DNA_PK pAb;human, mouse, rat, hamster
- Known as:
- DNA_PK pAb;H. sapiens, mouse, rat, hamster
- Catalog number:
- ASAKAP-PI001E
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- DNA_PK pAb;human mouse rat hamster
Related genes to: DNA_PK pAb;human, mouse, rat, hamster
- Gene:
- PRKDC NIH gene
- Name:
- protein kinase, DNA-activated, catalytic subunit
- Previous symbol:
- HYRC, HYRC1
- Synonyms:
- DNPK1, p350, DNAPK, XRCC7, DNA-PKcs, DNAPKc, DNA-PKC, p460
- Chromosome:
- 8q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-09
- Date modifiied:
- 2019-04-23
Related products to: DNA_PK pAb;human, mouse, rat, hamster
Related articles to: DNA_PK pAb;human, mouse, rat, hamster
- Hepatocellular carcinoma (HCC) remains a lethal malignancy with limited therapeutic options. While Poly (ADP-ribose) polymerase inhibitors (PARPi) exploit synthetic lethality in tumors with DNA repair defects, their clinical utility in HCC is hindered by the low prevalence of canonical repair gene mutations and the enhancing DNA repair capacity. Through proteomic analysis of two independent cohorts (=260), we identified the THO complex component THOC2 as a master regulator of DNA damage response (DDR) via mRNA nuclear export control. Clinically, THOC2 overexpression predicted poor survival (HR=2.68-6.84, <0.001) and correlated with enhanced DDR gene expression. Mechanistically, THOC2 chaperones mRNA nuclear export of DDR effectors (MDC1, PRKDC, MSH6) and proliferation drivers (TOP2A), thereby establishing a dual pro-repair/pro-growth program. Targeting this vulnerability, THOC2 knockdown induced synthetic lethality with PARPi, reducing Olaparib IC50 by up to 61% and suppressing tumor growth by 76% (<0.001). Our study illuminates mRNA transport as a druggable DDR modulator and establishes THOC2 as both a prognostic biomarker and a therapeutic target to overcome PARPi resistance in HCC. This work pioneers a strategy to expand synthetic lethality beyond genetic defects by targeting post-transcriptional regulation. - Source: PubMed
Publication date: 2026/06/10
Li XinliYang SongpengZhang MengxinGuo ZhaoyuWang YanMeng YanruLiu YuanpingZhang HuXu KaikunZhang XiuyuanZhai YuanjunJin JingzhuoHe FuchuTian ChunyanSun Aihua - Relapse and graft-versus-host disease (GvHD) remain primary causes of treatment failure in patients with B-cell acute lymphoblastic leukemia (B-ALL) undergoing allogeneic hematopoietic cell transplantation (allo-HCT). While abatacept (ABATA) effectively mitigates GvHD via CD28-costimulation blockade, there is significant concern that it concurrently diminishes graft-versus-leukemia (GvL) effects, potentially leading to higher relapse rates. We investigated whether blinatumomab (BLINA) retains antileukemic efficacy in the presence of ABATA using in vitro assays and humanized NOD.Cg-Prkdc Il2rg Tg(IL15)1Sz/SzJ (NSG-IL15) and NOD.Cg-Prkdc Il2rg/SzJ (NSG) mouse models. - Source: PubMed
Publication date: 2026/06/12
Leite Geovana S FSullivan JohnFilioglou DimitriosKounelis MatinaBatatinha HelenaSimpson Richard JKatsanis Emmanuel - Sjögren's syndrome (SS) is a systemic autoimmune disease characterized by lymphocytic infiltration of exocrine glands, leading to impaired glandular secretion. To elucidate the pathogenic mechanisms underlying SS, suitable preclinical animal models are essential. In this study, we developed a humanized murine model that captures key immunopathological features of SS patients, and assessed its therapeutic utility. - Source: PubMed
Publication date: 2026/05/22
Park Jin-SilChoi JeongWonJeong Ha YeonKang Hye YeonCho Sang HeeLee Su BeomCho Mi-LaPark Sung-Hwan - Indigenous sheep breeds represent valuable reservoirs of genetic diversity shaped by long-term adaptation to local environments and management systems. Greek autochthonous sheep breeds remain underrepresented in genomic and functional studies. The objective of this study was to characterize and compare coding sequence variation in three indigenous Greek sheep breeds-Lesvos (LES), Serres (SER), and Thrace (THR)-and to identify shared and breed-associated functional patterns. The study was designed using a two-stage approach, comprising a discovery (exploratory) phase and a validation phase. In the discovery phase, whole genome sequencing data (one animal per breed; total = 3; mean sequencing depth ~36.9×) were analyzed to identify protein-altering exonic variants, focusing on missense single-nucleotide polymorphisms (SNPs) and exonic insertions/deletions (indels). Variants were examined at breed-specific and comparative levels, followed by functional enrichment analyses using Gene Ontology (GO) and KEGG pathways. Normalized variant density metrics identified genes with elevated polymorphism levels. In the validation phase, a subset of prioritized missense SNPs was genotyped in an independent cohort of 54 animals (18 per breed) using MassARRAY genotyping. Genes harboring prioritized missense SNPs showed a conserved enrichment profile across breeds, dominated by genome maintenance, DNA repair, cytoskeletal organization, and core regulatory functions. Distinct breed-associated patterns were also observed. LES showed enrichment in metabolic, biosynthetic, and sensory-related processes, SER in regulatory and signaling functions, and THR in cytoskeletal, extracellular matrix, and organelle-associated pathways. Polymorphism density analyses highlighted highly variable genes across breeds, including olfactory receptor (OR) gene families, keratin-associated protein genes (), and loci involved in immune and regulatory functions (e.g., , ). The validation phase confirmed the expected allele frequency patterns for most prioritized SNPs, supporting the robustness of the approach. This study identifies functionally relevant coding variation across Greek indigenous sheep breeds, revealing conserved genomic patterns and breed-associated signatures linked to metabolic, structural, and regulatory processes. - Source: PubMed
Publication date: 2026/05/05
Kyrgiafini Maria-AnnaStamatellos GeorgiosStamatis CostasMamuris Zissis - The global spread of mpox continues to pose a threat to public health, with immunocompromised patients being at greater risk for severe disease. This study aimed to establish a lethal severe infection model using NPG (NOD.Cg-Prkdc Il2rg/Vst) mice, a strain with profound immunodeficiency, to simulate severe mpox in immunocompromised patients and investigate disease progression, viral replication kinetics, tissue tropism, and immune responses. In our study, mice were inoculated with three doses of mpox virus (high: 2 × 10, medium: 2 × 10, low: 2 × 10 TCID [50% tissue culture infective dose]) or phosphate-buffered saline as a negative control. Body weight, clinical signs, and survival were monitored. Viral loads in plasma and tissues, histopathological changes, and inflammatory responses were evaluated to systematically characterize the pathogenicity of mpox virus in severely immunodeficient mice. The results showed that NPG mice were highly susceptible to mpox virus, showing a clear dose-dependent response. The high-dose group exhibited 100% lethality, and the medium-dose group had a 50% survival rate, whereas the low-dose and control groups survived throughout the study. Plasma and tissue viral loads, as well as histopathological severity, followed a dose-dependent pattern. Viremia remained persistently high, and animals that died at different time points exhibited uniformly high viral loads across multiple tissues. By day 10 postinfection, markedly elevated levels of pro-inflammatory cytokines were detected in plasma, whereas anti-inflammatory cytokines remained largely uninduced. We found that the infection of severely immunodeficient mice with mpox virus results in dose-dependent lethality, persistent high viral loads, and a pronounced pro-/anti-inflammatory imbalance. These findings provide important insights into the pathogenesis of mpox in immunocompromised populations and develop a practical animal model for evaluating therapeutic interventions. - Source: PubMed
Publication date: 2026/05/21
Li NaJia ZiqingCong ZheMa JianrongLu JiahanHou YongzhiWang FeiYang JiasenChen TingZhang JingjingZhang DongXue Jing