Recombinant Human Thymidine Phosphorylase TYMP
- Known as:
- Recombinant Human Thymidine Phosphorylase TYMP
- Catalog number:
- enz-005
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Recombinant Human Thymidine Phosphorylase TYMP
Related genes to: Recombinant Human Thymidine Phosphorylase TYMP
- Gene:
- TYMP NIH gene
- Name:
- thymidine phosphorylase
- Previous symbol:
- MNGIE, ECGF1
- Synonyms:
- -
- Chromosome:
- 22q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-27
- Date modifiied:
- 2019-04-23
Related products to: Recombinant Human Thymidine Phosphorylase TYMP
Related articles to: Recombinant Human Thymidine Phosphorylase TYMP
- COVID-19 survivors exhibit increased interstitial lung fibrosis, a known risk factor for lung cancer. We investigated whether SARS-CoV-2 spike protein (SP)-induced lung injury and elevated thymidine phosphorylase (TYMP) promote lung tumorigenesis. - Source: PubMed
Publication date: 2026/03/31
Wallace CayleighGileles-Hillel AlexCox AmeliaGozal DavidLi WeiYue Hong - Psoriasis is a common, chronic, and recurrent immune-mediated disorder with global prevalence, underscoring the need for novel biomarkers to improve diagnosis and treatment. In this study, differentially expressed genes (DEGs) in psoriatic tissues were comprehensively identified through integrated single-cell and bulk RNA-seq analyses. Thymidine phosphorylase (TYMP) emerged as one of the most significantly upregulated biomarkers in psoriasis. Multiplex immunohistochemistry (mIHC) and IHC assays jointly confirmed marked overexpression of TYMP in psoriatic keratinocytes. Mechanistically, we demonstrated that IL-17-mediated inflammatory signaling transcriptionally induces TYMP expression via NF-κB1. TYMP overexpression promotes keratinocyte proliferation and activates signaling pathways associated with keratinization and neutrophil degranulation in psoriasis. Immune infiltration analysis, blood routine tests, and ELISA verified that TYMP upregulation is closely correlated with neutrophil degranulation in psoriasis. In the imiquimod (IMQ)-induced psoriasis-like mouse model, pharmacological inhibition of TYMP by tipiracil partially reverses the pathological effects of TYMP overexpression, including accelerated keratinocyte proliferation, aberrant keratinization, and neutrophil-driven inflammation. In summary, TYMP is overexpressed in psoriasis due to hyperactivation of the IL-17/NF-κB1 signaling. Targeting TYMP by Tipiracil ameliorates psoriasis symptoms by suppressing abnormal keratinization and neutrophil degranulation, thereby highlighting its potential as a therapeutic target for psoriasis. - Source: PubMed
Publication date: 2026/04/09
Wang JingZhou ZengChen YanyanLi QiangZhai LantianLi DandanQin ShanshanHe Yanling - Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is an extremely rare autosomal recessive disease caused by variants in the thymidine phosphorylase gene (TYMP), primarily characterized by severe gastrointestinal and neurological symptoms. The complete phenotype of MNGIE has not been linked to any gene other than TYMP. - Source: PubMed
Capece GiulianaCaumo LucaVolta SaraRiguzzi PietroSogus ElenaPetrosino AngelaVianello SaraSabbatini DanieleSalviati LeonardoManara RenzoViscomi CarloSorarù GianniBello LucaPegoraro Elena - Epilepsy is a common neurological disorder with a complex molecular pathogenesis. Approximately one-third of patients experience drug-resistant seizures, which severely impairs their quality of life. This study employed an integrated bioinformatics and machine learning approach to identify key genes associated with epilepsy. Epilepsy-related datasets from the GEO database were analyzed using differential expression analysis and weighted gene co-expression network analysis (WGCNA) for the initial identification of candidate genes. These candidates were subsequently refined using machine learning algorithms, including least absolute shrinkage and selection operator (LASSO), random forest (RF) and support vector machine (SVM), to filter key genes. TYMP and HES4 demonstrated robust diagnostic value for epilepsy (AUC: 0.770 for TYMP and 0.769 for HES4). Functional enrichment analysis indicated their involvement in key signaling pathways and a close association with immune cell infiltration, highlighting their role in modulating the immune microenvironment. The significant upregulation of TYMP and HES4 was validated in both epileptic mouse models and epilepsy cell lines using RT-qPCR and Western blot. Moreover, screening of a drug-gene interaction database identified Calpain inhibitor I as a potential therapeutic agent targeting TYMP. Overall, these findings provide novel insights into the pathogenesis of epilepsy and suggest promising targets for future research and therapeutic development. - Source: PubMed
Publication date: 2026/02/24
Wu LuluHuang YupingYang HuiZhang ChenyuFeng DandanZhou Guoping - Mitochondrial DNA (mtDNA) depletion disorders (MDDs) are rare, genetically diverse conditions marked by a significant reduction in mtDNA, primarily affecting energy-demanding tissues such as muscle, liver, and brain, sometimes leading to catastrophic multisystem failure. In a cohort of patients with MDDs, we measured telomere length in lymphocytes, granulocytes, T cells, and B cells, and compared to healthy controls. Telomere length was shorter overall in patients with MDDs, with the most significant differences observed in granulocytes. The observation that mtDNA depletion is associated with shorter telomeres may provide insight into MDD pathophysiology. Telomere length may have potential as a biomarker in mitochondrial disease, but further study is needed. - Source: PubMed
Publication date: 2026/02/10
Dille YumiRampakakis EmmanouilAubert GeraldineDassi ChristelleMannherz WilliamBerrahmoune SaoussenSrour MyriamBuhas DanielaAgarwal SuneetMyers Kenneth A