Ask about this productRelated genes to: GTF3C2 antibody
- Gene:
- GTF3C2 NIH gene
- Name:
- general transcription factor IIIC subunit 2
- Previous symbol:
- -
- Synonyms:
- KIAA0011, TFIIIC110
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-21
- Date modifiied:
- 2015-11-09
Related products to: GTF3C2 antibody
Related articles to: GTF3C2 antibody
- Type 1 diabetes mellitus (T1DM) is a metabolic disease leading threat to human health around the world. Here we aimed to explore new biomarkers and potential therapeutic targets in T1DM through adopting integrated bioinformatics tools. The gene expression Omnibus (GEO) database was used to obtain next generation sequencing data (GSE270484) of T1DM and normal control samples. Furthermore, differentially expressed genes (DEGs) were screened using the DESeq2 package in R bioconductor package. Gene Ontology (GO) and pathway enrichment analyses were performed by g:Profiler. The protein-protein interaction (PPI) network was plotted with IID PPI database and visualized using Cytoscape. Module analysis of the PPI network was done using PEWCC. Then, microRNAs (miRNAs) and transcription factors (TFs) in T1DM were screened out from the miRNet and NetworkAnalyst database. Then, the miRNA-hub gene regulatory network and TF-hub gene regulatory network were constructed by Cytoscape software. Moreover, a drug-hub gene interaction network of the hub genes was constructed and predicted the drug molecule against hub genes. The receiver operating characteristic (ROC) curves were generated to predict diagnostic value of hub genes. Finally we performed molecular docking, ADMET profiling and molecular dynamics simulation studies of marine derived chemical constituents using Schrodinger Suite 2025-1. A total of 958 DEGs were screened: 479 up regulated genes and 479 down regulated genes. DEG were mainly enriched in the terms of developmental process, membrane, cation binding, response to stimulus, cell periphery, ion binding, neuronal system and metabolism. Based on the data of protein-protein interaction (PPI), the top 10 hub genes (5 up regulated and 5 down regulated) were ranked, including FN1, GSN, ADRB2, CEP128, FLNA, CD74, EFEMP2, POU6F2, P4HA2 and BCL6. The miRNA-hub gene regulatory network and TF-hub gene regulatory network showed that hsa-mir-657, hsa-miR-1266-5p, NOTCH1 and GTF3C2 might play an important role in the pathogenesis of T1DM. The drug-hub gene interaction network showed that Clenbuterol, Diethylstilbestrol, Selegiline and Isoflurophate predicted therapeutic drugs for the T1DM. Molecular docking and molecular dynamics simulation study revealed that CMNPD5805 and CMNPD30286 as potential inhibitors of FN1 (pdb id: 3M7P) a key biomarker in pathogenesis of T1DM. These findings promote the understanding of the molecular mechanism and clinically related molecular targets for T1DM. - Source: PubMed
Publication date: 2026/01/14
Vastrad BasavarajPattanashetti ShivalingSadashivanavar VeereshPai K S RVastrad Chanabasayya - : Most studies investigating prognostic biomarkers in cervical cancer (CC) analyze patients irrespective of FIGO stage, potentially masking molecular features that underlie the aggressiveness of some FIGO II tumors. To address this, we investigated differential gene expression in a FIGO II CC cohort to identify a gene signature predictive of progression-free survival (PFS) within five years of treatment initiation. : Tumor samples from 15 CC patients were analyzed using RNA sequencing, bioinformatics, and machine learning to identify differentially expressed genes (DEGs) associated with prognosis. Findings were validated in an independent CC cohort ( = 174). : High expression of B3GALT1 (HR = 5.11), GTF3C2-AS1 (HR = 18.73), and ZKSCAN4 (HR = 5.18) was significantly associated with an increased risk of recurrence in our cohort. Elevated expression of these transcripts is also associated with shorter PFS in the external dataset. Notably, GTF3C2-AS1 expression alone was sufficient to classify all fifteen patients into their respective prognostic groups using a decision tree model, achieving 93.3% accuracy in leave-one-out cross-validation (LOOCV). Additional candidates, including RCAN2-DT, MYH9-DT, IGKC, IGHG1, and IGHG3, were associated with PFS in our cohort but could not be externally validated due to a lack of available data. : Transcriptomic profiling revealed potential biomarkers that refine prognostic stratification in cervical cancer beyond FIGO staging. Among them, GTF3C2-AS1 consistently emerged as a potential predictor of recurrence risk. Additional candidates, including B3GALT1, ZKSCAN4, and immunoglobulin transcripts, provided complementary insights but require further validation. These preliminary results highlight intra-stage heterogeneity in FIGO II CC and underscore the promise of molecular markers to improve risk assessment. - Source: PubMed
Publication date: 2025/10/16
Melo Carolina P SMelo Angelo BQueiroz Fábio RCosta Álvaro PAmaral Laurence RPereira Ramon AAmorim Izabela F GFerreira Jorge G GJeremias Wander JBertarini Pedro L LGomes Matheus SBraga Letícia CSalles Paulo G O - General transcription factor IIIC subunit 2 (GTF3C2) is one of the polymerase III transcription-related factors. Previous studies have revealed that GTF3C2 is involved in regulating cell proliferation. However, the role of GTF3C2 in hepatocellular carcinoma (HCC) remains unclear. This study aimed to determine its expression, biological function, and mechanism in HCC. - Source: PubMed
Publication date: 2025/02/11
Wu YaniYang YingnanZhang YoujuXu QiuranHuang DongshengTu Kangsheng - Spitz melanocytic neoplasms exhibit frequent chromosomal rearrangements leading to recurring gene fusions, such as ALK fusions. TPM3 and DCTN1 emerge as the predominant fusion partners of ALK , although less common partners such as NPM1 , TPR , CLIP1 , GTF3C2 , MLPH , EEF2 , MYO5A , and KANK1 have also been documented. Although ALK fusions are primarily associated with Spitz nevi or atypical Spitz tumors, instances of Spitz melanoma with ALK fusions documented in the English literature are exceedingly rare. Here, we present a case of Spitz melanoma harboring SLC20A1::ALK fusion, highlighting a novel fusion transcript not previously reported in Spitz melanocytic neoplasms, including Spitz melanomas. In addition, the tumor exhibits multiple aberrant chromosomal alterations characteristic of melanoma, along with a somatic mutation in GRM3 . - Source: PubMed
Publication date: 2024/06/28
Cho Woo ChealPrieto Victor GYang Richard K - The pulmonary endothelium is a dynamic and metabolically active monolayer of endothelial cells. Dysfunction of the pulmonary endothelial barrier plays a crucial role in the acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), frequently observed in the context of viral pneumonia. Dysregulation of tight junction proteins can lead to the disruption of the endothelial barrier and subsequent leakage. Here, the highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) served as an ideal model for studying ALI and ARDS. The alveolar lavage fluid of pigs infected with HP-PRRSV, and the supernatant of HP-PRRSV infected pulmonary alveolar macrophages were respectively collected to treat the pulmonary microvascular endothelial cells (PMVECs) in Transwell culture system to explore the mechanism of pulmonary microvascular endothelial barrier leakage caused by viral infection. Cytokine screening, addition and blocking experiments revealed that proinflammatory cytokines IL-1β and TNF-α, secreted by HP-PRRSV-infected macrophages, disrupt the pulmonary microvascular endothelial barrier by downregulating claudin-8 and upregulating claudin-4 synergistically. Additionally, three transcription factors interleukin enhancer binding factor 2 (ILF2), general transcription factor III C subunit 2 (GTF3C2), and thyroid hormone receptor-associated protein 3 (THRAP3), were identified to accumulate in the nucleus of PMVECs, regulating the transcription of claudin-8 and claudin-4. Meanwhile, the upregulation of ssc-miR-185 was found to suppress claudin-8 expression via post-transcriptional inhibition. This study not only reveals the molecular mechanisms by which HP-PRRSV infection causes endothelial barrier leakage in acute lung injury, but also provides novel insights into the function and regulation of tight junctions in vascular homeostasis. - Source: PubMed
Publication date: 2024/05/28
Sun WeifengWu WeixinFang XinyuGe XinnaZhang YongningHan JunGuo XinZhou LeiYang Hanchun