Ask about this productRelated genes to: USP39 antibody
- Gene:
- USP39 NIH gene
- Name:
- ubiquitin specific peptidase 39
- Previous symbol:
- -
- Synonyms:
- SAD1, CGI-21, SNRNP65
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-04
- Date modifiied:
- 2015-08-26
Related products to: USP39 antibody
Related articles to: USP39 antibody
- FOXA1 is a pioneer transcription factor that shapes lineage-specific regulatory programs in hormone-associated cancers. Here, we integrated FOXA1 cistromes, transcriptomes, GWAS loci, expression-associated quantitative trait loci (eQTL) datasets, clinical cohorts, and functional assays to examine how FOXA1-directed transcriptional networks contribute to prostate and breast cancer biology. We identified high-confidence FOXA1 direct target genes that converge on shared oncogenic pathways while retaining cancer-type-specific regulatory modules. These FOXA1-associated transcriptional programs generated prognostic signatures that stratified patient outcomes across independent cohorts. In prostate cancer, cancer-risk variants were enriched within FOXA1 binding regions, and selected functional variants modulated FOXA1 occupancy and downstream key effector gene (, , and ) expression. Functional validation supported roles for these genetically regulated targets in prostate cancer cell proliferation and migration. Together, our findings connect inherited noncoding variation, FOXA1 chromatin binding, transcriptional regulation, and tumor-associated phenotypes, providing a framework for understanding FOXA1-centered regulatory mechanisms in hormone-associated cancers. - Source: PubMed
Publication date: 2026/08/06
Luo BinjieZhang QinYang XiayunTan ZenglaiQin LongguangYang YuehongJokela RiittaGiannareas NikolaosManninen AkiWei Gong-Hong - Atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of mortality worldwide, yet its genetic architecture and underlying mechanistic hypotheses have not been fully elucidated. - Source: PubMed
Publication date: 2026/07/06
Liu QinHan XiaodiHu Yue-QingFu Liwan - Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy primarily driven by oncogenic KRAS signaling. The splicing factor SRSF1 plays a key oncogenic role in PDAC through reciprocal cross-interactions with KRAS signaling. However, the mechanisms regulating SRSF1 protein stability remain poorly understood. Here, we identify the deubiquitinase USP39 as a critical regulator of SRSF1 stability. It interacts with SRSF1 in an RNA-independent manner and suppresses its ubiquitination. USP39 is upregulated in PDAC and correlates with poor patient prognosis. Functional analyses demonstrate that USP39 promotes PDAC cell progression, in part through stabilization of SRSF1. Mechanistically, MYC activates USP39 transcription through direct promoter binding. These findings define a MYC-USP39-SRSF1 regulatory axis that integrates transcriptional and post-translational mechanisms in PDAC and suggest USP39 as a potential therapeutic target. Implications: USP39 functions as a central regulator that integrates transcriptional and post-translational regulation in pancreatic cancer through the MYC-USP39-SRSF1 axis and represents a potential therapeutic target. - Source: PubMed
Publication date: 2026/06/11
Ma BentengZhang XinKral Alexander JSingh NeeluDeschênes AstridCifani PaoloPark YoungkyuTuveson David AKrainer Adrian RWan Ledong - Ovarian cancer (OV) is a leading cause of mortality related to gynecological malignancies. Chemoresistance represents a major clinical obstacle. Carboplatin (CBP) is a first-line chemotherapeutic agent widely used for ovarian cancer treatment. Meanwhile, Zinc Finger CCCH-Type Containing 18 (ZC3H18) is aberrantly overexpressed in OV. However, its functional role and underlying regulatory mechanisms in CBP resistance remain undefined. Ovarian cancer cell lines A2780 and ES‑2 and their CBP‑resistant sublines (A2780/CBP and ES‑2/CBP) were used in this study. The resistant cell lines were established by exposing parental cells to gradually increasing concentrations of CBP for two months. Western blotting, IHC, and RT-qPCR were used to detect gene and protein expression. CCK-8, EdU, and flow cytometry analyses were used to measure cell viability, proliferation, and apoptosis. A Seahorse XFp extracellular flux analyzer and a commercial kit were used to evaluate mitochondrial function. Co-IP was used to validate protein interactions. MSP was performed to analyze BRCA1 methylation. ZC3H18 expression was significantly elevated in CBP-resistant OV tissues and cell lines and was associated with poor patient prognosis. ZC3H18 silencing in resistant cells reduced mitochondrial OCR and ATP production, suppressed proliferation, and enhanced CBP-induced apoptosis. Mechanistically, USP39 directly interacted with and deubiquitinated ZC3H18, thereby enhancing its protein stability. ZC3H18, in turn, promoted BRCA1 expression by reducing methylation of the BRCA1 promoter. Furthermore, USP39 knockdown sensitized resistant cells to CBP, an effect that was partially reversed by ZC3H18 overexpression, which restored BRCA1 expression, mitochondrial function, and chemoresistance. USP39-mediated deubiquitination stabilized ZC3H18, which suppressed BRCA1 promoter methylation and enhanced mitochondrial biogenesis, thereby promoting CBP resistance in ovarian cancer. Targeting the USP39/ZC3H18/BRCA1 axis may offer a novel strategy for overcoming chemoresistance. - Source: PubMed
Publication date: 2026/05/25
Wang JingLi XinyuChang JianmiaoHou XiaoxueYan YananChen JiangpingWu Xin - Opioid use disorder (OUD) is caused by a complex interplay between genetic and non-genetic factors. DNA methylation is an epigenetic mechanism that modulates gene expression. Data on DNA methylation and opioid addiction and treatment are limited. This association study was designed to assess the difference in genome-wide methylation patterns between individuals with OUD in methadone maintenance treatment (MMT) ( = 114) and those with OUD who achieved long-term abstinence (>10 years) without mu opioid receptor agonist treatment ( = 136). - Source: PubMed
Publication date: 2026/05/05
Levran OrnaLi JustinSason AnatAdelson MiriamPeles Einat