DAXX-01 Daxx mAb
- Known as:
- DAXX-01 Daxx mAb
- Catalog number:
- mc-485
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- DAXX-01 Daxx mAb
Related genes to: DAXX-01 Daxx mAb
- Gene:
- DAXX NIH gene
- Name:
- death domain associated protein
- Previous symbol:
- -
- Synonyms:
- DAP6
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-25
- Date modifiied:
- 2016-10-05
Related products to: DAXX-01 Daxx mAb
11A5 Anti-Prolyl 4-Hydroxylated FGA mAb13 X Anti INT HIV mAb14-3-3β, 30kD, Clone: 4E1, Mab anti-Mouse, Rat; WB/IP14-3-3β/ε/ζ, ~30kD, Clone: 3C8, Mab anti-Human, Mouse, Rat; WB14-3-3β/ζ, ~29-30kD, Clone: 22-ii-D8B, Mab anti-Human, Mouse, Rat, Monkey, Dog, Sheep, Swine, Bovine; WB/IH/IC14-3-3β/ζ, ~29-30kD, Clone: 22-ii-D8B, Mab anti-Human, Mouse, Rat, Monkey, Dog, Sheep, Swine, Bovine; WB/IH/IC14_3_3 beta mAb;mouse, rat (4E1)14_3_3 beta_epsilon_zeta mAb;human, mouse, rat (3C8)14_3_3 beta_zeta mAb (22_ii_D8B);h, mouse, rat, bovine, canin14_3_3 beta_zeta mAb (22_ii_D8B);h, mouse, rat, bovine, canin14_3_3, Mab anti_; Clone 6A1015K allergen of House Dust Mite Dermatophagoides, Mab anti-15K allergen of House Dust Mite Dermatophagoides, Mab anti_17-Beta-Estradiol, Mab anti-; Clone: 4S42, ELISA17-estradiol, Mab anti- Related articles to: DAXX-01 Daxx mAb
- The molecular characterization of Pituitary neuroendocrine tumors (PitNETs) has progressed pronouncedly in recent years, unraveling the molecular pathways driving initiation and progression of the different PitNET types, and allowing better understanding of their biology. The most frequent recurring somatic driver alterations were recognized in corticotroph PitNETs (USP8, USP48, BRAF) and somatotroph PitNETs (GNAS), and, much less frequently, in lactotroph PitNETs (SF3B1). Additional well-characterized somatic driver alterations, including TP53, ATRX, and DAXX, are enriched in aggressive corticotroph tumors. Identification of new molecular markers and delineation of their clinical phenotypes are enabling further subclassification of PitNETs based on tumor molecular profiles, with earlier recognition of more aggressive variants. These molecular markers also provide an opportunity for new targeted therapies. Beyond single-gene alterations, epigenetic modifications, such as DNA methylation, histone modifications, and non-coding RNA dysregulation, are emerging as important contributors to PitNET pathogenesis and potential therapeutic targets. Multi-omics approaches encompassing genomics, transcriptomics, epigenomics, and proteomics are transforming PitNET classification. In this review, we provide a comprehensive, data-driven update on somatic driver alterations, epigenetic alterations, converging signaling pathways, and the related emerging therapeutic targets in PitNETs, integrating pooled analyses from published cohorts. - Source: PubMed
Publication date: 2026/08/07
Schwarz YairHalperin ReutTirosh Amit - Although bovine herpesvirus 1 (BoHV-1) causes massive losses of cattle, the transition from mucosal replication to neuroinvasion remains poorly understood. Using a controlled calf model, we integrated quantitative virology and transcriptomics to map its pathogenesis and define the role of promyelocytic leukemia protein (PML). Calves inoculated intranasally and ocularly (1.4 × 10 plaque-forming units/head) were sampled daily (1-14 days post-infection, dpi) for glycoprotein B (gB) qPCR. Tissues were analyzed at 4 and 14 dpi to measure viral DNA via gB-specific qPCR, and for mRNA-seq of trigeminal ganglia (TG). Shedding peaked at 3-6 dpi, being highest in nasal samples, lower in ocular samples, and substantially lower in rectal samples, and declined by 10-14 dpi. At 4 dpi, among the tissues sampled, the tonsils exhibited the highest viral burden. TG exhibited low viral levels at 4 dpi, although they remained detectable at 14 dpi, indicating neuroinvasion. The TG program shifted from early proteostasis priming (4 dpi) to immune/extracellular matrix activation with synaptic repression (14 dpi). In MDBK/Vero cells, IFN-α resulted in higher bovine PML (bPML) levels and enlarged PML nuclear bodies (PML-NBs), reducing very early viral DNA levels, whereas BoHV-1 disrupted PML-NB integrity. The different bPML isoforms exerted different effects on viral infection. STRING analysis revealed a conserved PML-SUMO1-UBE2I-DAXX-SP100 core. These findings delineate the mucosal-to-neuronal trajectory, establish PML as both an effector and viral target in complementary systems, and identify SUMO/ubiquitin-linked proteostasis as a tractable target for antiviral intervention.IMPORTANCEAlthough bovine herpesvirus 1 (BoHV-1) remains a major challenge to cattle health, the early transition from mucosal replication to trigeminal neuroinvasion has not been clearly mapped in natural-host calves. By integrating daily shedding kinetics, tissue viral DNA profiling, and time-resolved trigeminal ganglion transcriptomics, we delineate when and how BoHV-1 reaches the sensory neurons. Promyelocytic leukemia protein (PML) is identified as a key intrinsic antiviral factor that is upregulated by IFN-α and restricts very early viral genome accumulation, while viral BoHV-1-encoded infected cell protein 0 actively dismantles PML nuclear bodies. The discovery of opposing isoform-specific PML functions and a conserved PML-SUMO proteostasis hub provides mechanistic insight into BoHV-1 immune evasion. These findings refine our understanding of the mucosal-to-neuronal trajectory of infection and highlight proteostasis-linked antiviral pathways as promising targets for intervention. - Source: PubMed
Publication date: 2026/07/23
Wang YongJin HuanWang FanyuCheng JingCao MengyaoZhou LinyiLiu WenxiaoLi Yongqing - Patients with pancreatic neuroendocrine tumours (PNETs) often have similar baseline clinical characteristics, including grade and molecular imaging phenotype, yet have highly variable responses to peptide receptor radionuclide therapy (PRRT). To identify genomic alterations and mutational patterns associated with PRRT treatment response and acquired somatic changes following PRRT exposure, whole genome or exome sequencing was applied to 40 PNET samples from 32 patients, including eight paired pre- or post-PRRT samples. The genomic profile of tumours reflected the known mutational landscape of PNET with MEN1 (34%), ATRX/DAXX (47%) alterations and a recurrent pattern of aneuploidy (38%) detected. A recurrent PSIP1::TBL1X fusion of unknown function was also identified in four tumours. The disease control rate following PRRT using RECIST1.1 and molecular imaging criteria was 88% (28/32). No mutational features were found to be statistically associated with progression-free survival. There was no significant increase in tumour mutational burden in the post-PRRT tumours, nor recurrent emergent mutational changes in cancer driver genes to explain progression to higher-grade disease, when observed. However, a small indel signature (ID8) previously associated with DNA damage repair by non-homologous end joining (NHEJ) was higher in PRRT-exposed compared with PRRT-naive samples (23.8 vs 4.8%, respectively; P < 0.001). Thus, comprehensive DNA analysis of pancreatic NETs did not identify biomarkers predictive of PRRT response nor evidence for high-level PRRT-induced genomic instability or hypermutation, yet mutation signature analysis supports NHEJ as being important for DNA repair and survival of neuroendocrine cells following exposure to beta-particle radiation. - Source: PubMed
Boehm EmmaFlynn AidanCaneborg AlexHatzimihalis AthenaHogg AnnetteWaldeck KellyJackett LouisePrall Owen W JMitchell CatherineKong GraceMichael MichaelAkhurst TimThomson Benjamin N JMurray William KChin KwangLawrence BenPrint Cristin GVissers Joseph H AGrimmond Sean MTothill Richard WHicks Rodney J - Alterations in alternative splicing are emerging as a novel cancer hallmark, offering new insights into tumor biology. However, integrative analyses of splicing are still scarce, particularly in rare cancers like pancreatic neuroendocrine tumors (PanNETs), whose striking heterogeneity complicates patient diagnosis and treatment. Here, we provide the first comprehensive characterization of the RNA splicing landscape in PanNETs through integrative analysis of RNA-seq data from 174 tumor samples. We identified three robust spliceosomic groups (SPN1, SPN2, SPN3) each associated with unique clinical and molecular characteristics. SPN1 displayed intermediate clinical behavior alongside enhanced mTOR signaling; SPN2 was characterized by a less secretory phenotype, enrichment in alpha-cell markers and somatostatin receptors, increased metastasis, and frequent mutations in MEN1 and DAXX/ATRX genes; in contrast, SPN3 was composed mainly by low grade tumors with beta-cell marker expression and the lowest mutational rate, yet it also contained all the highly proliferative neoplasms. Moreover, each group had a specific alternative splicing events signature, revealing an unprecedented discovery: the association between the expression profile of the splicing machinery and its product, the splicing variants. We provide a detailed characterization of the molecular and functional consequences of the splice variants defining each of the spliceosomic groups. These findings underscore the previously unrecognized yet significant impact of RNA splicing on PanNET heterogeneity and suggest that detailed splicing profiles could serve as valuable tools for identifying novel biomarkers and therapeutic targets. Thus, beyond providing crucial insights into PanNET molecular biology, our study offers a foundation for future studies exploring personalized therapeutic strategies based on splicing features. - Source: PubMed
Publication date: 2026/07/09
Blázquez-Encinas RicardoGarcía-Vioque VíctorMafficini AndreaLandoni LucaRuiz-Palacios DanielGutiérrez-Camacho LauraMoreno-Montilla María TrinidadAlcala NicolasVentura SebastiánEyras EduardoPaiella SalvatoreSalvia RobertoRovite VitaFoll MatthieuLuchini ClaudioFernandez-Cuesta LynnetteLawlor Rita TScarpa AldoIbáñez-Costa AlejandroPedraza-Arevalo SergioCastaño Justo P - Mutations in the ATRX chromatin remodeler confer a predisposition to a developmental genetic disorder and cancer, but how ATRX safeguards genome and telomere stability remains unresolved. Here, we uncover critical dependencies for the CTC1-STN1-TEN1 (CST) complex and RAD9A-HUS1-RAD1 (9-1-1) clamp in ATRX-deficient cells. ATRX-CST synthetic lethality manifests following accumulation of telomeric G-rich single-stranded DNA (ssDNA), which results in telomere loss and cell death. Conversely, we attribute ATRX-9-1-1 synthetic lethality to genome-wide ssDNA lesions, which compromise DNA replication. We further show that ATRX suppresses DNA damage during replication stress by counteracting the activity of the FAM111A protease. We demonstrate that roles of ATRX in telomere maintenance and replication are genetically separable, requiring its ATPase activity and PIP-box, respectively. We also show that such roles protecting genome stability are largely independent of the ATRX-DAXX interaction. Collectively, our data show that functions of ATRX in suppressing toxic ssDNA lesions are context-dependent and are key to global DNA replication and telomere integrity. - Source: PubMed
Publication date: 2026/06/30
Segura-Bayona SandraMaric MarijaTakaki TohruManova ZornitsaStanage Tyler HIdilli Aurora ILi ShudongHewitt GraemeMachour Feras EMillar RhonaAdamowicz MarekLow Ronnie Ren JieRuis PhilAzeroglu BenuraFallesen ToddPatel HarshilHowell StevenKotsantis PanagiotisHowell MichaelBoulton Simon J