Ask about this productRelated genes to: E2F1 antibody
- Gene:
- E2F1 NIH gene
- Name:
- E2F transcription factor 1
- Previous symbol:
- RBBP3
- Synonyms:
- RBP3
- Chromosome:
- 20q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-29
- Date modifiied:
- 2016-10-05
Related products to: E2F1 antibody
Related articles to: E2F1 antibody
- Endometriosis is a common gynecological disease in which lipid metabolic dysregulation has been increasingly implicated. However, the specific metabolic changes in ectopic lesions and stromal cells remain poorly understood. It is also unclear whether these changes contribute to lipid droplet accumulation or how this process is controlled at the transcriptional level. Here, we report that ectopic stromal cells exhibit broad lipid remodeling, showing changes in phosphatidylcholines, lysophosphatidylcholines, sphingomyelins, and acylcarnitines. Both ectopic lesions and ectopic stromal cells showed increased triacylglycerol and total cholesterol levels, lipid droplet accumulation, and reduced E2F1 expression. Integrated epigenomic and transcriptomic analyses of patient-derived ectopic stromal cells, together with mechanistic validation, revealed that E2F1 transcriptionally activates MGLL, which encodes monoacylglycerol lipase, a lipolytic enzyme involved in lipid mobilization. Both in vitro and in vivo experiments showed that downregulation of E2F1 increased lipid droplet accumulation, whereas restoring MGLL expression partially reversed this effect. Consistently, targeted lipidomic analysis of ectopic stromal cells following MGLL knockdown showed increased levels of several diacylglycerol species and alterations in sphingomyelin profiles. In summary, our findings suggest that E2F1 downregulation reduces MGLL expression and impairs lipid mobilization, which may contribute to lipid droplet accumulation and endometriotic lesion growth. - Source: PubMed
Publication date: 2026/09/28
Wang XiaorongZhu JingwenLi JieHuang YanXue Qing - Neuroendocrine neoplasms (NENs) are a biologically heterogeneous group of epithelial malignancies arising from neuroendocrine cells across multiple organs. Although considered rare in comparison to other solid tumors, their incidence has increased more than six-fold in recent decades. A major clinical challenge is the accurate stratification between aggressive, poorly differentiated (PD) neuroendocrine carcinomas (NECs) and slow growing well-differentiated (WD) neuroendocrine tumors (NETs), which differ significantly in prognostic outcomes and treatment response. Conventional histopathology is often insufficient for reliable classification or determination of tumor origin, motivating the need for molecularly informed diagnostic approaches. - Source: PubMed
Publication date: 2026/09/15
Khumpan TimothyChewe KasondeVijayvergia NamrataEleam EricQuiñones-Romero Juan NicolasPeri SurajYulan GongEngstrom Paul FCai Kathy QPei JianmingAlekbaeva Gulnaz DCampbell Kerry SWhetstine Johnathan RAstsaturov IgorLee Hayan - Patent ductus arteriosus (PDA) is a common congenital heart disease (CHD) with a complex genetic basis. The transcription factor MEF2C plays a critical role in cardiac development, but the role of promoter region variants in PDA has not been explored. This study aimed to identify MEF2C promoter variants in PDA patients and investigate their functional consequences. We sequenced the MEF2C promoter region in 318 children with PDA and 306 healthy controls. Identified variants were subjected to dual-luciferase reporter assays in A7r5 vascular smooth muscle cells to assess transcriptional activity. Bioinformatics (JASPAR) and electrophoretic mobility shift assays (EMSA) were used to predict and validate changes in transcription factor binding. Seventeen variants were identified, of which seven were present exclusively in PDA patients. Three variants were novel. Dual-luciferase assays showed that six variants significantly altered promoter activity compared to wild-type (range 69.6%-82.3%). JASPAR prediction revealed that these variants affected binding sites for 16 transcription factors, including GATA1, GATA2, GATA3, STAT3, ZEB1 and E2F1. EMSA confirmed altered DNA-protein binding patterns for all six variants, and super-shift assays further validated that the g.24571 A > G variant specifically disrupts GATA3 binding. This is the first study to identify functionally relevant MEF2C promoter variants in PDA. Our findings suggest that dysregulation of MEF2C through promoter variants may contribute to PDA pathogenesis by disrupting critical transcription factor interactions. These results extend the genetic landscape of PDA beyond coding regions and provide new insights into the molecular mechanisms of CHD. - Source: PubMed
Wang Shao-JieChen Huan-XinYang QinHe Guo-Wei - Alcohol consumption is associated with increased breast cancer risk, partly due to the accumulation of toxic aldehydes like acetaldehyde, a carcinogenic byproduct of ethanol metabolism. Acetaldehyde Dehydrogenase 2 (ALDH2), a key mitochondrial enzyme, detoxifies acetaldehyde and other reactive aldehydes that drive oxidative stress, DNA damage, and hormonal dysregulation-processes central to carcinogenesis. Although alcohol consumption has been implicated in breast cancer, the role of ALDH2 deficiency itself, in the absence of exogenous alcohol exposure, in mammary gland biology and cancer susceptibility remains unclear. Genetic variants that impair ALDH2 activity are highly prevalent in East Asian populations, where carriers of inactive ALDH2 alleles exhibit impaired aldehyde detoxification. While such individuals are more susceptible to alcohol-related cancers, the effects of ALDH2 deficiency on mammary gland development and homeostasis without alcohol exposure remain unexplored. To investigate the effects of ALDH2 deficiency on mammary proliferation and development, we utilized a C57BL/6-based ALDH2 knockout (Aldh2-/-) mouse model. Our findings revealed that Aldh2-/- mice displayed hyperproliferative mammary glands with increased epithelial cell density, ductal expansion, and increased numbers of Ki67+ cells. Flow cytometry analysis revealed expansion of luminal and basal epithelial subpopulations, accompanied by enhanced mammary epithelial stemness, as indicated by increased mammosphere formation and colony-forming efficiency. At the molecular level, ALDH2 deficiency activated oxidative stress pathways, reflected by elevated 8-OHdG, p38 MAPK, NF-κB, and Nrf2 signaling, along with DNA damage responses involving p53 and H2A.X. We also identified a novel upregulation of RANK and RANKL in Aldh2-/- mammary glands, identifying the RANK/RANKL upregulation associated with NF-κB/p38 MAPK activation and enhanced mammary stemness. Furthermore, hormonal dysregulation was observed, with a significant increase in ERα and PR expression and phosphorylation. Dysregulated ER signaling correlated with enhanced erbB3 activation and downstream signaling, including the cyclin D1-pRb-E2F1 axis. These findings suggest that ALDH2 deficiency, possibly through accumulated endogenous aldehydes, profoundly alters mammary morphogenesis, epithelial repopulation, and stemness. These effects are associated with activation of oxidative stress and DNA damage pathways, together with upregulation of RANKL, estrogen receptor and receptor tyrosine kinase signaling. This study is the first to identify ALDH2 deficiency as a novel factor associated with mammary epithelial alterations that may create a tissue state that could predispose to oncogenic transformation. - Source: PubMed
Publication date: 2026/09/09
Ma ZhikunParris Amanda BLester MilesGissendanner De'jaVasiliou VasilisYang Xiaohe - Gastric ulcer is a common gastrointestinal disorder associated with oxidative stress, inflammation, and disruption of the gastric mucosal barrier. This study investigated the gastroprotective and therapeutic effects of Phoenix dactylifera (Zaghloul) methanolic leaves extract against ethanol-induced gastric ulcer in male Wistar rats. Phenolic quantification of the extract revealed the presence of phenolic (2450.127 mg GAE/g) and flavonoid (2230.00 mg CE/g) contents. LC-ESI-MS-MS analysis led to detection of 23 compounds. Ethanol administration resulted in elevation of MDA, inflammatory modulators (TNF-α, ICAM-1 and IL-10) and reduction of TAC, GSH and cycloxygenase enzymes (COXI and COXII). Expression of E2F1, RAD21, NIBPL, and Vimentin genes was increased via ulcer induction. Treatment with the extract reversed ethanol effects by elevating TAC, GSH, COXI and COXII and reducing MDA, TNF-α, ICAM-1 and IL-10;TNF-α/IL-10 ratio was increased in the ulcerative group and reduced by treatment. Moreover, the extract modulated the expression of E2F1, RAD21, NIBPL, and Vimentin suggesting a potential association with attenuation of epithelial injury and mucosal repair. Histopathological examination demonstrated improvement of the mucosal architecture and mucin production, and reduction of fibrosis. Collectively, these findings demonstrate the impact of ulcer induction and extract treatment on the expression of the studied genes and support the gastroprotective and therapeutic effects of P. dactylifera leaves extract through antioxidant, anti-inflammatory, and mucosal healing activities. Further studies at the protein level using more dosages of the extract are needed to clarify the mechanistic significance of these gene expression changes and the appropriate dose of the extract. - Source: PubMed
Publication date: 2026/09/24
Aly Hanan FMabrouk Mohamed IShalaby Mohamed BHamed Karima AKhalil Wagdy K BSawi Salma ElEl-Feky Amal MElbatanony Marwa MSalim Mohamed SKiwan Hanan S