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)
- Homologous recombination repair (HRR) pathway defects are critical drivers of hereditary cancers, yet population-specific prevalence data from India remain limited. Current testing practices disproportionately focus on , potentially underidentifying patients with other HRR gene variants who could benefit from targeted therapies. - Source: PubMed
Publication date: 2026/08/13
Kapoor AkhilUthale SrushtiChain AnamikaRungta ArchiAnoop AnjanaGupta AnujSansar BipineshMishra Bal KrishnaPal AnkitaThakkar SoumyaSarin Rajiv - 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