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
- Nuclear mRNA transport is essential for maintaining mRNA homeostasis and normal cellular functions; however, the mechanisms regulating the nuclear transport of E2F transcription factor 1 () mRNA remain poorly understood. In this study, we show that the nuclear RNA transport factor 1 (NXF1) is upregulated in Hemin-treated HT22 cells and intracerebral hemorrhage (ICH) mice, suggesting its involvement in ICH pathogenesis. knockdown exerted a protective effect against Hemin-induced inflammatory responses in HT22 cells. Consistently, downregulation ameliorated neurological deficits, reduced cell death, and decreased cytokine levels . Mechanistically, NXF1-mediated neuroprotection was associated with mitophagy induction. Collectively, our findings provide novel insights into ICH progression and identify the RBM15/NXF1/E2F1 axis as a potential target for ICH intervention. - Source: PubMed
Publication date: 2026/09/16
Sun JiweiYin HaoyuSong JianLi NingFeng JieLu XuefengHan YiZhang Yesen - Nuclear pore complexes (NPCs) are embedded throughout the nuclear envelope of all eukaryotic cells and are composed of 30 unique proteins called nucleoporins (Nups). While Nups primarily function at NPCs, multiple Nups function in the nucleoplasm independent of the NPC. We previously found that is necessary for entry into S phase in Drosophila cells, however, the mechanism is unknown. Here, we demonstrate that is one of only a subset of Nup genes that can promote entry into S phase. We identify that transcripts dependent on in Drosophila cells are enriched in cell cycle processes and that many of these transcripts are also dependent on the cell cycle regulator, E2f1. Importantly, we find that entry into S phase can be rescued by co-depleting the CycE/CDK2 inhibitor, , in -depleted cells. Furthermore, promotes S phase entry across multiple cell and tissue types and cell cycle contexts. Critically, overexpression of has a dominant-negative effect on entry into S phase in larval salivary glands, suggesting that Nup98, not Nup96, promotes entry into S phase. Our work identifies Nup98 as a key regulator of the G1/S transition in metazoans. - Source: PubMed
Publication date: 2026/09/09
Malagise Evi MSherman AnnaCapelson MayaNordman Jared T - In utero alcohol exposure (IUE) can alter mammary development and increase mammary tumor susceptibility in experimental models. However, most previous studies have relied on carcinogen-induced or genetically tumor-prone models, leaving it unresolved whether prenatal alcohol exposure produces mammary developmental and molecular changes before the introduction of an oncogenic challenge. Here, we addressed this question using non-tumorigenic C57BL/6 mice. Pregnant dams received a Lieber-DeCarli liquid diet containing 1.7% (v/v) ethanol or an isocaloric control diet from gestational day 11 to 19, and mammary glands from female offspring were examined during puberty (postnatal day 40, PND40) and young adulthood (PND70). At PND40, IUE enhanced mammary ductal morphogenesis, increased terminal end bud numbers, and elevated epithelial proliferation. These developmental alterations persisted at PND70, with increased lateral branching and proliferative activity. IUE also altered mammary epithelial composition, expanding the basal/myoepithelial compartment and the CD24 CD49f mammary repopulating unit/stem cell-enriched population. Mammary epithelial cells from IUE-exposed offspring exhibited increased colony-forming cells (CFCs), mammosphere formation, and 3D Matrigel growth, indicating enhanced stem/progenitor-associated activity. At the molecular level, IUE increased ERα expression and phosphorylation together with Cyclin D1, c-Myc, E2F1, and Bcl-2, and enhanced AKT, ERK, and STAT3 phosphorylation, IL-6 expression, and SOX2 at PND40. Importantly, major components of this signaling phenotype remained altered at PND70, including ERα-associated signaling, AKT/ERK activation, and IL-6/STAT3 signaling, whereas the pubertal increase in SOX2 was not sustained. Together, these findings demonstrate that prenatal alcohol exposure induces profound and persistent histomorphological, cellular, and signaling alterations in the mammary gland in the absence of a carcinogenic challenge or genetically introduced oncogenic driver. These results identify intrinsic developmental reprogramming of normal mammary tissue as a potential basis through which prenatal alcohol exposure may modify subsequent responses to tumor-promoting or other environmental challenges. - Source: PubMed
Publication date: 2026/09/23
Ma ZhikunParris Amanda BEspinoza Evelyn IYang Xiaohe - Ataxia-telangiectasia (A-T) is a rare autosomal recessive genome-instability disorder due to pathogenic variants in ATM, a central kinase of the DNA double-strand break signaling, checkpoint activation and stress-response pathways. Although microRNAs (miRNAs) regulate DNA damage response (DDR), apoptosis, senescence and cell-cycle control, the stress-responsive behavior of selected ATM/DDR-associated miRNAs remains incompletely characterized in A-T fibroblast models. - Source: PubMed
Publication date: 2026/09/30
Iqbal Muhammad JunaidBucci CeciliaRicci AnastasiaMorganti GianlucaKhan Faez IqbalKhan Muhammad JawadMenotta Michele - Hepatocellular carcinoma (HCC) remains a major challenge threatening global health. It has a high incidence with poor prognosis, and its response to current conventional therapies is not satisfactory, so we need to explore new effective therapies to address this problem. Targeted therapy represents a promising approach, but the therapeutic efficacy of targeting ion transporters and nuclear transport proteins, such as Na+/K+/2Cl- cotransporter 1 (NKCC1) and Karyopherin β1 (KPNβ1), remains poorly investigated. This study aims to assess the therapeutic efficacy of targeting NKCC1 and KPNβ1 individually and in combination. We also explored the roles of these transporters in tumor cell proliferation and HCC progression. To achieve this aim, an HCC rat model was used, induced by diethylnitrosamine and phenobarbital. The evaluation included histopathological examination and assessment of liver function biomarkers (alanine aminotransferase and aspartate aminotransferase), cell cycle regulators (Cyclin D1, p21, E2F1), proliferation (Ki-67), apoptosis (Caspase-3), and expression of NKCC1 and KPNβ1. This study revealed that NKCC1 and KPNβ1 were upregulated in the HCC group. This increase was associated with increased proliferation and suppressed apoptosis. Targeting these proteins, particularly in combination, significantly improved liver function. It also induced cell cycle arrest, reduced proliferative markers, and enhanced apoptosis. These findings indicate that NKCC1 and KPNβ1 could serve as possible therapeutic targets in HCC treatment. - Source: PubMed
Abass Shimaa AElhasanein Doaa HEldomany Ramadan AZakaria Sherin