RAD50 Antibody (OASA09269)
- Known as:
- RAD50 Antibody (OASA09269)
- Catalog number:
- oasa09269
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RAD50 Antibody (OASA09269)
Related genes to: RAD50 Antibody (OASA09269)
- Gene:
- RAD50 NIH gene
- Name:
- RAD50 double strand break repair protein
- Previous symbol:
- -
- Synonyms:
- hRad50, RAD50-2
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-23
- Date modifiied:
- 2016-01-27
Related products to: RAD50 Antibody (OASA09269)
Related articles to: RAD50 Antibody (OASA09269)
- Cardiac fibrosis is a hallmark of ischemic heart failure and is driven by activated myofibroblasts. DNA damage and defective repair promote fibroblast activation, yet the upstream regulators that couple DNA damage responses to profibrotic remodeling remain unclear. - Source: PubMed
Publication date: 2026/07/31
Su ZhenyangShen HuiSun JinyuKong XiangqingSun Wei - Rheumatoid arthritis (RA) is characterized by persistent synovial inflammation in which fibroblast-like synoviocytes (RA-FLS) and B cells interact within a potentially genotoxic microenvironment. This study investigates how naive B cells respond to cytotoxic stress when supported by RA-FLS in a co-culture model, using viability assays, time resolved γ-H2AX MFI, RT-qPCR of DNA damage response and differentiation genes, and flow cytometric analysis of subsets and surface markers. Naive B cells exhibited greater loss of viability than RA-FLS, and time-resolved γ-H2AX MFI showed an earlier signal peak and decline in naive B cells versus prolonged retention in RA-FLS (0-24h post-treatment); these reflect overall damage-response dynamics rather than direct DSB repair. Importantly, γ-H2AX levels indicate DNA damage but do not directly quantify DNA break repair. Transcriptional profiling showed selective induction of ATM, APEX1, RAD50, BAX, and BCL6 following treatment, consistent with engagement of a focused DNA damage response program. Prolonged co-culture was associated with the expansion of B cell enriched compartments derived from naïve B cells, and with increased expression of stromal markers CD90 and podoplanin on both B cells and RA-FLS, while IL-10 secretion was reduced under cytotoxic conditions. Together, these findings define differential stress responses and phenotypic adaptations of B cells and RA-FLS within an inflammatory co-culture system and suggest that genotoxic stress may contribute to remodeling of immune-stromal interactions in the rheumatoid synovium. - Source: PubMed
Publication date: 2026/07/13
Bruci DenadaLowin TorstenFritz GerhardWolf FrancescaPongratz Georg - Hereditary cancer syndromes (HCSs) account for approximately 5-10% of all cancers and are frequently associated with pathogenic variants (PVs) in genes such as and . Nevertheless, a substantial proportion of individuals with strong familial cancer aggregation remain genetically unexplained after standard multigene panel testing. Clinical exome sequencing (CES) may overcome this limitation by enabling a broader exploration of cancer susceptibility genes. - Source: PubMed
Publication date: 2026/07/24
Dell'Elice AnastasiaPalmarini ClaudiaAnaclerio FedericoPilenzi LucreziaCalabrese GiuseppePalka ChiaraTinari NicolaGrassadonia AntoninoBallerini PatriziaGrossi SimonaVitali MarcoSecondi LorenzoAmerio PaoloGatta ValentinaStuppia LiborioAntonucci Ivana - Genomic sequencing has made precision oncology of pancreatic ductal adenocarcinoma (PDAC) feasible and is recommended by numerous clinical guidelines. The clinical significance of genomic alterations in PDAC remains to be revealed. This study was designed to bridge this gap by elucidating the clinical relevance of genomic profiling in a diverse PDAC population. From January 1, 2021 to April 30, 2023, we prospectively collected tumor tissues and peripheral blood from 1135 patients diagnosed with PDAC at Fudan University Shanghai Cancer Center (FUSCC). Germline and somatic mutations were identified using a 676-gene panel. PDAC with KRAS/ARID1A co-mutation was featured with early metastasis and poor prognosis. Patients with BRCA1/2 and PALB2 mutations showed a trend towards improved survival with platinum-containing regimens, although statistical significance was not reached. In contrast, we observed a statistical preference for platinum-containing adjuvant chemotherapy in KRAS wild-type PDAC patients. For the mutational landscape, the current cohort had a lower mutation rate of KRAS, while mutations related to the WNT, Hippo, and PI3K signaling pathways were more prevalent, compared with Caucasian PDAC. Somatic RAD50 p.L719fs, ATR p.I774fs, and germline RAD51D p.K91fs were homologous recombination repair (HRR) gene mutations enriched in this Chinese cohort relative to reported Caucasian series. These results highlighted that genomic sequencing could guide the management of PDAC, including prognosis prediction and chemotherapy regimen selection. Trial Registration: Chinese Clinical Trial Registry registration number: ChiCTR2500097983. - Source: PubMed
Dong MingweiHua JieMa ZhilongTang RongWei MiaoyanLv ZonglinLiu YuanChen KeDu QiongWang WeiYu XianjunXu Jin - Microsatellite instability-high (MSI-H) colorectal cancer cells depend on the Werner syndrome helicase (WRN) to resolve cruciform DNA structures that arise from expanded TA-dinucleotide repeats. Loss of WRN induces replication stress and double-strand breaks (DSBs), a vulnerability that can be recapitulated by the selective WRN inhibitor HRO761 in MSI cancer cells. To uncover the mechanisms governing sensitivity to WRN inhibition, we conducted genome-wide CRISPR/Cas9 screens in colorectal cancer cell lines treated with or without HRO761. These screens identified SMARCAL1 as a key modulator of WRN dependency. Depletion of SMARCAL1 rendered cells resistant to WRN inhibition, and rescue of this effect required the ATPase/translocase activity of SMARCAL1. Mechanistically, SMARCAL1 antagonized WRN and supported cruciform DNA structures, thereby enhancing cellular reliance on WRN. In addition, the MRE11-RAD50-NBS1 (MRN) complex, rather than MUS81 or ERCC1/XPF, was the principal mediator of cruciform DNA processing following WRN inhibition. Acute disruption of the MRN complex conferred profound resistance to WRN inhibition, whereas ATM deficiency produced a more modest resistant phenotype. Further genetic and pharmacological epistasis analyses demonstrated that the MRN complex regulates WRN inhibitor sensitivity through both ATM-dependent signaling and MRE11 nuclease-dependent functions. Importantly, the key resistance mechanisms identified in this study were independently validated using a structurally distinct clinical-stage WRN inhibitor VVD-214. Collectively, these findings identify the SMARCAL1-MRN-ATM axis as a critical regulator of WRN dependency and provide mechanistic insight into resistance to WRN-targeted therapy. - Source: PubMed
Publication date: 2026/07/22
Ma TiantianWu JiboLi SitingChen Junjie