GALK1 Antibody
- Known as:
- GALK1 Antibody
- Catalog number:
- XW-7213
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- GALK1 Antibody
Ask about this productRelated genes to: GALK1 Antibody
- Gene:
- GALK1 NIH gene
- Name:
- galactokinase 1
- Previous symbol:
- GALK
- Synonyms:
- -
- Chromosome:
- 17q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2015-08-25
Related products to: GALK1 Antibody
Related articles to: GALK1 Antibody
- Diabetic nephropathy (DN) is a leading cause of chronic kidney disease. Salvianolic acid A (SAA) has shown promising therapeutic potential against DN, yet its underlying mechanisms and precise molecular targets remain incompletely elucidated. Potential targets of SAA were predicted using SwissTargetPrediction and SuperPred, with its drug-like properties evaluated by ADMET analysis. Diabetic nephropathy (DN)-related targets were collected from GEO, CTD, and GeneCards databases. Shared targets underwent GO and KEGG enrichment analyses. Core targets were identified through topological analysis in Cytoscape, machine learning, and Mendelian randomization validation. Molecular docking and dynamics simulations assessed the binding affinity and stability between SAA and core targets. Single-cell RNA sequencing data revealed their cell type-specific expression in kidney tissues. Experimental validation was performed using an in vitro high glucose-induced podocyte injury model analyzed by RT-qPCR. The intersection of 212 drug targets with 5,097 disease targets yielded 134 potential therapeutic targets for salvianolic acid A in DN. Machine learning and Mendelian randomization further identified eight targets with causal relationships to DN. Molecular docking demonstrated strong binding affinities of salvianolic acid A to the domains of FYN, AKR1B1, TNF, GALK1, HMGCR, MAP2K2, SCN4A, and ITGA5. Single-cell analysis revealed distinct expression patterns across different renal cell types. In vitro experiments demonstrated that SAA effectively protected podocytes from HG-induced injury. SAA alleviates diabetic nephropathy through multi-target mechanisms, influencing key genes involved in disease progression. This study provides a systematic elucidation of the therapeutic basis for SAA and supports its further clinical development. - Source: PubMed
Publication date: 2026/06/24
Fu TongfeiXiong ZhiliTao HongwuZhan Yongli - Bladder cancer (BCa) is the second most common cancer of the genitourinary tract globally. It has limited treatment options, high recurrence rate, and acquires resistance to platinum-based therapy. Therefore, identifying novel therapeutic targets is urgently needed. Analysis of the TCGA data revealed that the enzyme galactokinase-1 (GALK1) is overexpressed ( < 0.0001) in bladder tumors compared to normal tissue. Our data also confirmed GALK1 protein upregulation in multiple human BCa cell lines and rodent bladder tumors. However, the precise role of GALK1 in BCa progression and effects of its specific inhibitor remain unexamined. In this study, we demonstrate that GALK1 gene silencing using shRNA resulted in a significant reduction in BCa cell proliferation, migration, and invasion. Pharmacological inhibition of GALK1 using small molecule Cpd36 resulted in anticancer efficacy against BCa. Cpd36 inhibited proliferation, migration, and invasion of BCa cells. Further, Cpd36 induced G1 phase cell cycle arrest, apoptosis, mitochondrial membrane depolarization, and ROS production in the BCa cells. Mechanistically, Cpd36-induced reduction in cell proliferation was associated with a decrease in expression of GALK1, PCNA proteins. Inhibition of metastatic potential was accompanied by decreased migration, invasion, and MMP-9 expression. Cell cycle arrest was associated with decrease in Cyclin D1 and increased expression of p21 and p27. Induction of apoptosis was linked with increased expression of cleaved caspase-3 and cleaved PARP, while downregulating p-AKT. Additionally, Cpd36 in combination with cisplatin or gemcitabine showed a strong synergistic effect on BCa cells. Taken together, our findings suggest that GALK1 plays a significant role in BCa cell survival and validates its inhibitors as promising therapeutic options for managing this disease. - Source: PubMed
Publication date: 2026/03/23
Singh Surya PLiu RonghaoYan FengTang QinggongRao Chinthalapally VMadka Venkateshwar - Chronic liver disease (CLD) is a major global health burden, causing ~ 2 million deaths annually. In a substantial proportion of cases, extensive hepatology and metabolic evaluations fail to determine the etiology, leading to classification as idiopathic liver disease, which may harbor rare genetic causes. This study assessed the clinical utility of whole-exome sequencing (WES) and clinical-exome sequencing (CES) in idiopathic liver disease patients and explored candidate variants using in silico approaches. - Source: PubMed
Bozkurt Kekilli SerayKaralar Pekuz Ozge KamerKekilli ArdaBinicier Hatice CilemSahin Uyar Sibel BurcakOzkan EtkinArslan Gülten ZumrutAydogan AycaAkarsu MesutArslan NurUlgenalp AyferCaglayan Ahmet Okay - Bladder cancer (BLCA) is a highly heterogeneous malignancy with high morbidity and mortality. Massive lactate production and hypoxia are characteristics of the tumor microenvironment (TME). However, our understanding of the clinical value of hypoxia and lactate metabolism (HLM) in BLCA remains limited. - Source: PubMed
Publication date: 2025/11/21
Zhao YihaoLi PeixinShen ZheYao ShengwenZhang XiaoyiZhang NianzhaoChen Jun - The influence of supplementing glycerol, vitamin C and niacinamide on the liver of growing-finishing pigs has not yet been examined. This study investigated the effect of 10% glycerol, 0.06% vitamin C and 0.05% niacinamide supplementation at single or combination on liver of growing-finishing pigs. Compared with pigs supplemented with 0% glycerol, 0% vitamin C and 0% niacinamide, pigs supplemented only with 10% glycerol had higher ( < 0.05) TNF- concentration, partially hepatic steatosis, higher ( < 0.05) relative abundances of , , , , and , lower ( < 0.05) solute carrier family 7 member 11 () expression in liver tissue. However, pigs offered the diet with a mixture of 0.06% vitamin C and 0.05% niacinamide had higher ( < 0.05) relative abundance of and expression of , lower ( < 0.05) relative abundances of and in liver tissue. Supplementation of 10% glycerol, 0.06% vitamin C and 0.05% niacinamide simultaneously to pigs increased ( < 0.05) the ferrous ion level, the relative abundances of , and , the expressions of gene Cryptochrome-1() and , but decreased ( < 0.05) the expressions of gene C-reactive protein () and galactokinase 1 () in liver tissue. Supplementation with 0.06% vitamin C and 0.05% niacinamide can alleviate the damage in liver of pigs fed a diet containing 10% glycerol. - Source: PubMed
Publication date: 2025/06/18
Sun WenchenDeng LinglanZou WanjieWei PantingHao ShaobinWu HuadongLu WeiHe Yuyong