Ask about this productRelated genes to: Eif4e antibody
- Gene:
- EIF4E NIH gene
- Name:
- eukaryotic translation initiation factor 4E
- Previous symbol:
- EIF4EL1, EIF4F
- Synonyms:
- EIF4E1
- Chromosome:
- 4q23
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-09
- Date modifiied:
- 2015-08-25
Related products to: Eif4e antibody
Related articles to: Eif4e antibody
- Onvansertib (ONV) is a selective inhibitor of polo-like kinase 1 (PLK1) and has promise in treating cancer. However, its potential effects on male reproductive function remain insufficiently characterized. In this study, male mice received clinically relevant doses of ONV by intragastric gavage for five consecutive days. Evaluations conducted on day 1, day 6, and day 35 after treatment revealed a marked increase in germ cell apoptosis accompanied by a significant reduction in epididymal sperm counts, whereas somatic cell architecture was preserved. Mechanistically, PLK1 inhibition by ONV led to a pronounced decrease in eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1) phosphorylation. This disruption is likely linked to impaired meiotic centrosome maturation and aberrant spindle organization in germ cells. Collectively, these findings demonstrate that ONV preferentially induces apoptosis in germ cells via PLK1 suppression, thereby compromising spermatogenic capacity. - Source: PubMed
Publication date: 2026/09/18
Qi Xiao-XuanFeng XinZhu Wen-RuiSong Tian-YiLi Hui-LingLiu QiangXu Chao-YangYuan YanCheng QingLi Lai-Hua - Eukaryotic cap-dependent translation initiation is regulated by binding of the predominantly folded eukaryotic initiation factor 4E (eIF4E) to the intrinsically disordered eIF4E binding proteins (4E-BPs). Here, we report full-length atomistic conformational ensembles generated by IDPConformerGenerator and optimized by X-EISDv2 workflow for both apo 4E-BP2, the neuronal 4E-BP, and 4E-BP2 in complex with eIF4E, using data from single-molecule fluorescence and nuclear magnetic resonance (NMR), together with select coordinates from a 4E-BP1:eIF4E crystal structure. Structural sampling within dynamic complexes is often underappreciated, with NMR and crystal structure data for 4E-BP:eIF4E suggesting different degrees of structural heterogeneity. Our ensemble models validated by solution spectroscopy data enable comparison of free 4E-BP2 and its complex with eIF4E. This shows a delocalization of contacts around canonical regions, which supports previous findings of unidirectional conditional occupancy of the binding sites. Two new contact regions emerged: one between the disordered N-termini of eIF4E and 4E-BP2, which may play an allosteric role in tuning the binding affinity, and the other between the C-terminus of 4E-BP2 and an extended region of eIF4E, which is consistent with the extended, dynamic binding interface that we reported previously. These results support a model of translation regulation in which the dynamic 4E-BP2:eIF4E complex facilitates accessibility of regulatory sites of 4E-BP2 when bound. - Source: PubMed
Smyth SpencerLiu Zi HaoTsangaris Thomas EHead-Gordon TeresaForman-Kay Julie DGradinaru Claudiu C - Through fasting and feeding (both in vivo and in vitro), nutrient availability fluctuates over time. Pancreatic β-cells must respond to nutrients not only by regulated insulin secretion but also by insulin synthesis, which depends upon proinsulin. β-cells respond biosynthetically to glucose, but little is known about amino acids as regulators of proinsulin levels. We find that in INS1E (rat) β-cells, isolated murine islets, and isolated human islets-even in the presence of abundant glucose, proinsulin levels remain sensitive to reduced availability of other nutrients contained in β-cell/islet bathing medium. A low proinsulin level upon in vitro fasting is accompanied by diminished ribosomal phospho-S6 and phospho-eIF4E-BP1 plus increased phospho-eIF2α, reversed upon re-feeding. Even as extracellular glucose levels remained steady, INS1E cells consumed the majority of extracellular glutamine and serine (measured by mass spectrometry); concurrently, six nonessential amino acids (most notably proline and alanine, plus glutamic and aspartic acid) were actually exported from cells to media. Proinsulin suppression in response to amino acid limitation appears to be β-cell-autonomous, is linked to proinsulin biosynthesis, and is ameliorated upon GCN2 inhibition in INS1E cells. Upon re-feeding amino acid-containing medium, the mTORC1 inhibitor rapamycin fully suppressed phospho-S6 but did not block the recovery of proinsulin levels, whereas Torin1 inhibition of mTOR inhibited the amino acid-dependent increase in proinsulin biosynthesis. Altogether, these data indicate that inadequate amino acid-triggered β-cell signaling can blunt the proinsulin biosynthetic response, contributing to insulin deficiency-a finding that has potential relevance to the pathogenesis of malnutrition-related diabetes. - Source: PubMed
Publication date: 2026/08/31
Ruan YutingGleason Noah FArvan Peter - Chronic allograft dysfunction, driven by interstitial fibrosis and tubular atrophy, remains a major cause of long-term renal allograft loss. Everolimus (EVR), a mammalian target of rapamycin (mTOR) inhibitor, may reduce fibrosis through antifibrotic effects and calcineurin inhibitor minimization. This study aimed to evaluate the impact of EVR-involving immunosuppression on renal allograft fibrosis and to identify predictors of fibrotic progression. A total of 104 living-donor kidney transplant recipients transplanted between 2011 and 2017 were retrospectively analyzed (EVR, = 61; non-EVR, = 43). Interstitial fibrosis was quantified in protocol biopsies using digital image analysis. Phosphorylation of the mTOR-signaling proteins p70 ribosomal S6 kinase and eukaryotic translation initiation factor 4E-binding protein 1 was assessed using a semiquantitative immunoreactive score. Multivariable regression analyses identified independent predictors of fibrotic progression. Cytomegalovirus infection was less frequent in the EVR group, whereas acute rejection, graft function, and graft survival were comparable between groups. At 1-year posttransplantation, interstitial fibrosis was significantly lower in the EVR group. EVR significantly suppressed p-4EBP1 phosphorylation and effectively modulated the mTOR-signaling pathway. Multivariable analysis identified the absence of EVR therapy as an independent predictor of accelerated fibrosis. EVR-involving immunosuppression attenuated renal interstitial fibrosis, likely through suppression of mTOR-signaling. - Source: PubMed
Publication date: 2026/08/26
Saito TakuroSaito MitsuruYamamoto RyoheiSagehashi RyuichiroAoyama YuMori MizukiKajiwara ChikaFurihata KengoKagaya HideakiYagishita HironobuFujiyama NobuhiroKashima SokiNumakura KazuyukiNarita ShintaroKikuchi MasafumiMiura MasatomoHabuchi Tomonori - Diabetic foot ulcers (DFUs) are severe complications of diabetes, and treatment options for DFUs are limited. Current research on impaired angiogenesis in DFUs predominantly relies on generic endothelial cells, which inadequately reflect the pathophysiological microenvironment of the diabetic microvasculature. In contrast, this study focused specifically on human dermal microvascular endothelial cell (HDMEC) senescence as a central mechanism in DFU progression. We used a self-feeder layer 3D (SFL-3D) culture system to reprogram adipose-derived mesenchymal stem cells (ADSCs) to prepare functionally enhanced three-dimensional adipose stem cells (tdASCs) and their extracellular vesicles (tdASC-EVs) to mitigate HDMEC senescence and improve diabetic healing. - Source: PubMed
Publication date: 2026/06/22
Wang YunweiHu ZhihanShi AoCao PengZhao LuyangDi XiaoyuKang YuchenWang JiatongGong LiChen WenjiaoWang GangCao GuangtongLuo LiangZhao RuomeiZhang XiLiu Yi