Ask about this productRelated genes to: RNF169 antibody
- Gene:
- RNF169 NIH gene
- Name:
- ring finger protein 169
- Previous symbol:
- -
- Synonyms:
- KIAA1991
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-13
- Date modifiied:
- 2018-11-19
Related products to: RNF169 antibody
Related articles to: RNF169 antibody
- Ubiquitination of the C-terminus of histone H2B (H2BK120ub) is a key histone modification with functions in a wide array of DNA-related processes, best characterized in gene transcription and repair. A role for H2B ubiquitination in DNA replication has been postulated and investigated in yeast but is still elusive in human cells. Here, we uncovered a critical function of H2BK120ub in replication fork dynamics. H2BK120ub is present at replication forks and accumulates upon replication stress in a manner dependent on ATR and RAD51. Loss of RNF20, the main ubiquitin ligase promoting H2BK120ub, leads to RECQ1-mediated unrestrained replication fork progression and defective fork reversal upon mild replication stress, restoring fork stability in BRCA2-deficient cells. Furthermore, we identified RNF169, a factor involved in the DNA damage response and repair, as a reader of the H2BK120ub mark at stalled replication forks, where it is required to protect the nascent DNA from excessive nucleolytic degradation. Hence, RNF20, H2BK120ub and RNF169 are key novel players orchestrating replication stress response and fork plasticity in human cells. - Source: PubMed
Publication date: 2025/10/27
Duzanic Filip DMohana-Natarajan VaishnaviFisicaro SamueleBakker CollinAouami MosesAmaral GabrielLopes MassimoTaneja NitikaPenengo Lorenza - The prognosis prediction of breast cancer is a challenging problem in the clinic. Identifying reliable biomarkers and revealing the regulatory mechanism underlying the progression of breast cancer cells would benefit the treatment and outcomes of breast cancer patients. - Source: PubMed
Publication date: 2025/10/17
Chang YanSun ZheminXu Meiling - Spatiotemporal recruitment of DNA repair factors is crucial to coordinate repair across DNA lesions. MacroH2A1.2 (mH2A1.2), which accumulates in subgenomic regions that are difficult to replicate (e.g., common fragile sites, telomeres, and repeated sequences), selectively promotes homology-driven DNA repair; however, the mechanisms remain elusive. We report an unexpected role for RNF168-mediated mH2A1.2 ubiquitination in preventing aberrant RAD18 recruitment to subgenomic loci experiencing prolonged replication arrest in human cancer cells. Biochemical reconstitution revealed that RAD18 cannot bind ubiquitinated mH2A1.2-containing nucleosomes. In cells, loss of mH2A1.2 ubiquitination increases RAD18 and γH2AX levels at collapsed forks and sensitizes cells to replication stress. Depletion of RAD18, fork remodelers, or the endonuclease MUS81 rescues these phenotypes, indicating that mH2A1.2-ubiquitination prevents toxic RAD18 engagement at MUS81-dependent double-strand breaks (DSBs), which arise at collapsed forks in difficult-to-replicate sites experiencing prolonged arrest. Our findings highlight the detrimental consequences of inappropriate DNA processing by MUS81 at these loci. - Source: PubMed
Publication date: 2025/08/13
Galloy MaximeBlondeau AndréanneVion ÉlodieKim DaeinBakker Collin AGaggioli VincentThomas MélissaLavoie Élise GMarois IsabelleDelgado Monterroso Alberto DavidMasson Jean-YvesTaneja NitikaMiller Kyle MMaréchal AlexandreFradet-Turcotte Amélie - We performed an integrated analysis of genome-wide DNA methylation and expression datasets in normal cells and healthy animals exposed to polyphenols with estrogenic activity (i.e. phytoestrogens). We identified that phytoestrogens target genes linked to disrupted cellular homeostasis, e.g. genes limiting DNA break repair () or promoting ribosomal biogenesis (). Existing evidence suggests that DNA methylation may be governed by sirtuin 1 (SIRT1) deacetylase via interactions with DNA methylating enzymes, specifically DNMT3B. Since SIRT1 was reported to be regulated by phytoestrogens, we test whether phytoestrogens suppress genes related to disrupted homeostasis via SIRT1/DNMT3B-mediated transcriptional silencing. Human MCF10A mammary epithelial cells were treated with phytoestrogens, pterostilbene (PTS) or genistein (GEN), followed by analysis of cell growth, DNA methylation, gene expression, and SIRT1/DNMT3B binding. SIRT1 occupancy at the selected phytoestrogen-target genes, and , was accompanied by consistent promoter hypermethylation and gene downregulation in response to GEN, but not PTS. GEN-mediated hypermethylation and SIRT1 binding were linked to a robust DNMT3B enrichment at and promoters. This was not observed in cells exposed to PTS, suggesting a distinct mechanism of action. Although both SIRT1 and DNMT3B bind to and promoters upon GEN, the two proteins do not co-occupy the regions. Depletion of SIRT1 abolishes GEN-mediated decrease in expression, suggesting SIRT1-dependent epigenetic suppression of by GEN. These findings enhance our understanding of the role of SIRT1-DNMT3B interplay in epigenetic mechanisms mediating the impact of phytoestrogens on cell biology and cellular homeostasis. - Source: PubMed
Publication date: 2025/03/03
Ma YuexiBoycott CaylaZhang JiaxiGomilar RekhaYang TonyStefanska Barbara - Prostate cancer (PCa) remains a significant global health challenge, with approximately 1.6 million new cases and 366,000 deaths annually. Despite high survival rates for localized prostate cancer, recurrence poses a substantial risk due to inherent biological factors and residual disease. Early detection and intervention are essential for enhancing patient outcomes and reducing mortality. However, traditional diagnostics such as PSA tests, digital rectal examinations, and biopsies often lack specificity resulting in overdiagnosis. There is a pressing need for novel biomarkers to enhance precision medicine approaches for PCa. This study employs a machine learning approach to identify DNA methylation and RNA expression biomarkers predictive of PCa recurrence using datasets from The Cancer Genome Atlas (TCGA). We analyzed 49,133 genes, identifying 684 differentially methylated genes (DMGs) and 691 differentially expressed genes (DEGs) between recurrence and non-recurrence groups. Ten genes (TNNI2, SPIN2, COL5A3, RNF169, CCND1, FGFR1, SLC17A2, FAMM71F2, RREB1, AOX1) were found to have significant correlations between methylation and expression, forming the basis for our predictive model. A support vector machine (SVM) model was developed using these ten genes, achieving an area under the curve (AUC) of 0.773, demonstrating robust predictive capability. Multivariate regression analysis confirmed the SVM score as an independent predictor of recurrence (HR = 0.45; 95% CI 0.28-0.69, P < 0.001). The analysis of recurrence-free survival suggested that patients with low-risk scores experienced significantly better outcomes compared to those with high-risk scores. Functional enrichment analyses of DMGs revealed significant involvement in biological processes such as transcription regulation, signal transduction, and immune response, highlighting the potential mechanistic pathways of these biomarkers. Validation using real-time PCR confirmed differential expression and methylation patterns of the identified genes in prostate cancer (PC3) and non-cancerous cell lines (PNT2). In conclusion, our study hihglights the DNA methylation biomarkers linked to PCa recurrence and introduces a promising SVM model for early prediction, potentially improving treatment outcomes. Further research is needed to explore the biological roles of these genes in PCa aiming to refine therapeutic approaches. - Source: PubMed
Publication date: 2025/02/01
Aldakheel Fahad MAlnajran HadeelAlduraywish Shatha AMateen AyeshaAlqahtani Mohammed SSyed Rabbani