AMPD1
- Known as:
- AMPD1
- Catalog number:
- Y213846
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AMPD1
Related genes to: AMPD1
- Gene:
- AMPD1 NIH gene
- Name:
- adenosine monophosphate deaminase 1
- Previous symbol:
- -
- Synonyms:
- MAD, MADA
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-19
- Date modifiied:
- 2016-10-05
Related products to: AMPD1
Related articles to: AMPD1
- Programmed cell death protein (PD-1) inhibitors constitute the standard adjuvant therapy for cutaneous melanoma (CM), but well-established strategies for acral melanoma (AM) remain limited. - Source: PubMed
Publication date: 2026/04/22
Du YuChen YuWang JiaxiangLin JingWei XiaotingGu JunjieGuo JunSi LuMao Lili - The flavor of chicken meat is formed by a series of complex chemical reactions, and the flavor precursors are affected by regulatory genes. In order to study the differences of muscle flavor precursors between Tengchong Snow chickens and AA broilers, integrated metabolomics and transcriptomics analyses were used to investigate muscle metabolite profiles and the key genes involved in the metabolism of muscle flavor compounds. The results showed that 42 significantly differentially metabolites were detected, and (5-L-Glutamyl)-L-glutamate, gamma-Glutamylalanine, S-Adenosylhomocysteine, Homo-L-arginine and GMP were important flavor metabolites. The key candidate genes with high correlation with flavor precursor metabolites were identified through correlation analysis as , , , , , and . In addition, the gene-metabolite interaction network for flavor formation in chicken breast muscle was constructed. This study could provide some basic data for the formation mechanism of local chicken excellent meat quality, and provide reference for the development and utilization of local chicken breeds and the selection and breeding of high-quality broilers. - Source: PubMed
Publication date: 2026/03/10
Yang MinZhang RuifangZhao JingyingJian ZonghuiWu HaoZi XiannianWang KunXu ZhiqiangGe ChangrongJia JunjingLiu LixianDou Tengfei - Lung cancer, primarily non-small cell lung cancer (NSCLC), causes the highest cancer-related mortality. Although PD-1/PD-L1 inhibitors have improved survival in advanced NSCLC, they can cause immune-related adverse events. (), a traditional Chinese medicine used for tonifying the lung and kidney and enhancing immune function, has shown therapeutic promise in combination with anti-PD-1 therapy for NSCLC. This study aimed to explore the anti-tumor effect of wild combined with anti-mouse PD-1 in the treatment of Lewis lung adenocarcinoma (LLC) and to elucidate the underlying pharmacodynamic mechanism. LLC mouse model was established via inoculation with LLC cells, followed by treatment with anti-mouse PD-1, , or their combination. The tumor volume, weight, and histological changes of LLC mice were evaluated. The proportions of tumor-infiltrating immune cells in blood and tumors were evaluated by flow cytometry, immunohistochemistry, and immunofluorescence. The underlying mechanisms of the combination of and anti-mouse PD-1 therapy in LLC mice were investigated using an integrated transcriptomics and metabolomics analysis. Treatment with anti-mouse PD-1, , or their combination significantly reduced tumor volume and weight, and attenuated the histopathological changes of LLC mice tumors. Among which, medium-dose combination exhibited significant improvements. Furthermore, the combination of and anti-mouse PD-1 significantly increased the proportion of CD8 T cells and decreased the abundance of Tregs and PMN-MDSCs. Integrated transcriptomics and metabolomics analysis revealed that the combination of and anti-mouse PD-1 can enhance anti-tumor immunity in LLC mice by acting on key immune-related genes, including DGKA, PLA2G7, AMPD1, ATP8B4, and BST1, thereby modulating glycerophospholipid metabolism, the TCA cycle, purine metabolism, and nicotinate-nicotinamide metabolism. Wild combined with anti-mouse PD-1 therapy exerts therapeutic effects against LLC by targeting immune-related genes, modulating associated pathways, increasing the proportion of CD8 T cells, and reducing the infiltration of Tregs and PMN-MDSCs, thereby suppressing tumor growth and inhibiting LLC progression. Further research and clinical studies are needed to validate and expand upon these promising findings. - Source: PubMed
Publication date: 2026/02/04
Liu YingyingGao YaqiSuonanlamao Ma YuananXiao YuancanWei LixinZhou Wenbin - Neuroblastoma RAS viral oncogene homolog (NRAS) mutations occur in 20-30% of cutaneous melanomas, defining a distinct molecular subtype. While NRAS mutations drive unique gene expression programs, locus-specific transcriptional regulation has not been systematically explored. This study characterized coordinated transcriptional upregulation in NRAS-mutant melanoma, focusing on chromosome 1p13.2. RNA-seq and mutation data for 472 melanoma samples from The Cancer Genome Atlas Skin Cutaneous Melanoma were analyzed. Differential expression, coexpression assessment, and copy number variation (CNV) correlation were performed for 45 protein-coding genes within 1p13.2. Findings were validated in MSK-IMPACT 2021 ( n = 696). In NRAS-mutant melanomas, 56% of 1p13.2 genes were upregulated (false discovery rate < 0.05) versus 12% genome-wide ( P < 0.001), including TRIM33, AMPD1, GNAI3, and SLC25A24. Upregulation was NRAS-specific: 84% showed higher expression versus BRAF-mutant tumors. Six of the 10 most NRAS-correlated genes localized to 1p13.2. CNV gains showed dose-dependent effects (gains: 1.8-3.2 fold; amplifications: 3.5-5.4 fold), with strong correlations (AMPD1 ρ = 0.68, GNAI3 ρ = 0.62, TRIM33 ρ = 0.58; P < 0.001). MSK-IMPACT validation confirmed 1p13.2 upregulation. As these findings are based on transcriptomic and copy number analyses, additional protein-level and functional studies across independent cohorts are required to confirm biological significance. NRAS-mutant melanomas harbor a coordinated transcriptional program within 1p13.2, driven by CNV gains. This locus contains genes with potential druggability, offering new avenues for combinatorial targeting alongside mitogen-activated protein kinase pathway inhibition. - Source: PubMed
Publication date: 2026/01/29
Bilik Sophie MBurke Olivia MElman Scott A - The integration of omics technologies, including genomics, proteomics, metabolomics, and microbiomics, has transformed sports science, particularly soccer, by providing new opportunities to optimize player performance, reduce injury risk, and enhance recovery. This systematic literature review was conducted in accordance with PRISMA 2020 guidelines and structured using the PICOS/PECOS framework. Comprehensive searches were performed in PubMed, Scopus, and Web of Science up to August 2025. Eligible studies were peer-reviewed original research involving professional or elite soccer players that applied at least one omics approach to outcomes related to performance, health, recovery, or injury prevention. Reviews, conference abstracts, editorials, and studies not involving soccer or omics technologies were excluded. A total of 139 studies met the inclusion criteria. Across the included studies, a total of 19,449 participants were analyzed. Genomic investigations identified numerous single-nucleotide polymorphisms (SNPs) spanning key biological pathways. Cardiovascular and vascular genes (e.g., , , , , , ) were associated with endurance, cardiovascular regulation, and recovery. Genes related to muscle structure, metabolism, and hypertrophy (e.g., , , , , , , , , ) were linked to sprint performance, metabolic efficiency, and muscle injury susceptibility. Neurotransmission-related genes (, , , , , , ) influenced motivation, fatigue, cognitive performance, and brain injury recovery. Connective tissue and extracellular matrix genes (, , , , , , , , , , , , ) were implicated in ligament, tendon, and muscle injury risk. Energy metabolism and mitochondrial function genes (, , , , , , ) shaped endurance capacity, substrate utilization, and body composition. Oxidative stress and detoxification pathways (, , , ) influenced recovery and resilience, while bone-related variants (, , were associated with bone density and remodeling. Beyond genomics, proteomics identified markers of muscle damage and repair, metabolomics characterized fatigue- and energy-related signatures, and microbiomics revealed links between gut microbial diversity, recovery, and physiological resilience. Evidence from omics research in soccer supports the potential for individualized approaches to training, nutrition, recovery, and injury prevention. By integrating genomics, proteomics, metabolomics, and microbiomics data, clubs and sports practitioners may design precision strategies tailored to each player's biological profile. Future research should expand on multi-omics integration, explore gene-environment interactions, and improve representation across sexes, age groups, and competitive levels to advance precision sports medicine in soccer. - Source: PubMed
Publication date: 2026/01/12
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