Ask about this productRelated genes to: 4E-BP1 antibody
- Gene:
- EIF4EBP1P1 NIH gene
- Name:
- eukaryotic translation initiation factor 4E binding protein 1 pseudogene 1
- Previous symbol:
- EIF4EBP1P
- Synonyms:
- -
- Chromosome:
- 14q11.2
- Locus Type:
- pseudogene
- Date approved:
- 2003-01-13
- Date modifiied:
- 2014-11-28
Related products to: 4E-BP1 antibody
Related articles to: 4E-BP1 antibody
- Diabetic ulcers (DU) are a severe complication of diabetes mellitus and are associated with infection, recurrence, amputation, and excess mortality. Robust molecular markers that distinguish ulcer tissue from non-ulcer tissue and clarify the biological basis of impaired healing remain limited. - Source: PubMed
Publication date: 2026/10/01
Jiang YueCai YunxiLiu QingkaiJiang JingsiShen FangZhang YingFei XiaoyaKuai LeZhang ZhanLuo YingSong JiankunMa XinLi BinMa XiaoxuanRu Yi - 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 - Eukaryotic initiation factor 4E-binding protein 1 (EIF4EBP1/4E-BP1) is a pivotal translational regulator with context-dependent roles in breast cancer pathogenesis. Its phosphorylation status, dynamically controlled by mammalian target of rapamycin (mTOR), mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK), and AMP-activated protein kinase (AMPK) signaling, dictates a dualistic function: hypophosphorylated EIF4EBP1 suppresses oncogenesis by sequestering eIF4E and inhibiting cap-dependent translation of pro-tumorigenic mRNAs (e.g., cyclin D1 and c-MYC), while hyperphosphorylation promotes tumor progression and therapeutic resistance. EIF4EBP1 amplification (8p11-p12) is correlated with endocrine resistance and poor prognosis. EIF4EBP1 modulates cell cycle checkpoints, metabolic adaptation under stress, and resistance to cyclin-dependent kinase (CDK) 4 and 6 inhibitors and rapalogs via feedback loops (e.g., SGK3/Akt reactivation). Emerging therapeutic strategies, such as ATP-competitive mTOR inhibitors, bisteric compounds, and agents targeting polyamine metabolism or upstream kinases, exploit the dynamics of EIF4EBP1 phosphorylation. As a biomarker, phosphorylated EIF4EBP1 levels predict tumor aggressiveness and treatment failure, positioning it as a critical node for precision oncology. Future research must address spatial heterogeneity and leverage multi-omics/AI-driven approaches. - Source: PubMed
Liu WeijiaHou LiliTang DandanMou HaiyuWang WeijieLiu Song-BaiLi Xiaohua - is a human-specific gene with unexplored functions. This study investigated its regulation, molecular mechanism, and clinical significance in gastric cancer. expression was consistently down-regulated in primary tumors and cancer cell lines across various cancer types, including gastric cancer, as indicated by TCGA data and quantitative PCR analysis. Its down-regulation in gastric cancer cells is mediated by promoter methylation, confirmed through bisulfite genomic sequencing, with expression restored following demethylation treatment. A progressive reduction in expression was observed from normal stomach mucosa to adjacent non-tumor tissues and primary tumors, along with increased methylation. inhibited cancer cell viability, clonogenicity, cell cycle progression, migration, and invasion while promoting apoptosis. It also suppressed subcutaneous tumor growth and distant metastasis in mice. Transcriptomic analysis revealed that disrupted PI3K/AKT/mTOR signaling. Western blotting confirmed that reduced protein levels of PI3K, p-AKT, and mTOR. This led to the down-regulation of EIF4E and EIF4EBP1, oncogenic protein synthesis genes and effectors of mTOR signaling, as well as p-EIF4EBP1(Thr70), which is regulated by mTOR. Notably, expression was inversely correlated with EIF4E, EIF4EBP1, and p-EIF4EBP1 (Thr70) in gastric tumors (all < 0.001). Multivariate analysis revealed that expression in primary gastric tumors independently predicted survival ( = 0.027). Kaplan-Meier survival analysis showed that low expression was associated with shortened survival in gastric cancer patients ( = 0.0009). Overall, plays a tumor-suppressive role by inhibiting the PI3K/AKT/mTOR/EIF4E pathway, and its down-regulation serves as an independent marker for poor prognosis in gastric cancer patients. - Source: PubMed
Publication date: 2025/10/31
Xu FeiZhang MengwenZhang SuzhanZeng YaoZheng ShuLiang Jessie Qiaoyi - The mammalian/mechanistic Target of Rapamycin Complex 1 (mTORC1) orchestrates cell growth and metabolism in response to diverse extracellular and intracellular cues. mTORC1 phosphorylates a broad range of substrates, each of which plays important physiological roles. Emerging evidence suggests that mTORC1 can respond to upstream signals in a nuanced manner, enabling differential regulation of individual substrates and, consequently, specific downstream biological processes. Phosphorylation of non-canonical mTORC1 substrates, such as the lysosome biogenesis regulator transcription factor EB (TFEB), can be regulated independently of phosphorylation of canonical substrates. However, the nature of signals that determine the signaling selectivity of mTORC1 remains incompletely understood. Here, we studied mTORC1 regulation by G protein-coupled receptors (GPCRs). We found that phosphorylation of TFEB responds to GPCRs differently compared with canonical mTORC1 substrates controlling protein synthesis, such as S6K1 and 4EBP1. In particular, the muscarinic acetylcholine receptor M5 (M5R) promoted phosphorylation of S6K1 and 4EBP1 while triggering TFEB dephosphorylation. Consequently, M5R stimulated protein synthesis without inhibiting lysosome biogenesis. mTORC1 can thus separately regulate anabolic and catabolic processes under the control of M5R. The present study highlights the importance of reassessing the effects of GPCRs on mTORC1 by concurrently monitoring individual substrates, a critical consideration to be made when evaluating GPCR ligands as therapeutic agents targeting the mTORC1 pathway. - Source: PubMed
Atkinson Samuel JNegoita FlorentinaIoi YuichiroRitchie William VThompson KyleGardner MaxAshdown Peter THellberg KristinaTakahara TerunaoSakamoto KeiThompson DawnHislop James NHatakeyama Riko