Peptides: E2F6 Protein Length:12-25 amino acids.
- Known as:
- Peptides: E2F6 Protein Length:12-25 amino acids.
- Catalog number:
- bs-1750P
- Product Quantity:
- 200ug lyophilized
- Category:
- -
- Supplier:
- Bios
- Gene target:
- Peptides: E2F6 Protein Length:12-25 amino acids.
Related genes to: Peptides: E2F6 Protein Length:12-25 amino acids.
- 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: Peptides: E2F6 Protein Length:12-25 amino acids.
Related articles to: Peptides: E2F6 Protein Length:12-25 amino acids.
- Human glial progenitor cells (hGPCs) exhibit diminished expansion competence with age, as well as after recurrent demyelination. Using RNA-sequencing to compare the gene expression of fetal and adult hGPCs, we identify age-related changes in transcription consistent with the repression of genes enabling mitotic expansion, concurrent with the onset of aging-associated transcriptional programs. Adult hGPCs develop a repressive transcription factor network centered on MYC, and regulated by ZNF274, MAX, IKZF3, and E2F6. Individual over-expression of these factors in iPSC-derived hGPCs lead to a loss of proliferative gene expression and an induction of mitotic senescence, replicating the transcriptional changes incurred during glial aging. miRNA profiling identifies the appearance of an adult-selective miRNA signature, imposing further constraints on the expansion competence of aged GPCs. hGPC aging is thus associated with acquisition of a MYC-repressive environment, suggesting that suppression of these repressors of glial expansion may permit the rejuvenation of aged hGPCs. - Source: PubMed
Publication date: 2024/05/08
Mariani John NMansky BenjaminMadsen Pernille MSalinas DennisKesmen DenizHuynh Nguyen P TKuypers Nicholas JKesel Erin RBates JannaPayne CaseyChandler-Militello DevinBenraiss AbdellatifGoldman Steven A - Prostate cancer (PCa) is the most prevalent cancer affecting American men. Castration-resistant prostate cancer (CRPC) can emerge during hormone therapy for PCa, manifesting with elevated serum prostate-specific antigen (PSA) levels, continued disease progression, and/or metastasis to the new sites, resulting in a poor prognosis. A subset of CRPC patients shows a neuroendocrine (NE) phenotype, signifying reduced or no reliance on androgen receptor (AR) signaling and a particularly unfavorable prognosis. In this study, we incorporated computational approaches based on both gene expression profiles and protein-protein interaction (PPI) networks. We identified 500 potential marker genes, which are significantly enriched in cell cycle and neuronal processes. The top 40 candidates, collectively named as CDHu40, demonstrated superior performance in distinguishing NE prostate cancer (NEPC) and non-NEPC samples based on gene expression profiles compared to other published marker sets. Notably, some novel marker genes in CDHu40, absent in the other marker sets, have been reported to be associated with NEPC in the literature, such as DDC, FOLH1, BEX1, MAST1, and CACNA1A. Importantly, elevated CDHu40 scores derived from our predictive model showed a robust correlation with unfavorable survival outcomes in patients, indicating the potential of the CDHu40 score as a promising indicator for predicting the survival prognosis of those patients with the NE phenotype. Motif enrichment analysis on the top candidates suggests that REST and E2F6 may serve as key regulators in the NEPC progression. - Source: PubMed
Publication date: 2024/03/31
Liu ShengNam Hye SeungZeng ZiyuDeng XuehongPashaei ElnazZang YongYang LeiLi ChenglongHuang JiaotiWendt Michael KLu XinHuang RongWan Jun - CircRNAs participate in the development of hepatocellular carcinoma (HCC). This work aims to explore the key tumor promoting circRNA as a gene therapy target. - Source: PubMed
Publication date: 2024/01/02
Ai JiaoyuZhang WanlinDeng WenshengYan LikunZhang LidongHuang ZongjingWu ZiyiAi JunhuaJiang Hai - EN1 encodes a homeodomain-containing transcription factor and is a determinant of bone density and fracture. Previous powerful genome-wide association studies (GWASs) have identified multiple single-nucleotide polymorphisms (SNPs) near EN1 at 2q14.2 locus for osteoporosis, but the causal SNPs and functional mechanisms underlying these associations are poorly understood. The target genes regulated by the transcription factor EN1 are also unclear. In this study, we identified rs188303909, a functional CpG-SNP, as a causal SNP for osteoporosis at 2q14.2 through the integration of functional and epigenomic analyses. Functional experiments demonstrated that unmethylated rs188303909 acted as a strong allele-specific distal enhancer to regulate EN1 expression by modifying the binding of transcription factor E2F6, but rs188303909 methylation attenuated the active effect of E2F6 on EN1 expression. Importantly, transcription factor EN1 could differentially bind osteoporosis GWAS lead SNPs rs4869739-T and rs4355801-G to upregulate CCDC170 and COLEC10 expression, thus promoting bone formation. Our study provided a mechanistic insight into expression regulation of the osteoporosis susceptibility gene EN1, which could be a potential therapeutic target for osteoporosis precision medicine. KEY MESSAGES: CpG-SNP rs188303909 is a causal SNP at the osteoporosis susceptibility locus 2q14.2. Rs188303909 distally regulates EN1 expression by modulating DNA methylation and E2F6 binding. EN1 upregulates CCDC170 and COLEC10 expression through osteoporosis GWAS lead SNPs rs4869739 and rs4355801. - Source: PubMed
Publication date: 2023/12/28
Wang YaHuang XinyaoZhang QiongdanCheng ChenQin ZixuanLu LiHuang Qingyang - E2F6 is a member of the E2F transcription factor family. Numerous studies have demonstrated that E2F6 is critical to cancer development and progression, but its role in cancer immunotherapy remains unclear. - Source: PubMed
Publication date: 2023/12/09
Gong ChuandongTu ZeweiLong XiaoyanLiu XinjunLiu FengLiu JiaZhu XingenLi JingyingHuang Kai