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)
- 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 - 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 - White spot syndrome virus (WSSV) devastates shrimp aquaculture, yet safe antivirals remain scarce. Here we identify a druggable host-directed pathway centered on hemocyanin (HMC). This pathway coordinates endoplasmic reticulum (ER)-mitochondrial crosstalk to promote WSSV replication, which could be counteracted by the natural anthraquinone emodin. In , emodin suppressed viral replication with a half maximal inhibitory concentration (IC) of 1.174 μM, improved survival in both therapeutic and prophylactic regimens, remained effective after per os administration, and retained antiviral activity in water for up to 4 d. Target fishing, orthogonal biophysics, and docking analyses show that emodin binds HMC (K = 4.49 μM) and interferes with HMC-HSPA5/BiP (heat shock protein family A (Hsp70) member 5) association. Mechanistically, emodin weakens the ITPR/IPR (inositol 1,4,5-trisphosphate receptor)-VDAC (voltage dependent anion channel)-MCU (mitochondrial calcium uniporter) conduit at ER-mitochondrial contact sites, thereby limiting Ca transfer, restoring mitochondrial membrane potential and organelle spacing, and attenuating ER stress. Untargeted metabolomics revealed that WSSV induced phosphoinositide and amino acid dysregulation, whereas emodin selectively normalizes phosphatidylinositol (PtdIns) and phosphatidylinositol 1,4,5-trisphosphate (PtdIns[1,4,5]P) signaling and rebalances amino acid, tricarboxylic acid (TCA) intermediates. Correspondingly, emodin inhibited phosphoinositide 3-kinase (PI3K)-AKT/protein kinase B-MTOR (mechanistic target of rapamycin kinase) complex 1 (MTORC1) signaling and restored lysosome-dependent macroautophagy/autophagy. RNAi or ITPR and MCU inhibition phenocopied emodin, whereas exogenous HMC or ER stress activation exacerbated infection and was mitigated by emodin or MCU blockade. These findings establish HMC-anchored ER-mitochondrial contact as a central proviral vulnerability and position emodin as a practical scaffold for next-generation antivirals in aquaculture. 2-APB: 2-aminoethyl diphenylborinate; 3-MA: 3-methyladenine; ΔΨm: mitochondrial membrane potential; AKT/protein kinase B: AKT serine/threonine kinase; ATG1/ULK1: autophagy related 1; ATG13: autophagy related 13; BSA: bovine serum albumin; CETSA: cellular thermal shift assay; Co-IP: co-immunoprecipitation; DAPI: 4',6-diamidino-2-phenylindole; DDIT3/Chop: DNA damage inducible transcript 3; DMSO: dimethyl sulfoxide; EAS6B: epoxy-activated sepharose 6B; EGTA: ethylene glycol tetraacetic acid; EIF4EBP1: eukaryotic translation initiation factor 4E binding protein 1; EPC: epithelioma papulosum cyprini; ER: endoplasmic reticulum; HMC: hemocyanin; HPLC-MS: high performance liquid chromatography-mass spectrometry; HRP: horseradish peroxidase; HSPA5/BiP: heat shock protein family A (Hsp70) member 5; HSPA9/GRP75: heat shock protein family A (Hsp70) member 5; ITPR/IPR: inositol 1,4,5-trisphosphate receptor; KEGG: Kyoto Encyclopedia of Genes and Genomes; LAMP1: lysosome associated membrane protein 1; LC-MS: liquid chromatography-mass spectrometry; MAMs: mitochondria-associated ER membranes; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MCU: mitochondrial calcium uniporter; MTOR: mechanistic target of rapamycin kinase; MTORC1: MTOR complex 1; OPLS-DA: orthogonal partial least squares-discriminant analysis; PA: phosphatidic acid; PBS: phosphate-buffered saline; PC: phosphatidylcholine; PCA: principal component analysis; PE: phosphatidylethanolamine; PI3K: phosphoinositide 3-kinase; PLS-DA: partial least squares-discriminant analysis; PS: phosphatidylserine; PtdIns: phosphatidylinositol; PtdIns(1,4,5)P: phosphatidylinositol (1,4,5)-trisphosphate; PtdIns(3,4,5)P: phosphatidylinositol (3,4,5)-trisphosphate; PtdIns(4,5)P: phosphatidylinositol (4,5)-bisphosphate; RPS6KB1/S6K1: ribosomal protein S6 kinase B1; SDS-PAGE: sodium dodecyl sulfate-polyacrylamide gel electrophoresis; SQSTM1/p62: sequestosome 1; TCA: tricarboxylic acid cycle; TEM: transmission electron microscopy; TFEB: transcription factor EB; UPR: unfolded protein response; VDAC: voltage dependent anion channel; WSSV: white spot syndrome virus; XBP1: X-box binding protein 1. - Source: PubMed
Publication date: 2026/07/01
Zhang XuShan Li-PengLiu LeiChen Jiong - The study aimed to evaluate the effects of full-fat rice bran (FFRB; Tainung No. 81, Taiwan) at various doses on insulin resistance, muscle atrophy, and gut microbiota composition in middle-aged ovariectomized (OVX) mice fed a high-fat diet (HFD), using young sham-operated mice as a life-stage reference group. Thirty-six female ICR mice were assigned to six groups, including OVX mice fed HFD with or without 5%, 10%, or 20% FFRB. Compared with HFD-fed OVX controls, 20% FFRB reduced body weight gain by 43%, decreased visceral fat mass, and improved insulin resistance (homeostasis model assessment of insulin resistance, HOMA-IR reduced by 65%, = 0.001). FFRB attenuated the decline in relative grip strength (forelimb, = 0.013; four-limb, < 0.001), and upregulated muscle protein synthesis genes, including insulin receptor substrate 1 (IRS-1), mammalian target of rapamycin (mTOR), eukaryotic translation initiation factor 4E binding protein 1 (eIF-4EBP1), while downregulating forkhead box protein O1 (FOXO1), muscle RING-finger protein-1 (MuRF-1), and interleukin (IL)-6. FFRB was also associated with higher fecal acetate levels ( < 0.001), upregulated colonic tight junction genes (occludin and zonula occludens (ZO)-1), and greater relative abundance of . Correlation analyses revealed positive associations between short-chain fatty acids (SCFAs) and muscle strength, muscle anabolic markers, genus , and . Dietary inclusion of FFRB was associated with favorable metabolic and muscle-related parameters in HFD-fed middle-aged OVX mice, with potential involvement of gut microbiota and SCFA alterations. - Source: PubMed
Publication date: 2026/05/30
Loe Pei YuOhsaki YusukeYang Suh-ChingShirakawa HitoshiChiu Wan-Chun