Ask about this productRelated genes to: E2F6 antibody
- Gene:
- E2F6 NIH gene
- Name:
- E2F transcription factor 6
- Previous symbol:
- -
- Synonyms:
- E2F-6
- Chromosome:
- 2p25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-07
- Date modifiied:
- 2015-08-25
Related products to: E2F6 antibody
Related articles to: E2F6 antibody
- Colorectal cancer (CRC) is the third most common malignancy worldwide, and the role of E2F transcription factor 6 (E2F6) in CRC remains controversial. - Source: PubMed
Publication date: 2026/05/08
Zeng Da TongWu Ke JunLi Jian DiChen Guo QiangZhang WeiLi Zong YuLing Jing WenHuang Wei JianChen GangLi Hui - FZD8, a GPCR, is involved in various physiological processes, such as cell differentiation, bone growth and stem cell regulation, by binding to various Wnt ligands. Though FZD receptors have low mutation rates in cancer, aberrant Wnt or FZD expression leads to deregulated Wnt/FZD signaling pathways that may result in tumorigenesis. The structural and functional effects of most of the coding and non-coding SNPs of human FZD8 gene are yet to explore. In the present study, we analyzed 450, 109, and 390 SNPs in the CDS, 3'UTR, and 5'UTR of the FZD8 gene, respectively, using advanced state-of-the-art bioinformatics tools to explore their structural and functional consequences in tumorigenesis. We identified 10 highly deleterious nsSNPs among which 6 nsSNPs were located within the Wnt1 binding CRD region of FZD8. Additionally, these nsSNPs were also predicted to affect post-translational modifications in FZD8. The highly deleterious variant P120Q, causes significant structural change in secondary structure of FZD8 mRNA. Structure based stability prediction revealed 4 destabilizing variants among 6 highly deleterious variants. Wnt1 binds most strongly with FZD8-CRD among other FZD-CRDs. MD simulation analyses revealed that the binding energies of the mutated complexes were less stabilizing compared to the wild-type Wnt1-FZD8-CRD complex, with the P74L and A119E complexes predicted to be the most destabilizing. SNPs, rs1408188233 (34.T > C) in 3'UTR and rs1588706985 in 5'UTR may lead to AGO2 mediated and E2F6 mediated silencing of the FZD8 gene, respectively, whereas nsSNPs-rs1322411573 and rs1410965895 in the CDS may abolish miRNA-mediated gene silencing. Differential expression of FZD8 was observed across various normal, tumor, and metastatic tissues, and its deregulation was associated with reduced survival outcomes in patients with different types of cancer. Additionally, several biomarkers involving FZD8 mutations have been identified in patients with gastric cancer, multiple myeloma, and uterine cancer. Furthermore, these computationally prioritized high risk SNPs of FZD8 can be investigated in population based genetic studies and may serve as potential targets for future drug development against FZD8-associated diseases. - Source: PubMed
Publication date: 2026/02/24
Mondal AmaleshPaul DebaratiMondal TithiGoswami Achintya Mohan - This study aimed to investigate the expression and prognostic significance of genes associated with copper-induced cell death in glioblastoma multiforme (GBM). Using a suite of bioinformatics tools and databases, the researchers analyzed gene expression, survival rates, and immune infiltration in GBM. Complementary in vitro experiments were performed to evaluate the effects of LIPT1 inhibition on GBM cell behavior in the context of copper-induced cell death. The team further explored upstream mechanisms leading to LIPT1 overexpression in GBM, specifically focusing on transcription factors and the role of ubiquitination degradation. The findings indicated a significant upregulation of LIPT1 in GBM, correlating with increased sensitivity to copper-induced cell death. Inhibition of LIPT1 was observed to exacerbate malignant behaviors in GBM cells post-copper exposure. Subsequent analysis pinpointed three transcription factors—CBX3, E2F6, and GTF2B—as regulators of LIPT1. Notably, GTF2B was also found to be co-expressed with LIPT1 and positively associated with recurrence-free survival in patients. ChIP-seq data analysis revealed significant GTF2B binding peaks near the LIPT1 promoter. Further exploration using UbiBrowser 2.0 identified E3 ubiquitin ligases that potentially target GTF2B, with RBX1 emerging as a viable anti-cancer target in GBM. Data from the UALCAN database showed a notable decrease in RBX1 protein expression in GBM tissues. Moreover, several ubiquitination modification sites were detected on the GTF2B protein. In conclusion, the study proposes a novel scientific hypothesis: RBX1 inhibits LIPT1 transcription by promoting the ubiquitin-mediated degradation of GTF2B, thereby suppressing copper-induced cell death in GBM cells. These findings offer new insights into the molecular mechanisms governing copper death sensitivity in GBM and identify potential therapeutic targets for further exploration. - Source: PubMed
Publication date: 2026/01/31
Zeng JianpingLiu JingHua ShushanLiu ShuaiTong ShoufangZhang JieMungur RajneeshChen ShangshiFeng JiugengDing Cong - MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs) regulate broad gene networks through distinct mechanisms, which govern normal brain development and function but are dysregulated in schizophrenia (SCZ). However, how disease-risk miRNAs and lncRNAs co-operate to form pathogenic pathways in SCZ brains remain poorly understood. In this study, we identified a novel miRNA-lncRNA pathway in which the well-recognized SCZ-risk factor miR-137 enhances expression of the SCZ-risk lncRNA GOMAFU in human neuron development. We found significant up-regulation of GOMAFU during differentiation of multiple types of human neurons in vivo and in culture. Interestingly, the accumulation of histone acetylation, which activates numerous neuronal genes, down-regulates GOMAFU in iPSC-derived human neurons through inducing transcription repressors of GOMAFU, represented by the miR-137-target E2F6. We further demonstrated that miR-137 is necessary and sufficient for enhancing GOMAFU expression in a human neuronal progenitor cell (NPC) line and observed co-regulation of MIR137 with GOMAFU during normal human neuronal development and in SCZ brains. Moreover, we identified human NPC transcriptomic changes induced by miR-137 and discovered that miR-137 integrates functional co-operation of histone acetylation and transcription factors to promote GOMAFU expression. Notably, a significant number of miR-137-regulated transcription factors are predicted to bind the GOMAFU promoter and affected in SCZ brains, forming a highly interactive molecular network. Together, these results unveil the SCZ risk miR-137-GOMAFU non-coding RNA pathway connected by SCZ-affected transcription factors, providing a new mode of functional integration of non-coding and coding risk genes of SCZ that contributes to the complex etiology. - Source: PubMed
Publication date: 2025/11/18
Teng PengZhou YingJi XingyuLi YangpingKu LiWang FengWen ZhexingYao BingFeng Yue - To investigate the biological functions of the transcription factor LRR binding FLII interacting protein 1 (LRRFIP1) in white adipocyte differentiation (WAD) and elucidate the underlying molecular regulatory mechanisms involved. - Source: PubMed
Publication date: 2025/11/12
Zhou LeiJiao YuwenXue JiamingZhan XiaoqiangWang DongmeiTang Liming