Daxx Blocking Peptide target: Daxx
- Known as:
- Daxx Blocking Peptide target: Daxx
- Catalog number:
- 3229BP-50
- Product Quantity:
- 50 μg
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- Daxx Blocking Peptide target:
Related genes to: Daxx Blocking Peptide target: Daxx
- 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 Blocking Peptide target: Daxx
Related articles to: Daxx Blocking Peptide target: Daxx
- Corticotroph adenomas include functioning tumors causing Cushing disease (CD) and silent corticotroph adenomas (SCA), which differ markedly in size, clinical presentation, and aggressiveness. The molecular basis for these differences remains incompletely understood. - Source: PubMed
Publication date: 2026/06/11
Paes TicianaZhang QilinBorges Clarice OrangeMohan Dipika RVaz VictorSoares Beatriz SantanaCarroll Rona SKaiser Ursula BSmith Timothy RBi Wenya LindaMeredith DavidLerario Antonio MAbreu Ana Paula - The antiviral protein MORC3 is frequently inhibited by viruses. To counteract viral antagonism, MORC3 represses a noncanonical pathway of type-I-interferon (IFN) such that viral inhibition of MORC3 triggers ( > 10,000-fold) IFN induction. How MORC3 represses this pathway, and why IFN induction upon MORC3 loss is so potent without canonical IRF3/7 transcription factors, is unknown. Here, we show that MORC3 restricts chromatin accessibility at tandem repeat elements harboring up to 61 homotypic transcription factor motifs. One such element becomes a potent enhancer of IFNB1 upon MORC3 loss. Its motif cluster contains 45 PU.1 binding sites and is necessary and sufficient for MORC3-mediated repression and enhancer activity upon MORC3 loss. PU.1 recruits MORC3 to repress this enhancer by recruiting DAXX and enabling H3.3 incorporation. Upon MORC3 loss, PU.1 drives IRF3/7-independent IFN induction. Other restricted tandem repeats contain homotypic motif clusters of SPI, AP-1, and SP/KLF transcription factors. Our findings uncover a TF motif cluster-driven repression mechanism by MORC3 at tandem repeats, enabling specific repression of an IFNB1 enhancer such that viral antagonism of MORC3 induces interferon. - Source: PubMed
Publication date: 2026/06/05
Krumwiede LuisaHollaus DavidValeri ErikaSchindler-Schumitsch KarinaBazyl Monika ASchiedlbauer JohannaBecht Nanette NJaritz Markusde Almeida Bernardo PSchloissnig SiegfriedBurdette Dara LSchreiber JacobStark AlexanderGaidt Moritz M - 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