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 goal of this study was to explore the biological mechanisms that may influence the development of myofibromas, noninvasive soft tissue tumors with a variable clinical course. While solitary lesions are usually benign, multicentric infantile myofibromatosis can range from indolent disease with spontaneous regression to severe forms with visceral involvement and life-threatening complications. - Source: PubMed
Publication date: 2026/05/29
Boulouadnine BoutainaZurriaga Carlota RoviraGofflot StéphanieBrichard BénédicteDecottignies AnabelleDemoulin Jean-Baptiste - Pancreatic neuroendocrine tumors (PanNETs) are clinically heterogeneous, and conventional risk stratification based on tumor size, grade, and stage often fails to capture the full spectrum of biological behavior, especially among small (≤ 2 cm), non-functioning tumors where management remains controversial. - Source: PubMed
Publication date: 2026/05/29
Cheong Kai XuanZhang Lu-TingWang Ya-ZhouGan WeiLiu Chen-ChenYing YingPeng Mao-ZhenTang Lin-HuiLiu LiangWang Wen-Quan - Gene therapy holds significant potential for treating genetic disorders, but the use of viral vectors is limited by factors such as immunogenicity, payload capacity, and high manufacturing costs. Nonviral gene delivery (NVGD) using plasmid DNA presents an attractive alternative; however, it typically provides a limited magnitude or duration of transgene expression. One potential reason for these shortcomings is the host cell's epigenetic regulation mechanisms, which can silence both viral and nonviral transgenes. Specifically, when foreign DNA enters the nucleus, it is detected by nuclear DNA sensors, such as IFI16, which initiate the assembly of a "restrictosome" or nuclear domain 10 (ND10) body. This multiprotein complex contains several components, such as PML, Speckled Proteins (e.g., SP100), DAXX, and ATRX that act as a scaffold for recruiting various epigenetic modifiers that subsequently deposit repressive histone modifications like H3K9me3 and H3K27me3 on the transgene chromatin. These marks induce DNA methylation and the subsequent condensation of plasmids or episomes into heterochromatin, which represses transgene expression. Alternatively, unmethylated CpG motifs in bacterial plasmid DNA can trigger innate immune responses in the cytosol, but this review will specifically focus on the detailed mechanisms of epigenetic regulation responsible for silencing plasmid DNA within the host cell nucleus. Addressing these nuclear defense mechanisms, potentially through strategies that manipulate DNA methylation or inhibit restrictosome activity, is crucial for advancing the development of safe, effective, and long-lasting plasmid viral and non-viral gene therapies. - Source: PubMed
Publication date: 2026/05/28
Mwangi LeilaWarga EricElmer Jacob - Pancreatic neuroendocrine neoplasms (PanNENs) constitute a heterogeneous group of tumors distinguished by substantial variability in morphology, immunophenotype, molecular characteristics, and clinical behavior. In recent years, the advent of multiple omics-based methodologies has significantly enhanced our understanding of these neoplasms. Integrating histology and genomics with survival analyses has clarified that the fundamental distinction within this disease spectrum lies between well-differentiated neuroendocrine tumors (NETs) and poorly differentiated neuroendocrine carcinomas (NECs). Furthermore, genomics, transcriptomics, and epigenetic profiling have deepened the granularity of the PanNET landscape, revealing marked differences even within the same diagnostic category, with important clinical implications. For example, DAXX/ATRX mutations, activation of the alternative lengthening of telomeres pathway, BEND2 gene fusions, and an α-cell transcriptional profile are more frequently associated with adverse outcomes. Additional omics approaches, including metabolomics, proteomics, radiomics, and the more recently developed spatially resolved methodologies, are further expanding current knowledge in this challenging field. In this review, we provide an integrated overview of PanNENs, synthesizing insights generated across diverse multi-omics platforms. - Source: PubMed
Publication date: 2026/05/29
Bevere MicheleGkountakos AnastasiosValentinuzzi SilviaDe Fabritiis SimoneWong Chee SDe Robertis RiccardoMattiolo PaolaGentiluomo ManuelFassan MatteoPea AntonioCrinò Stefano FSimbolo MicheleMafficini AndreaCampa DanieleCingarlini SaraLandoni LucaLawlor Rita TSalvia RobertoD'Onofrio MirkoMilella MicheleAdsay VolkanBrosens Lodewijk AHeaphy Christopher MHong Seung-MoSinghi Aatur DScarpa AldoLuchini Claudio - Recent studies have identified ATRX/DAXX and PDX1/ARX as biomarkers defining novel pancreatic neuroendocrine tumor (PanNET) subtypes, while the clinical significance of somatostatin receptors (SSTRs) remains incompletely understood. - Source: PubMed
Publication date: 2026/05/11
Ciobanu Oana AMartin Carmen SorinaFica SimonaHerlea VladTudose IrinaVasilescu FlorinaSandra IrinaBarbu Carmen G