RAD54B Antibody
- Known as:
- RAD54B Antibody
- Catalog number:
- GWB-MM381C
- Product Quantity:
- 50ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- RAD54B Antibody
Related genes to: RAD54B Antibody
- Gene:
- RAD54B NIH gene
- Name:
- RAD54 homolog B
- Previous symbol:
- -
- Synonyms:
- RDH54
- Chromosome:
- 8q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-22
- Date modifiied:
- 2018-01-31
Related products to: RAD54B Antibody
Related articles to: RAD54B Antibody
- Bladder cancer remains one of the most common malignancies of the urinary tract. Although the treatment landscape has expanded rapidly in recent years, gemcitabine still occupies a central position in intravesical treatment for non-muscle-invasive bladder cancer, in perioperative systemic therapy for muscle-invasive disease, and in platinum-based first-line regimens for advanced urothelial carcinoma. Yet the long-term benefit of gemcitabine is frequently curtailed by primary non-response or acquired resistance. In practice, this problem is often recognized only after radiographic progression or clear clinical deterioration has occurred. This review summarizes recent progress in bladder cancer therapy and translational research, with a particular emphasis on the biological basis and hierarchical evolution of gemcitabine resistance. We establish a 3-stage operational model of resistance, distinguishing: (1) early pharmacologic resistance driven by impaired drug uptake/activation or enhanced inactivation; (2) intermediate resistance driven by enhanced DNA damage repair, replication stress tolerance, and pro-survival autophagy signaling; and (3) late adaptive resistance driven by epithelial-mesenchymal transition (EMT), stemness maintenance, metabolic reprogramming, non-coding RNA-mediated epigenetic regulation, inflammatory microenvironmental remodeling, and extracellular vesicle-based intercellular transmission. These layers function as an interactive network, with sequential emergence under treatment pressure and parallel activation in context-dependent clinical settings. We stratify key mechanistic nodes (including the HYAL4-V1/CD44/JAK2-STAT3/CDA axis, AKR1C3, AP1M2-RAD54B, PRPF19-DDB1, AKT/mTOR signaling, Beclin-1-dependent autophagy, the MINCR/ZEB1/PHGDH axis, and IL-6-associated inflammatory states) by their clinical evidence quality and translational readiness, explicitly distinguishing preclinical discovery from clinically validated findings. Critically, most mechanistic findings remain at the preclinical or retrospective validation stage, with no markers yet approved for routine clinical use. Future work must prioritize longitudinal paired clinical samples, standardized analytic assays for dynamic biomarkers, and the integration of functional models (organoids, microfluidic systems), multi-omics technologies (single-cell sequencing, spatial transcriptomics), and liquid-biopsy approaches to translate mechanistic discoveries into clinically actionable predictive tools and therapeutic strategies. - Source: PubMed
Publication date: 2026/05/29
Jin MingCai ZhenzhenBu MingLiu JichengZhang Xiaojie - Breast cancer is prevalent and deadly, affecting women worldwide. Increasing research suggests that lysine lactylation (KLA) and DNA damage repair (DDR) play critical roles in tumor progression and that KLA and DDR are interconnected, as KLA can modulate DDR protein function, thereby influencing genome stability and drug response, while DDR signaling can reciprocally reshape lactate metabolism and KLA activity. In this study, we developed a novel prognostic gene signature (KLA and DDR index, KLDRI) based on KLA- and DDR-related genes. Model genes (, , , , ) were generated via LASSO-Cox regression. Patients were stratified into high- and low-risk groups according to KLDRI, the robust prognostic value of which was demonstrated via survival and validation analyses in the TCGA cohort and the METABRIC and GSE96058 cohorts, respectively. Tumor microenvironment analysis indicated an immunologically suppressed phenotype in high-risk patients, whereas low-risk patients exhibited an immune-inflamed microenvironment. Drug sensitivity analysis indicated reduced sensitivity to multiple chemotherapy and targeted therapy drugs in the high-risk group. Single-cell transcriptomic analysis revealed differential gene expression patterns between risk groups. A prognostic nomogram based on KLDRI was developed to predict overall survival. Furthermore, functional experiments demonstrated that knockdown suppressed cancer cell proliferation and migration, sensitized cells to cisplatin treatment, and reduced global lactylation, which may serve as a novel biomarker and potential therapeutic target. These findings enhance our understanding of the interplay between KLA, DDR, and breast cancer progression, facilitating the development of personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/05/17
Zhu LiangYuan ChenweiLi YaorongFeng YuanLiang LuoqiZhu PinxuanYin WenjinLu Jinsong - The commercial viability of relies on efficient depuration. While extract dramatically accelerates this process, its physiological and molecular mechanisms remain unknown. To address this, we integrated behavioural, histological, ultrastructural, and transcriptomic (RNA-seq) analyses to characterize the acute stress and subsequent recovery phases of exposed to the botanical extract. Extract exposure induced severe neuromuscular hyperextension response, with histological analysis revealing acute interstitial oedema and neuronal chromatolysis. This structural damage caused sustained cephalopodium extension and muscle fibre uncoupling. Transcriptomic profiling linked this neuromuscular dysfunction to conserved calcium-dependent adrenergic signalling modules and profound endogenous neuroendocrine disruption. The extract also induced cellular stress, downregulating the apoptosis inhibitor and eliciting transcriptomic signatures consistent with a DNA damage response. Crucially, during the short-term recovery phase, surviving tissues mounted a robust transcriptomic repair response. The snails systemically suppressed the cell cycle via downregulation while upregulating and , suggesting a prioritization of genomic repair alongside partial morphological reorganization. Ultimately, accelerates depuration via acute phytochemical stress and neuromuscular dysfunction. Importantly, this stress is accompanied by a highly coordinated transcriptomic repair response and partial short-term restoration, providing foundational molecular insights essential for evaluating and optimizing botanical depuration protocols. - Source: PubMed
Publication date: 2026/05/13
Wang ZhiqiangChua EnjieLuo FuguangZhou XiaoyunHuang JiePeng JinxiaPan XianhuiWen Yanhong - BACKGROUND: The rapid differentiation between autoimmune and infectious encephalitis in children is a critical clinical decision that dramatically impacts treatment and outcome. Metagenomic next-generation sequencing (mNGS) of cerebrospinal fluid (CSF) is a powerful but often underutilized tool, as its host-derived RNA component is typically discarded. We hypothesized that this host response data could be translated into a diagnostic tool for autoimmune encephalitis (AE). METHODS: We enrolled 180 pediatric patients with suspected encephalitis to evaluate the clinical performance of CSF mNGS against conventional methods. Host transcriptomic analysis was performed on CSF cells from 88 patients (autoimmune, bacterial, and viral encephalitis). A novel biomarker was validated using RT-qPCR in an independent cohort, and its functional role was investigated in neuronal cultures challenged with NMDAR1 antibodies. A diagnostic model was developed and validated. RESULTS: mNGS demonstrated a significantly higher pathogen detection rate than conventional methods (29.4% vs. 16.7%). Host transcriptomic profiling revealed that AE shared a hyperinflammatory signature with viral encephalitis but was uniquely associated with dysregulation of receptor tyrosine kinase and heme signaling pathways. Furthermore, memory B cells and activated mast cells were specifically elevated in AE. We identified and validated RAD54B as a novel biomarker specifically upregulated in AE. Functionally, RAD54B upregulation protected neurons from DNA damage stress induced by NMDAR1 antibodies. A multi-gene diagnostic model based on host-response genes robustly differentiated AE from infectious encephalitis (AUC > 0.923) in a validation set. CONCLUSIONS: We present a validated translational pipeline that repurposes routine CSF mNGS data into a dual-purpose diagnostic tool. By leveraging the host RNA data inherent in CSF mNGS, clinicians can now simultaneously investigate infectious and autoimmune etiologies in a single, rapid test. This strategy has the immediate potential to reduce diagnostic delay, guide timely therapy, and improve outcomes in children with encephalitis. - Source: PubMed
Publication date: 2026/04/22
Han DingdingPan XiaozhouPan FenHan BiyunWu QianyueZhou YipingLiu HuifangXu HuanSun WeifenCheng HongyiLiu WenxinWan RujiaWeng WenhaoZhang Hong - Genome stability is essential for cellular viability yet constantly threatened by endogenous and exogenous DNA-damaging agents. Among these, DNA double-strand breaks (DSBs) are particularly harmful and in S/G2 phases are faithfully repaired through homologous recombination (HR), a high-fidelity pathway utilising homologous sequences in sister chromatin. The RAD51 recombinase forms nucleoprotein filaments on single-stranded DNA (ssDNA) to mediate homology search, strand invasion and subsequent D-loop formation that leads to DNA synthesis and repair. The efficiency of HR depends on precise regulation of RAD51 filament dynamics by accessory factors, including RAD54 and RAD54B, which belong to the SWI2/SNF2-family DNA translocases. While RAD54 is well-characterized, RAD54B's molecular functions remain poorly understood. Here, we define RAD54B's role in HR using cryo-electron microscopy, mutagenesis, biochemical and cellular assays. We show that RAD54B stabilizes RAD51-DNA filaments, inhibits RAD51 ATPase activity, and promotes strand invasion, D-loop formation and strand exchange. The N-terminal domain (NTD) alone supports filament stabilization and strand exchange, while the C-terminal ATPase domain is required for D-loop formation. Structural and biochemical analyses reveal three RAD51-interacting sites within the NTD and a unique domain (β-domain) that bridges RAD51 protomers and contacts donor dsDNA. This β-domain also regulates RAD54B's ATPase activity and higher-order oligomer organization on dsDNA. Cellular assays reveal that the NTD RAD51-interacting sites as well as the β-domain are required for repairing camptothecin-induced DSBs by HR in human cells. Our findings uncover a modular architecture and mechanistic framework for RAD54B function in HR, highlighting its critical role in genome maintenance. - Source: PubMed
Publication date: 2026/03/24
Liang PengtaoTye StephanieErtl da Costa JohannaMaharshi NeelamArgunhan BilgeKuhlen LucasBattley MeganMcCormack Elizabeth AHeyer Wolf-DietrichLöbrich MarkusZhang Xiaodong