Ask about this productRelated genes to: UCK1 antibody
- Gene:
- UCK1 NIH gene
- Name:
- uridine-cytidine kinase 1
- Previous symbol:
- -
- Synonyms:
- URK1, FLJ12255
- Chromosome:
- 9q34.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-28
- Date modifiied:
- 2016-10-05
Related products to: UCK1 antibody
Related articles to: UCK1 antibody
- Genome-wide association studies identified a melanoma- and nevus count-associated locus on chromosome band 9q34.13. Fine-mapping and melanocyte expression data collectively suggest two potential causal genes with opposite association with risk: higher levels of Rap guanine nucleotide exchange factor 1 ( ) and lower levels of uridine-cytidine kinase 1 ( ). Colocalization analyses and conditional TWAS suggest multiple causal -regulatory sequence variants in partial linkage disequilibrium (LD) to each other. Melanocyte capture-HiC and CRISPR-inhibition demonstrated regulatory interactions between fine-mapped variants and the and promoters. Focusing on , we demonstrate expression promotes melanocyte growth and drives malignant transformation of human immortalized melanocytes. Following treatment with human EGF, overexpression activated both RAP1 and RAS. Further, we show expression is significantly enriched in melanomas lacking strongly activating RAS-MAPK mutations, suggesting that may promote oncogenic RAS-MAPK signaling in melanomas. Furthermore, in these tumors, we provide preliminary evidence to support the prognostic relevance of expression in patients lacking or mutations. Together with other recent studies, these data suggest that germline variation influencing RAS activation may play a key role in nevus development and melanoma risk. - Source: PubMed
Publication date: 2026/02/08
Thakur RohitXu MaiThornock Alexandra MYon JoshuahAnyaso-Samuel SamuelLauss MartinRehling ThomasBui-Raborn LinhSowards HayleyDuncan GerardJessop LeaMyers TimothyChari RajLong ErpingFunderburk KarenYin JinhuHennessey RebeccaHseih EmoryLevin HannahMachiela Mitchell JZhang TongwuJonsson GoranBishop D TimothyNewton-Bishop JuliaNsengimana JeremieIles Mark MLandi Maria TeresaLaw Matthew HAndresson ThorkellChoi JiyeonZon Leonard IShi Jianxin Brown Kevin M - One critical aspect of cell proliferation is increased nucleotide synthesis, including pyrimidines. Pyrimidines are synthesized through de novo and salvage pathways. Prior studies established that the mammalian target of rapamycin complex 1 (mTORC1) promotes pyrimidine synthesis by activating the de novo pathway for cell proliferation. However, the involvement of mTORC1 in regulating the salvage pathway remains unclear. Here, we report that mTORC1 controls the half-life of uridine cytidine kinase 2 (UCK2), the rate-limiting enzyme in the salvage pathway. Specifically, UCK2 is degraded via the CTLH-WDR26 E3 complex during mTORC1 inhibition, which is prevented when mTORC1 is active. We also find that UCK1, an isoform of UCK2, affects the turnover of UCK2 by influencing its cellular localization. Importantly, altered UCK2 levels through the mTORC1-CTLH E3 pathway affect pyrimidine salvage and the efficacy of pyrimidine analog prodrugs. Therefore, mTORC1-CTLH E3-mediated degradation of UCK2 adds another layer of complexity to mTORC1's role in regulating pyrimidine metabolism. - Source: PubMed
Publication date: 2025/01/13
Pham Brittany QYi Sang AhOrdureau AlbanAn Heeseon - The pyrimidine salvage pathway plays a critical role in tumor progression and patient outcomes. The roles of pyrimidine salvage pathway-related genes (PSPGs) in cancer, however, are not fully understood. This study aims to depict the characteristics of PSPGs across various cancers. - Source: PubMed
Publication date: 2024/01/06
Li YinJiang ManlingWei YongqiHe XiangLi GuopingLu ChunlaiGe Di - Hepatocellular carcinoma (HCC) is currently one of the most life-threatening diseases worldwide. However, the factors, genes, and processes involved in the mechanisms of HCC initiation, development, and metastasis remain to be identified. WNT signalling pathways may play important roles in cancer initiation and progression. Thus, it would be informative to construct a WNT signature-based gene model for the prognosis of HCC and the prediction of therapeutic efficacy. We curated genomic profiles for HCC from The Cancer Genome Atlas (TCGA) and divided them into training and internal validation datasets. We also used samples from GSE14520 and HCCDB18 as validation datasets and clustered them by ConsensusClusterPlus analysis. We applied WebGestaltR to the WNT score-associated differentially expressed genes (DEGs) and conducted a signalling pathway enrichment analysis. We assessed the tumour immune microenvironment with ESTIMATE, Microenvironment Cell Populations (MCP)-counter, single-sample gene set enrichment analysis (ssGSEA), and tumour immune dysfunction and exclusion (TIDE). We performed a least absolute shrinkage and selection operator (LASSO) regression analysis to identify the prognosis-related hub genes, identified the risk and protective factor genes associated with HCC, classified them into two clusters, and found that Cluster 2 had a significantly better prognosis than Cluster 1. Moreover, the latter had advanced clinical features compared with the former. Uridine-cytosine kinase 1 (UCK1), myristoylated alanine-rich C-kinase substrate-like protein 1 (MARCKSL1), P-antigen family member 1 (PAGE1), and killer cell lectin-like receptor B1 (KLRB1) were detected and used to construct a simplified prognostic model for HCC. The high risk score subgroup showed a poorer prognosis than the low risk score subgroup, and the model assessed HCC prognosis consistently and effectively. The WNT score-related gene-based model designed and evaluated herein had strong prognostic and predictive ability for HCC and could, therefore, facilitate decision-making in the prognosis and therapeutic efficacy assessment of HCC. - Source: PubMed
Li PenghuiMa XiaoHuang DiGu Xinyu - Three AML cell variants (M/A, M/A* from MOLM-13 and S/A from SKM-1) were established for resistance by the same protocol using 5-azacytidine (AZA) as a selection agent. These AZA-resistant variants differ in their responses to other cytosine nucleoside analogs, including 5-aza-2'-deoxycytidine (DAC), as well as in some molecular features. Differences in global DNA methylation, protein levels of DNA methyltransferases, and phosphorylation of histone H2AX were observed in response to AZA and DAC treatment in these cell variants. This could be due to changes in the expression of uridine-cytidine kinases 1 and 2 (UCK1 and UCK2) demonstrated in our cell variants. In the M/A variant that retained sensitivity to DAC, we detected a homozygous point mutation in UCK2 resulting in an amino acid substitution (L220R) that is likely responsible for AZA resistance. Cells administered AZA treatment can switch to de novo synthesis of pyrimidine nucleotides, which could be blocked by inhibition of dihydroorotate dehydrogenase by teriflunomide (TFN). This is shown by the synergistic effect of AZA and TFN in those variants that were cross-resistant to DAC and did not have a mutation in UCK2. - Source: PubMed
Publication date: 2023/06/05
Šimoničová KristínaJanotka LubosKavcova HelenaSulova ZdenaMessingerova LuciaBreier Albert