Daxx (C-Terminus) Peptide
- Known as:
- Daxx (C-Terminus) Peptide
- Catalog number:
- 1163P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- Daxx (C-Terminus) Peptide
Related genes to: Daxx (C-Terminus) Peptide
- 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 (C-Terminus) Peptide
Related articles to: Daxx (C-Terminus) Peptide
- Epigenetic modifications play a crucial role in various diseases, including cancer. Targeting chromatin modulators to normalize these epigenetic markers is a promising avenue for overcoming cancer drug resistance and improving treatment efficacy. Histone chaperones, implicated in cancer due to their imperfect compensatory mechanisms, represent potential targets for epidrugs. To identify these targets, we performed enrichment and network analyses of histone chaperone interactions, both among themselves and with other proteins. This approach provided insights into structure-function relationships. The selective binding of histone chaperones to canonical histones highlights their potential as epidrugs targets. Network analysis of common histone chaperones identified key hub proteins: HSP90AB1, RBBP4, NPM1, DAXX, and SET. These hub proteins, particularly RBBP4, which formed the largest protein cluster was found associated with oncogenesis, suggesting RBBP4 as prime candidates for therapeutic intervention. Druggability prediction of these hub protein pockets further identified RBBP4 as the most promising target, with Ritonavir emerging as a potential epidrugs. These findings provide a crucial foundation for future epidrugs discovery targeting cancer. - Source: PubMed
Publication date: 2025/03/10
Malik SonamKumar PramodYadav Chander PrakashKumar DineshKumar Anuj - The classification of neuroendocrine neoplasms has evolved significantly. In the current World Health Organization (WHO) classification, well-differentiated grade 3 neuroendocrine tumors (G3-NETs) are distinguished from poorly-differentiated neuroendocrine carcinomas (NECs) based on morphology despite using the same proliferation indices, which poses diagnostic challenges. This review aims to assist pathologists in making an accurate diagnosis, which is crucial for patient management as G3-NETs and NECs have different prognoses and chemotherapy responses. - Source: PubMed
Publication date: 2025/03/04
Sun Belinda LDing HongxuSun Xiaoguang - Pancreatic neuroendocrine neoplasia (panNEN) is a tumor disease with distinctive morphology and often poses diagnostic challenges. - Source: PubMed
Publication date: 2025/03/04
Rindi GuidoInzani Frediano - Predicting metachronous metastases in localized pancreatic neuroendocrine tumors (PanNETs) and improving survival of patients with advanced disease are some of the most important goals in PanNET research. Both are addressed by a study published recently in this journal. First, the results suggest that heterozygous DAXX mutations are already present in tumor cells but only become potentiated after a single massive chromosomal event that causes loss of heterozygosity and biallelic loss of DAXX. Second, the significant finding that the alkylating agent streptozocin may also induce a hypermutator phenotype with aggressive high-grade progression is further explored. The literature on temozolomide and peptide receptor radionuclide therapy-induced and spontaneous high-grade PanNET progression shows that the cause of high-grade progression is likely multifactorial. High-grade progressed PanNETs may show histopathological features normally seen in neuroendocrine carcinomas. Although it is not clear how often alkylating treatment induces progression, increasing evidence suggests that after an initial response, some patients indeed progress due to streptozocin or temozolomide. © 2025 The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2025/02/25
Hackeng Wenzel MDreijerink Koen MaBrosens Lodewijk Aa - Telomere maintenance is essential for the unlimited proliferation of cancer cells. While most cancers reactivate telomerase to preserve telomeres, approximately 10-15% utilize the alternative lengthening of telomeres (ALT), a telomerase-independent mechanism driven by homologous recombination. ALT is primarily observed in sarcomas and neuroepithelial tumors and it is characterized by hallmarks such as heterogeneous telomere lengths, the presence of ALT-associated PML bodies (APBs), extrachromosomal telomeric repeats (ECTRs), and elevated replication stress. This review has a threefold aim: (1) to examine the mechanisms of ALT activation, (2) to highlight existing therapeutic interventions targeting ALT components and telosomic complexes, and, (3) to pinpoint potential molecular targets for novel anticancer treatments. Therapeutic strategies focus on disrupting APBs, stabilizing G-quadruplex structures, and inhibiting replication stress proteins such as FANCM and SMARCAL1. Emerging evidence highlights the role of shelterin proteins like TRF1 and TRF2, chromatin remodeling factors such as ATRX and DAXX, and the dysregulated cGAS-STING pathway in facilitating ALT activity. Moreover, the inhibitory role of RAP1-SUN1 protein interactions in telomere recombination provides a novel therapeutic avenue. Recent advances have elucidated the intricate balance of replication stress, DNA damage response, and recombination in ALT regulation. These insights can help overcome challenges posed by ALT + cancers, including their ability to transition from telomerase-dependent states. Targeting ALT-specific vulnerabilities offers a promising direction for developing innovative therapies that exploit the unique biology of ALT-driven tumors. - Source: PubMed
Publication date: 2025/02/18
Mishra ApurwaPatel Trupti N