Ask about this productRelated genes to: SulT1C2 antibody
- Gene:
- SULT1C2 NIH gene
- Name:
- sulfotransferase family 1C member 2
- Previous symbol:
- SULT1C1
- Synonyms:
- ST1C1
- Chromosome:
- 2q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-01-10
- Date modifiied:
- 2015-11-06
Related products to: SulT1C2 antibody
Related articles to: SulT1C2 antibody
- Liver cancer (LC) is the second leading cause of cancer-related deaths globally, yet the molecular mechanisms linking its progression with associated risk factors (RFs) remain poorly understood. To address this, we developed an integrative multi-stage framework combining bioinformatics, machine learning-based feature selection, survival modeling, and network analysis to identify robust biomarkers and pathways involved in LC progression. Unlike conventional biomarker discovery approaches, our strategy integrates multi-cohort transcriptomic and clinical datasets, enhancing robustness and reliability of findings. Initially, differentially expressed genes were identified from three Gene Expression Omnibus datasets for LC and its RFs. Next, using shared biomarkers, we constructed a gene-disease association (diseasome) network, revealing 230 unique genes, including 126 shared between LC and liver cirrhosis. Subsequently, RNA-seq and clinical data from The Cancer Genome Atlas (TCGA) were analyzed through combined and multivariate Cox survival models, identifying 70 prognostic genes. Among these, we identified RGS5, SULT1C2, CSM3, and CXCL14 as consistent survival-associated markers. Functional investigation of the 70 genes using enrichment and protein-protein interaction networks uncovered ten hub genes involved in key oncogenic pathways, including Oocyte meiosis, Lysine degradation and cell cycle regulation. These findings were further validated through literature and expression-level analysis. Additionally, an independent survival analysis using the full TCGA transcriptomic dataset identified 76 significant genes, with 18 overlapping the risk-associated gene set, reinforcing their prognostic value. Overall, this study demonstrates the potential of an integrative computational approach to uncover meaningful biomarkers and pathways in LC, offering valuable insights for future clinical and therapeutic strategies. - Source: PubMed
Asa Tania AkterHossain Md AliAli Md ShahjahanMahmud Md ZulfikerAzad A K MRahman Mohammad ZahidurMoni Mohammad Ali - Genetic variants can affect signaling pathways that are important in the pathophysiology of Parkinson's disease (PD). Comprehending their relationship is crucial for the development of diagnostic instruments and preventative drugs for PD. We thoroughly analyzed data from 68 genome-wide association studies to uncover significant genetic variations and clarify the molecular pathways underlying the etiology of Parkinson's disease (PD) resulting from genetic variants. Six common biomarkers linked to PD were found in all 68 investigations: SNCA, TMEM175, BST1, RIT2, LRRK2, and MCCC1. SNCA (↑rs5019538 and ↑rs356182), LRRK2 (↑rs34637584 and ↑rs76904798), and SH3GL2 (↑rs10756907 and ↓rs13294100) were the main biomarkers associated with PD. The clinical traits of PD, such as age at onset, cognitive progression, motor progression, composite progression, tremor dominant, and postural instability gait difficulty, have been found to be underpinned by additional biomarkers, including APOE, NTRK2, SLCO1B3, SLC28A3, AQP10, SNCAIP, ANO2, CADM1, PTPRD, GPR32, GPR321, SQOR, SULT1C2, GABRG2, CYP4Z1, CDH13, and FANCF. Significant evidence was found linking genetic variants linked to an increased risk of PD to reduced dopamine production, receptor recycling, oxidoreductase activity, and increased amyloid-beta accumulation. Considerable evidence links genetic variations with a lower risk of PD due to improved synaptic vesicle signaling, neuron projection development, controlled histone methylation, and excitatory postsynaptic potential. Additionally, we found MYT1L and hsa-miR-20a-5p, which are essential for understanding the genetic variations linked to PD. These findings provide a solid underpinning for future therapeutic approaches aimed at PD, with a focus on the genetic variants and processes connected to the illness. - Source: PubMed
Publication date: 2025/09/30
Nguyen Hai Duc - Autosomal dominant polycystic kidney disease is the most prevalent inherited kidney disease and leads to bilateral kidney enlargement and progressive loss of renal function, often over decades. Comorbidities include hypertension, flank pain, and bacterial infections. The condition often necessitates prolonged multidrug therapy. Given the kidneys' critical role in drug excretion, the progressive functional impairment in the disease can lead to complications such as drug overdosing and unexpected levels of drug-drug interactions. Studies of drug-metabolizing enzyme and transporter expression in this patient group remain scarce. We conducted comprehensive global liquid chromatography-tandem mass spectrometry proteomic analyses of microsomal and cytosolic fractions from early-stage (chronic kidney disease stage: 13, n = 16) and end-stage autosomal dominant polycystic kidney disease patients (chronic kidney disease stage: 5, n = 14), comparing them with age-matched healthy controls (n = 11). In the early-stage ADPKD samples, most drug-metabolizing enzymes and drug transporters did not differ significantly from the healthy controls. Exceptions were EPHX2 and SULT1C2 in the cytosolic fraction, which showed a more than 2-fold decrease in abundance (P < 0.05). In contrast, the end-stage ADPKD kidney samples showed a decrease in the abundance of most measured proteins. Several drug-metabolizing enzymes, including CYP4F2, UGT1A6, UGT1A9, and UGT2B7, exhibited statistically significant reductions (P < 0.05). Among the drug transporters, OAT1, OAT3, and OCT2 were below the limit of quantification in most ES-ADPKD samples. MDR1 was the only efflux drug transporter consistently measured, with an average abundance of 1.24 pmol/mg microsomal protein across all samples. - Source: PubMed
Publication date: 2025/05/15
Tillmann Annika CPeters Dorien J MRostami-Hodjegan AminWilson PatriciaNorman JillBarber JillAl-Majdoub Zubida M - In this communication, we test the hypothesis that sulfotransferase 1C2 (SULT1C2, UniProt accession no. Q9WUW8) can modulate mitochondrial respiration by increasing state-III respiration. - Source: PubMed
Publication date: 2024/08/28
Kolb Alexander JCorridon PeterUllah MahbubPfaffenberger Zechariah JXu Wei MinWinfree SethSandoval Ruben HHato TakeshiWitzmann Frank AMohallem RodrigoFranco JackelineAryal Uma KAtkinson Simon JBasile David PBacallao Robert L - Human studies of genetic risk factors for neural tube defects, severe birth defects associated with long-term health consequences in surviving children, have predominantly been restricted to a subset of candidate genes in specific biological pathways including folate metabolism. - Source: PubMed
Tindula GwenIssac BijuMukherjee Sudipta KumerEkramullah Sheikh MuhammadArman D MIslam JoynulSuchanda Hafiza SultanaSun LiangRockowitz ShiraChristiani David CWarf Benjamin CMazumdar Maitreyi