4E_BP1 Antibody (T45)
- Known as:
- 4E_BP1 Antibody (T45)
- Catalog number:
- AE1002a
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- 4E_BP1 Antibody (T45)
Related genes to: 4E_BP1 Antibody (T45)
- Gene:
- ABCB6 NIH gene
- Name:
- ATP binding cassette subfamily B member 6 (Langereis blood group)
- Previous symbol:
- -
- Synonyms:
- EST45597, umat, MTABC3
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2019-04-23
- Gene:
- CT45A1 NIH gene
- Name:
- cancer/testis antigen family 45 member A1
- Previous symbol:
- -
- Synonyms:
- CT45-1, CT45.1
- Chromosome:
- Xq26.3
- Locus Type:
- gene with protein product
- Date approved:
- 2009-03-09
- Date modifiied:
- 2016-08-04
- Gene:
- CT45A2 NIH gene
- Name:
- cancer/testis antigen family 45 member A2
- Previous symbol:
- -
- Synonyms:
- CT45-2, CT45.2
- Chromosome:
- Xq26.3
- Locus Type:
- gene with protein product
- Date approved:
- 2009-03-09
- Date modifiied:
- 2016-08-04
- Gene:
- CT45A3 NIH gene
- Name:
- cancer/testis antigen family 45 member A3
- Previous symbol:
- CT45A4
- Synonyms:
- CT45-3, CT45.3, CT45-4, CT45.4
- Chromosome:
- Xq26.3
- Locus Type:
- gene with protein product
- Date approved:
- 2009-03-09
- Date modifiied:
- 2016-08-04
- Gene:
- CT45A5 NIH gene
- Name:
- cancer/testis antigen family 45 member A5
- Previous symbol:
- -
- Synonyms:
- CT45-5, CT45.5
- Chromosome:
- Xq26.3
- Locus Type:
- gene with protein product
- Date approved:
- 2009-03-09
- Date modifiied:
- 2016-08-04
Related products to: 4E_BP1 Antibody (T45)
Related articles to: 4E_BP1 Antibody (T45)
- 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 - Tryptophan metabolism undergoes marked alterations in OSCC, leading to an abnormal accumulation of the metabolite kynurenine. Nonetheless, how kynurenine, a key intermediate of tryptophan metabolism, contributes to tumor metabolic reprogramming is still not well clarified. Here, we identify Kyn as a metabolic signal that drives glycolytic reprogramming and promotes tumor progression. Mechanistically, Kyn functionally associates with AKT and enhances AKT-dependent mTOR phosphorylation, leading to subsequent activation of the mTOR which facilitates the dissociation of eIF4EBP1 from eIF4E, thereby enhancing cap-dependent translation of HIF-1α. Elevated HIF-1α upregulates glycolytic enzymes, accelerating glycolytic flux and increasing lactate production. The accumulated lactate in turn stabilizes HIF-1α through lysine lactylation, thereby establishing a reinforcing feedback cycle that enhances glycolytic activity and supports continuous tumor expansion. Collectively, our results uncover an unappreciated metabolic regulatory loop in which kynurenine promotes glycolysis via AKT/mTOR-mediated translational activation and HIF-1α lactylation, highlighting a mechanistic link between tryptophan metabolism and glucose metabolism. These insights provide a rationale for combined therapeutic strategies targeting the kynurenine pathway and glycolysis in OSCC. - Source: PubMed
Publication date: 2026/07/23
Lin ShuoqiYan YuxiangZhou JunlinZheng GenggengLiao TesenLu YouguangSu BohuaZheng Dali - Alopecia areata (AA) is a common autoimmune alopecia disease. Evidence suggests that autophagy-related genes (ARGs) may contribute to its pathophysiology. This study aims to explore and identify potential autophagy-related biomarkers and molecular subtypes in AA. In this study, autophagy-related differential expression genes (ARDEGs) in AA were identified by comparing the differentially expressed genes (DEGs) in the GSE68801 dataset with the ARGs. Then, we applied three different machine learning methods to identify key hub genes and further verified them on independent datasets. We used the receiver operating characteristic (ROC) curve to evaluate the diagnostic potential of these hub genes and constructed a predictive nomogram. In addition, this study also used the consensus clustering method to define two AA subtypes and explored their immune characteristics and functional pathways through ssGSEA, MCPcounter and enrichment analysis. Experimental validation included qRT-PCR for four hub genes and Western blotting for critical autophagy markers. Our analysis detected 10 ARDEGs in AA. Applying three machine learning algorithms, we identified four candidate hub genes, , , and , and verified their expression patterns in independent cohorts. The combined four-gene model and nomogram showed potential diagnostic performance. Consensus cluster analysis divided AA cases into two subtypes, each associated with different immune infiltration and functional pathways. Downregulation of and and upregulation of were verified by qRT-PCR. Western blotting further suggested altered autophagy-related protein expression in AA lesions, characterized by a reduced LC3B-II/I ratio and Beclin-1 expression and increased SQSTM1 expression. This study identified four candidate autophagy-related genes and two exploratory molecular subtypes in AA and may provide clues for understanding autophagy-related immune dysregulation and support further validation of candidate diagnostic markers. - Source: PubMed
Publication date: 2026/05/23
Li YufenZhang XiaolinWang JiatingJiang Yiqun