumar SourabhSharma JyotiPandey HimaniJain VisheshDhua Anjan KumarYadav Devendra KumarDivya GaliLal DeviGoel PrabudhAgarwala Sandeep - Familial prostate cancer (PCa) accounts for nearly 20% of all PCa cases and is associated with increased genetic susceptibility and earlier disease onset. However, early detection and risk stratification in genetically predisposed individuals remain challenging. Circulating cell-free DNA (cfDNA) provides a minimally invasive source of tumor-derived genomic and epigenomic information. Integrating multi-omic cfDNA analyses may enhance the discovery of biomarkers relevant to familial PCa biology. We conducted a pilot feasibility study employing whole-genome, strand-specific sequencing of cfDNA from eight patients with familial PCa. A unified analytical pipeline was used to jointly profile genomic alterations and epigenomic features. Variant calling, methylation mapping, and allele-specific methylation (ASM) analysis were performed to identify somatic mutations, characterize epigenetic dysregulation, and explore potential interactions between genetic and epigenetic mechanisms. Sequencing revealed 18,878 genetic variants, including 2276 potentially pathogenic alterations. We identified 26 recurrent high-impact mutations, such as stop-gain and start-loss variants, in genes including , , and . Epigenomic profiling demonstrated widespread gene-specific hypermethylation, consistent with transcriptional repression in these loci. ASM events were detected in , , , , and , suggesting coordinated interactions between somatic variation and epigenetic regulation in familial PCa. This proof-of-concept study highlights the feasibility and potential of integrating whole-genome and epigenome profiling of cfDNA to decode the molecular architecture of familial prostate cancer. By jointly capturing genomic alterations and epigenetic signatures, including allele-specific methylation, this multi-omic liquid biopsy approach supports a high-resolution exploration of biologically relevant molecular features. Moreover, this integrated profiling strategy provides a minimally invasive and clinically scalable tool that may substantially improve risk assessment. These findings offer a promising foundation for future validation studies in larger cohorts, with the aim of advancing multi-omic cfDNA analysis as a next-generation technology in the field of precision oncologic epigenetics. - Source: PubMed
Publication date: 2026/04/03
Truda AnnaCordella AngelaDe Leo IleniaDi Palo ArmandoIorio RobertaMarino SimonaLa Rocca RobertoCollà Ruvolo ClaudiaPotenza NicolettaRavo MariaMarchese Giovanna - Conventional target screening repertoires provide limited coverage of proteome-level interactions, leaving critical gaps in the mechanistic toxicology of per- and polyfluoroalkyl substances (PFAS). In this study, thermal proteome profiling (TPP) was applied for unbiased, proteome-wide characterization of PFAS-protein interactions across five representative PFAS, identifying 173 proteins with significant ligand-induced stabilization. Specifically, legacy PFAS converged on small COPII coat GTPase SAR1A/SAR1B, consistent with potential mechanistic Target of Rapamycin (mTOR)-linked metabolic reprogramming, whereas the replacement ether PFAS hexafluoropropylene oxide dimer acid (HFPO-DA, commercially known as GenX) showed a distinct targetome highlighted by WD repeat-containing protein 89 (WDR89), suggesting non-nuclear-receptor mechanisms plausibly related to chromatin/complex assembly. Cellular thermal shift assay and molecular docking independently verified target engagement and provided a structural rationale for the observed stabilization patterns. Further ontology-based annotation linked the stabilized targets to 279 standardized disease entities, with a predominance of neoplastic outcomes. These findings demonstrate TPP as a new approach methodology for PFAS target discovery, reveal divergent early events for legacy versus replacement chemistries, and provide a proteome-scale framework to prioritize mechanism-based validation and to support evidence-weighted risk assessment of emerging fluorinated alternatives. - Source: PubMed
Publication date: 2026/03/26
Zheng XuehanLi YananQin HuaRuan ChengfeiYao LinlinLiu XianYe MingliangQu GuangboJiang Guibin - Glioblastoma (GBM) is one of the most aggressive cancers due to its high mortality rate in spite of intensive treatment. It may be happened because of drug resistance against their typical receptors, since these receptor genes are often mutated by environmental stress. So identifying mutated oncodriver genes which could be used as potential drug target is essential in order to develop effective new therapeutic drugs as well as better prognosis for GBM patients. In this study, we analyzed whole exome sequencing (WES) profiles of NCBI database on GBM and matched-normal (control) samples originated from astrocyte like neural stem cells (NSC) of subventricular zone (SVZ) to explore GBM-causing mutated oncodriver genes, since SVZ is considered as the origin of GBM development. We detected 16 mutated oncodriver genes. Then, filtering by differential co-expression analysis based on independent RNA-Seq profiles of CGGA database revealed 10 genes as dysregulated oncodriver genes. Following that, 3 significantly overexpressed oncodriver genes (MTCH2, VWF, and WDR89) were identified as potential drug targets. Then molecular mechanisms of GBM development were investigated by these three overexpressed driver genes through gene ontology (GO), KEGG-pathways, Gene regulatory network (GRN) and mutation analysis. Finally, overexpressed oncodriver genes guided top-ranked six drug agents (Irinotecan, Imatinib, etoposide, pazopanib, trametinib and cabozanitinib) were recommended against GBM through molecular docking study. Most of our findings received support by the literature review also. Therefore, the findings of this study might carry potential values to the wet-lab researchers for further investigation in terms of diagnosis and therapies of GBM. - Source: PubMed
Publication date: 2025/01/16
Sarker ArnobUddin BurhanAhmmed ReazMahmud SabkatAjadee AlviraPappu Md Al AminAziz Md AbdulMollah Md Nurul Haque - Circular RNAs are a single-stranded non-coding RNAs and play an important role in the development of many diseases. Alternative polyadenylation (APA) regulates the gene 3'UTR length for controlling gene expressions. Although the APA mechanism has been widely studied in the development of diseases, there is no data on its role in the burned intestinal mucosa. We thus herein assessed the role of the circSugp1-initiating APA mechanism in the burned intestinal mucosa. CircSugp1 was downregulated in the intestinal mucosa of burned mice. CircSugp1 promoted proliferation and migration in vitro and in vivo. CircSugp1 promotes the expression of CPSF6; the overexpression of CPSF6 can shorten the gene 3'UTR within the transcript APA range. The promoting effect of circSugp1 on value-added migration was mediated by the APA regulation of the Wdr89 short 3'UTR isoform. CircSugp1 targeted the upregulation of the expression of CPSF6, followed by upregulation of the expression of Wdr89 through APA, promoting the repair of intestinal mucosal damage in burned mice. - Source: PubMed
Publication date: 2024/12/11
Liao YuLi RanZhang HaoLi QiXu XiaoqingMeng FanzeSun Yong