DNA PKcs antibody
- Known as:
- Desoxyribonucleic acid PKcs (anti-)
- Catalog number:
- 20r-2017
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- DNA PKcs antibody
Related genes to: DNA PKcs antibody
- 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 PKcs antibody
Related articles to: DNA PKcs antibody
- Focal articular cartilage defects lack intrinsic regenerative capacity and can progress to osteoarthritis as no effective treatment exists to slow, stop or reverse cartilage degeneration. Cellular senescence, characterized by elevated p21 (CDKN1A) expression, impairs chondrocyte proliferation and cartilage repair. We hypothesized that targeted p21 suppression via lentiviral delivery would enhance cartilage regeneration. Lentiviral shRNA vectors targeting p21 or non-sense controls with a tdTomato reporter were constructed. In vitro, murine synovial progenitor cells and MC3T3E1 preosteoblasts were transduced and p21 mRNA was quantified by qRT-PCR. Cell cycle analysis was performed using flow cytometry. In vivo, immunocompromised (B6.Cg-Prkdc/SzJ) and immunocompetent (C57BL6) mice received full-thickness cartilage defects followed by intraarticular p21 shRNA or nonsense control injection. Cartilage repair was assessed by Safranin O staining and tissue cytometry quantified lentiviral transduction and p21 knockdown in chondrocytes. In vitro, p21 shRNA achieved ~80% reduction in p21 mRNA and increased G2M phase cells. In vivo, p21 shRNA treatment significantly improved cartilage repair in both strains. Tissue cytometry revealed 90% transduction efficiency with p21 cells reduced from ~90% to ~30%. Spearman correlation showed significant negative correlation between p21 expression and repair outcomes. Hepatic off-target transduction was minimal in uninjured animals but increased in injured animals, yet morphological hepatotoxicity was not observed. p21 knockdown via lentiviral shRNA effectively promotes cartilage regeneration, supporting the concept of targeting p21 and/or the p21 pathway as a therapeutic strategy for cartilage repair. - Source: PubMed
Larijani LeilaAhadzadeh Ardebili AriaOrtiz Vales NiniStürmer Andreas TKrawetz Roman J - Chronic rhinosinusitis is a difficult-to-treat, recurrent inflammatory condition of the nose and paranasal sinuses with global prevalence. Despite its impact on patient quality of life and its cost to the healthcare system, the pathogenesis of chronic rhinosinusitis (CRS) remains poorly understood. Additionally, while the presence of bacteria in CRS has been confirmed by numerous studies, their influence on disease symptoms is unclear. Disease-relevant models can help resolve these questions. We hypothesized that bacterial inoculation could drive CRS-associated symptoms in a murine model. To characterize host-microbe interactions in a murine model of sinonasal bacterial infection. and/or were inoculated in the nasal cavity of Swiss Webster, C57Bl/6, Balb/c and B6.Cg- /SzJ severe combined immunodeficient (SCID) mice. Systemic cytokine response was quantified with a multiplexed enzyme-linked immunosorbent assay, and local histological alterations were quantified using haematoxylin and eosin as well as Alcian Blue-Periodic Acid-Schiff-stained sinonasal sections. Intranasal bacterial inoculation induced symptoms of CRS in murine sinonasal cavities. Dual species inoculation generated a unique response compared to single species. Repeated inoculations did not result in bacterial clearance from immunological priming. While Swiss Webster and C57Bl/6 mice demonstrated the greatest magnitude of responses, Balb/c mice demonstrated a protective response, generally downregulating cytokines and attempting to prevent further tissue damage. SCID mice demonstrated effective clearance of by innate immunity, but maintenance of . Pathogenic bacteria are able to persist and drive the development of symptoms associated with clinical CRS in a murine model. Bacterial interactions and host factors influence CRS-associated inflammation. By investigating host responses from a number of mouse genetic backgrounds, the heterogeneity of disease presentation in CRS can be modelled, and strategies for infection management can be evaluated as potential therapeutic targets. - Source: PubMed
Vanderpool Emily JRumbaugh Kendra P - BRAF, a serine/threonine kinase, functions as a key effector of the MAPK signaling cascade and regulates cell proliferation and survival. Oncogenic BRAF mutations disrupt MAPK pathway homeostasis, contributing significantly to cancer progression and pathogenesis. BRAF phosphorylation is pivotal for modulating downstream signaling events. In this study, we performed a comprehensive analysis of global human phosphoproteomic datasets to elucidate BRAF phosphorylation dynamics and associated regulatory networks. The systematic annotation identified BRAF phosphorylation in 912 qualitative profiles across 166 studies and 234 quantitative differential datasets from 73 studies, revealing 44 and 21 distinct phosphosites, respectively. Class I phosphosites with localization probability ≥75% or A-score > 13 were filtered. A fold-change threshold of ≥1.3 for upregulation and ≤ 0.76 for downregulation was applied. Particularly, six predominant phosphorylation sites, S446, S729, S151, T401, S365, and S447, were frequently observed. Further analysis of melanoma-melanoma-specific phosphoproteomic datasets and correlations with gene expression data from melanoma cell lines revealed several key co-regulated proteins associated with the predominant BRAF phosphosites, including STAT3, BAD, CDK16, ITPKB, NPM1, MDC1, CHEK2, PRKDC, EIF3A, TP53BP1, RB1, and CDK14. These co-regulated proteins highlight the integration of BRAF signaling with critical processes, such as cell cycle control, apoptosis, DNA damage response, and protein synthesis in melanoma. Our analysis suggests that targeting BRAF-interacting proteins may also modulate oncogenic signaling pathways and represent promising biomarkers for melanoma diagnosis and therapy. - Source: PubMed
Publication date: 2026/04/03
Dcunha LeonaEdakkad BhavanaJohn LevinShivamurthy Prathik BasthikoppaBera PritamDas DebodiptaRaju RajeshBalaya Rex Devasahayam ArokiaKanekar Saptami - Reliable experimental platforms are essential for evaluating transmission-blocking interventions against Plasmodium falciparum (P. falciparum). Although the standard membrane feeding assay (SMFA) is widely used to assess transmission-blocking activity, it is performed in vitro and does not fully represent physiological conditions. In this study, we developed and applied a luciferase-based assay using NSG (NOD.Cg-Prkdc^scid Il2rg^tm1Sug/JicTac) mice engrafted with human red blood cells (hRBCs) to establish an hRBC-engrafted NSG (hRBC-NSG) humanized mouse model for evaluating the transmission-blocking activity of anti-CelTOS monoclonal antibodies (mAbs) against P. falciparum. - Source: PubMed
Publication date: 2026/04/01
Xu ShulinRoth Alison EThomson-Luque RichardSalinas NicholeBarnes SamanthaHerman CourtneyTolia Niraj HAdams John H - V(D)J recombination is the fundamental process by which developing T and B lymphocytes generate diverse antigen receptors, enabling adaptive immunity. This tightly regulated program operates exclusively in lymphoid precursors during G1 phase and depends on the lymphocyte specific RAG1-RAG2 recombinase to introduce programmed DNA double-strand breaks at recombination signal sequences, followed by repair through the classical non-homologous end-joining (c-NHEJ) pathway. Disruption of any step in this molecular choreography compromises antigen receptor diversity and underlies a spectrum of inborn errors of immunity (IEI), ranging from severe combined immunodeficiency (SCID) to immune dysregulation with autoimmunity and granulomatous disease. In this review, we place disorders of V(D)J recombination within the broader framework of T-cell development, detailing the temporal waves of recombinase activity, chromatin accessibility, and DNA damage responses that guide thymocyte differentiation. We discuss pathogenic variants affecting the cleavage phase (RAG1, RAG2, and the recently identified RAG co-chaperone NudC domain-containing 3, NUDCD3), end processing (ARTEMIS), ligation and repair (LIG4, XLF, XRCC4, PRKDC), and genome surveillance pathways (ATM, MRN complex, RNF168), highlighting genotype-phenotype correlations and mechanisms driving immune deficiency and dysregulation. We briefly review recent diagnostic advances, including newborn screening using T-cell receptor excision circles, repertoire sequencing, and functional assays, alongside current therapeutic strategies. Finally, we outline key unanswered questions and argue that continued integration of clinical observation with molecular discovery is essential to improve outcomes and deepen understanding of adaptive immune development. - Source: PubMed
Publication date: 2026/03/28
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