XTP3TPA Blocking Peptide
- Known as:
- XTP3TPA Blocking Peptide
- Catalog number:
- 33r-4552
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- XTP3TPA Blocking Peptide
Related genes to: XTP3TPA Blocking Peptide
- Gene:
- DCTPP1 NIH gene
- Name:
- dCTP pyrophosphatase 1
- Previous symbol:
- -
- Synonyms:
- MGC5627, RS21C6, CDA03, XTP3TPA
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-12-18
- Date modifiied:
- 2014-11-19
Related products to: XTP3TPA Blocking Peptide
Related articles to: XTP3TPA Blocking Peptide
- Defects in nucleotide metabolism and imbalances in deoxynucleotide triphosphate (dNTP) pools are associated with several human diseases, including cancer and mitochondrial disorders. In non-replicative cells, while DNA synthesis is reduced, a continuous supply of nucleotides is essential to sustain mitochondrial DNA (mtDNA) replication and repair. Human all-α dCTP pyrophosphatase 1 (DCTPP1), a nucleotido hydrolase with high specificity for dCTP, plays a critical role in maintaining nucleotide homeostasis, however its participation in mtDNA stability remains unexplored. In this study we performed a detailed analysis of pyrimidine metabolism enzymes in non-dividing cells. We found that during quiescence, DCTPP1 is predominantly localized to mitochondria. Depletion of the enzyme leads to upregulation of the de novo thymidylate synthesis pathway and expansion of both the dCTP and dGTP pools, highlighting its pivotal role in regulating the dNTP balance. To explore the potential therapeutic relevance of these observations, we used an in vitro model of mitochondrial neurogastrointestinal encephalomyopathy (MNGIE), a rare mitochondrial disorder caused by thymidine phosphorylase (TP) deficiency and characterized by dCTP depletion and mtDNA loss. Long-term thymidine overloading in quiescent cells (a model mimicking TP deficiency) led to reduced dCTP levels and the depletion of mtDNA, effects that were reversed upon DCTPP1 knockdown. Hence, reduced DCTPP1 levels restored dCTP availability and increased mtDNA copy number. These findings suggest that DCTPP1 plays a critical role in regulating mitochondrial dNTP pools and that down-regulation of the enzyme may serve as a compensatory mechanism in disorders marked by secondary dCTP depletion. DCTPP1 may therefore represent a promising therapeutic target for mitochondrial DNA depletion syndromes such as MNGIE. - Source: PubMed
Publication date: 2026/03/26
Fernández BelénPérez-Moreno GuiomarMartínez-Arribas BlancaVidal Antonio ERuiz-Pérez Luis MiguelGonzález-Pacanowska Dolores - Breast cancer (BRCA) remains a major cause of cancer-related mortality among women, underscoring the need for reliable prognostic biomarkers and immunologically informed therapeutic targets. Deoxycytidine triphosphate pyrophosphatase 1 (DCTPP1) has been implicated in tumor progression, but its role in the BRCA immune microenvironment remains unclear. Here, we integrated multi-omics analyses, tissue microarray (TMA) profiling, and functional assays to investigate the clinical and immune significance of DCTPP1 in BRCA. DCTPP1 was upregulated at both the mRNA and protein levels, and high DCTPP1 expression was associated with adverse clinicopathological features and poor overall survival (OS), and remained an independent prognostic factor in multivariable analyses. Computational immune infiltration analyses indicated that elevated DCTPP1 expression was associated with an immunosuppressive microenvironment, characterized by increased M2 macrophage infiltration and reduced CD8⁺ T-cell and M1 macrophage signatures; these findings were corroborated by multiplex immunohistochemistry(mIHC) in a TMA cohort. In Transwell co-culture, DCTPP1 knockdown in MCF-7 cells shifted THP-1–derived macrophages toward an M1-like phenotype, increasing the proportion of CD11b⁺CD86⁺ cells while decreasing CD11b⁺CD206⁺ cells, and concomitantly upregulating CD86 and TNF-α while downregulating CD163 and CD206. - Source: PubMed
Publication date: 2026/02/13
Chi JiuqingLiu WenyanZhai ZhihaoWang LiuWang XiaowuMa Zhijun - The complexities of nucleotide metabolism in breast cancer (BC) cells are not yet fully understood. A deeper exploration of the various tumor subpopulations and their interactions with the tumor microenvironment (TME) could provide important insights into these clinically relevant signaling pathways. - Source: PubMed
Publication date: 2026/01/14
Pan YuejunXu YongGong KeYuan Songlin - Chromochloris zofingiensis is recognized as a promising resource for the production of carotenoids. However, current knowledge regarding its capacity for zeaxanthin accumulation remains limited, which restricts its potential for commercial application. The development of high-yielding strains and an understanding of the underlying metabolic and regulatory mechanisms are critical to advancing large-scale zeaxanthin production. - Source: PubMed
Publication date: 2026/01/05
Chen QiaohongLiu MingmengWan DongMi WujuanZhu YuxuanSong GaofeiBi Yonghong - Placental trophoblast dysfunction is one of the main causes of missed abortion (MA). The expression and regulation of specific molecules play crucial roles in this complex process. Among these, human deoxycytidine triphosphate pyrophosphatase 1 (DCTPP1), a key enzyme, not only participates in nucleotide metabolism but also plays an indispensable role in maintaining genomic stability. To delve deeper into the mechanism of DCTPP1 in placental trophoblast cell function, we used an immortalized human first-trimester extravillous trophoblast cell line (HTR8/SVneo) as an experimental model for functional studies. A decrease in DCTPP1 expression leads to an increase in oxidative stress and decreased cell viability ultimately leading to apoptosis. Further analysis revealed an interaction between DCTPP1 and the AU-rich element RNA-binding protein 1 (AUF1). A decrease of AUF1 induced oxidative stress imbalance, leading to apoptosis in HTR8/SVneo cells. These findings highlight DCTPP1 as a potential biomarker and an effective drug target for the treatment or prevention of MA. - Source: PubMed
Publication date: 2025/08/23
Lu YajuanWu XueHe LeiPan PengZhao AnqiKan TangliChu YutingDong JinglinXu ShuangkaiTan XiaofangYang Xiaoqing