4E_BP1 Antibody (Ab_45), pAb, Rabbit
- Known as:
- 4E_BP1 Antibody (Ab_45), pAb, Rabbit
- Catalog number:
- A00461
- Product Quantity:
- 40ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- 4E_BP1 Antibody (Ab_45) pAb Rabbit
Related genes to: 4E_BP1 Antibody (Ab_45), pAb, Rabbit
- 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 (Ab_45), pAb, Rabbit
Related articles to: 4E_BP1 Antibody (Ab_45), pAb, Rabbit
- Early liver metastasis is a major factor contributing to the poor prognosis of pancreatic ductal adenocarcinoma (PDAC). Single-cell RNA sequencing (scRNA-seq) can analyze the heterogeneity between the primary tumor and metastatic lesions, but its wide clinical application is limited by costs, tissue requirements, and analytical complexity. In contrast, H&E-stained sections are more commonly available. However, it is not clear whether the risk signals derived from images can truly reflect the biological characteristics related to metastasis. We integrated the single-cell RNA sequencing data (GSE154778) of primary and metastatic pancreatic ductal adenocarcinoma (PDAC) with TCGA transcriptome, clinical pathological, and H&E image data. The copy number pattern based on InferCNV was used to distinguish malignant ductal cells with high copy numbers from ductal cells with low copy numbers. Differential expression and LASSO screening identified a transfer-related feature consisting of four genes (ARHGAP18, ASPH, EIF4EBP1, LY6D), and this feature was subsequently associated with image-derived features extracted through a dual-stream pathomics pipeline. The reproducibility of transcriptional levels in prognosis was evaluated in six independent GEO PDAC subgroups, and the locked pathological model was further tested on an external CPTAC subset using frozen cutoff values from TCGA. Pseudotime analysis suggested that a subset of metastatic malignant ductal cells occupied a progenitor-like transcriptional state. Cell-cell communication analysis indicated reduced antigen-presentation/prostaglandin-related signaling and relative enrichment of MIF- and laminin-associated pathways in metastases. The pathology model retained prognostic stratification in the internal TCGA validation split, although discrimination was lower than in training. Across six external GEO cohorts analyzed with cohort-specific optimal cutoffs, LY6D showed significant adverse survival associations in four cohorts, ARHGAP18 and ASPH in three cohorts each, and EIF4EBP1 in one cohort. In the external CPTAC cohort, the locked pathomics score also remained prognostic (HR 1.60, 95% CI 1.11-2.30; log-rank P = 0.011), with 12-, 24-, and 36-month time-dependent AUCs of 0.635, 0.617, and 0.639. This study presents an integrative genotype-to-phenotype workflow linking scRNA-seq-derived metastatic features to routine pathology images. External transcript-level validation and supportive CPTAC pathomics evaluation strengthen the findings, but larger independent validation studies and mechanistic experiments remain necessary before any clinical translation. - Source: PubMed
Publication date: 2026/05/26
Bao WenhaoLeng KaimingXia XiaodanChang JingyuYing PengchaoLuan ShaohaiYuan Qihua - Metabolic dysfunction-associated steatohepatitis (MASH) is emerging as a leading cause of chronic liver disease. MTOR (mechanistic target of rapamycin kinase) complex 1 (MTORC1) is a potential therapeutic target, whereas suppression of total MTORC1 activity can lead to unwanted effects. Here, we found that byakangelicin (Bya), a natural compound, selectively inhibited MTORC1-mediated phosphorylation of TFEB (transcription factor EB), without affecting canonical MTORC1 substrates. Knockout of hepatic blocked the alleviation effects of Bya on hepatic steatosis, inflammation, insulin resistance, and fibrosis in mice, while reintroduction of TFEB restored these effects. We identified Bya directly bound to MET370 and PHE552 of FLCN (folliculin), suppressing the function of the FLCN-FNIP1 (folliculin interacting protein 1)/FNIP2 complex, which in turn inhibited MTORC1-mediated cytoplasmic sequestration of TFEB. Mutation of FLCN (M370A and F552A) in the liver abolished Bya-induced protection against MASH. Thus, Bya is a promising therapeutic natural compound for MASH, and selective inhibition of MTORC1 is a potential approach to treat this disease. aa, amino acids; AAV, adeno-associated virus; Bio, biotin; Bio-Bya, biotin-conjugated Bya; BSA, bovine serum albumin; BW, body weight; Bya, byakangelicin; CETSA, cellular thermal shift assay; CHIP-atlas, chromatin immunoprecipitation atlas; C, maximum concentration; CQ, chloroquine; DARTS; drug affinity responsive target stability assay; EIF4EBP1/4E-BP1, eukaryotic translation initiation factor 4E binding protein 1; FBS, fetal bovine serum; FDA, food and drug administration; FIMO-JASPAR, find individual motif occurrences-JASPAR; FLCN, folliculin; FNIP1, folliculin interacting protein 1; GAP, GTPase-activating protein; GOT1/AST, glutamic-oxaloacetic transaminase 1; GPT/ALT, glutamic-pyruvic transaminase; GTRD, gene transcription regulatory database; GTT, glucose tolerance test; H&E, hematoxylin and eosin; Hbonds, hydrogen bonds; HFD, high-fat diet; HFHC, high-fat and high-cholesterol; HOMA-IR, homeostatic model assessment of insulin resistance; HSCs, hepatic stellate cells; IP, immunoprecipitation; ITT, insulin tolerance test; K, dissociation constant; KEGG, kyoto encyclopedia of genes and genomes; KPBS, potassium phosphate-buffered saline; LC-MS/MS, liquid chromatography-tandem mass spectrometry; LW/BW, liver-to-body weight ratio; MAP1LC3/LC3, microtubule associated protein 1 light chain 3; MASH, metabolic dysfunction-associated steatohepatitis; MASLD, metabolic dysfunction-associated steatotic liver disease; MCD, methionine and choline deficient; MST, microscale thermophoresis assay; MTOR, mechanistic target of rapamycin kinase; MTORC1, MTOR complex 1; ND, normal diet; NFKB/NF-κB, nuclear factor kappa B; NFKBIA/IKBA, NFKB inhibitor alpha; OP, oleate acid and palmitate acid; PBS, phosphate-buffered saline; PCA, principal component analysis; qRT-PCR, real-time quantitative PCR; RELA/p65, RELA proto-oncogene, NF-kB subunit; Res, resmetirom; Rg, radius of gyration; RMSD, root-mean-square deviation; RMSF, root-mean-square fluctuation; RPS3, ribosomal protein S3; RPS6KB1/S6K1, ribosomal protein S6 kinase B1; RRAGC, ras related GTP binding C; SASA, solvent-accessible surface area; SNRPD2, small nuclear ribonucleoprotein D2 polypeptide; SQSTM1/p62, sequestosome 1; T, half-life; TFE3, transcription factor binding to IGHM enhancer 3; TFEB, transcription factor EB; TMEM192, transmembrane protein 192; VIM, vimentin; WT, wild-type. - Source: PubMed
Publication date: 2026/05/25
Du XiliangFang ZhiyuanLiu GuowenWang LiJu LingxueGao WenwenSong YuxiangLei LinLi Xinwei - Traumatic brain injury (TBI) is a leading cause of mortality and long-term neurological disability, while effective pharmacological therapies for its neurobehavioral consequences remain limited. This systematic review evaluates the therapeutic potential of Ginkgo biloba (GB), particularly the standardized extract EGb 761, in TBI management. A comprehensive literature search was conducted in PubMed, Scopus, and Web of Science up to February 2026. Sixty-five studies met the inclusion criteria, including 42 in vivo experimental studies and 23 clinical trials examining neuroprotective, cognitive, behavioral, or functional outcomes following GB administration. Preclinical evidence consistently demonstrates that Ginkgo biloba (GB) exerts neuroprotective effects through attenuation of oxidative stress, as evidenced by increased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, alongside reduced malondialdehyde (MDA) levels. These effects are accompanied by modulation of the Slc7a11-Eif4ebp1 signaling axis, suppression of pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α, and regulation of key molecular pathways. Specifically, GB inhibits JAK/STAT and TXNIP/NLRP3 signaling while activating PI3K/AKT-associated pathways and autophagy. Clinical studies indicate potential improvements in cognitive and functional outcomes. However, adverse events, particularly bleeding, have been reported, especially when GB is co-administered with anticoagulants or nonsteroidal anti-inflammatory drugs. This underscores the importance of careful patient monitoring. The current evidence supports the promising neuroprotective potential of GB in traumatic brain injury. Nevertheless, clinical data remain insufficient to justify routine therapeutic use. Large-scale, well-designed, randomized controlled trials are necessary to confirm efficacy, optimize dosing regimens, and establish long-term safety profiles. - Source: PubMed
Nazeam Jilan AMahmoud OmniaSaad AmiraHassan AmiraSaleh OmniaAlaaeldein AmiraAli EtharEzzat AndrewBahaa EhdaaMgahd AndrewEl-Shazly MohamedElgayed Sabah H - Colorectal cancer (CRC) persists as a significant public health burden due to its high morbidity and mortality rates worldwide, yet the molecular events that govern its initiation and progression remain incompletely understood. We recently conducted microRNA (miRNA) profiling and identified multiple dysregulated miRNAs in CRC compared to adjacent normal tissue. Among those, miR-138-5p emerged as a potential tumor suppressor due to its marked downregulation in CRC tissue; however, the stage-specific expression of this miRNA during CRC progression and underlying molecular mechanisms remains to be unraveled. In this study, we performed differential expression profiling of healthy colon, adenomatous polyp (AP), and CRC tissues based on public datasets, revealing significant downregulation of miR-138-5p in CRC compared to controls, but not during the AP stage, suggesting a role in later stages of malignant progression. Forced expression of miR-138-5p in HCT116 and HT-29 CRC models suppressed clonogenic survival, proliferation, and migration while inducing cell death. Additionally, miR-138-5p significantly inhibited tumor formation under three-dimensional culture settings, reinforcing its tumor-suppressive function in a physiologically relevant context. Transcriptomic profiling of miR-138-5p-overexpressing CRC models revealed widespread changes in the pathways related to zinc ion binding, cilium morphogenesis, smoothened signaling, and nuclear transport. Integrated computational and experimental analyses identified 41 potential gene targets, among which , and were validated as potential miR-138-5p-regulated genes. Collectively, these findings establish miR-138-5p as a stage-specific tumor suppressor in CRC, acting through coordinated regulation of oncogenic networks across multiple pathways. Downregulation of miR-138-5p appears to be a late oncogenic event, conferring proliferative, survival, and invasive advantages to tumor cells. Restoration of miR-138-5p or therapeutic targeting of its downstream effectors may represent promising avenues for CRC therapeutic intervention. - Source: PubMed
Publication date: 2026/04/09
Shaath HibahVishnubalaji RadhakrishnanAlajez Nehad M - Cardiac fibrosis is a defining pathological feature of diabetic cardiomyopathy (DCM), and excessive activation of cardiac fibroblasts plays a critical role in regulating cardiomyocyte function through paracrine signaling. CCN1 (cellular communication network factor 1), an extracellular matrix protein involved in intercellular communication, has been suggested to influence cardiac remodeling, although its specific impact on cardiomyocytes in DCM has remained unclear. In this study, we found that CCN1 expression was markedly elevated in cardiac tissues from DCM mouse models and in insulin-resistant cell models, with fibroblasts serving as the primary source. Proteomic analysis and co-culture experiments demonstrated that CCN1 suppressed cardiomyocyte macroautophagy/autophagy. To determine its role in vivo, we generated fibroblast-specific knockout mice and established a DCM model, demonstrating that deletion ameliorated cardiac dysfunction and restored autophagic activity. We further identified ITGAV-ITGB1/integrin αvβ1 as the receptor mediating CCN1 signaling in cardiomyocytes. Molecular dynamics simulations and co-immunoprecipitation experiments confirmed that CCN1 engaged ITGAV-ITGB1/integrin αvβ1 through its cysteine-knot-containing (CT) domain. Mechanistically, this interaction activated the downstream PTK2/FAK-MTOR signaling pathway, leading to inhibition of cardiomyocyte autophagy. Together, these findings reveal a previously unrecognized fibroblast-cardiomyocyte signaling axis in which fibroblast-derived CCN1 drives DCM progression by suppressing autophagy through ITGAV-ITGB1/integrin αvβ1-dependent signaling. This work provides mechanistic insight into the pathogenesis of DCM and identifies CCN1 as a potential therapeutic target for mitigating disease onset and progression.: AAV9: adeno-associated virus serotype 9; ADGRE1/EMR1/F4/80: adhesion G protein-coupled receptor E1; BafA1: bafilomycin A; BSA: bovine serum albumin; C8: compound 8; CCN1: cellular communication network factor 1; CF: cardiac fibroblast; CSA: cross-sectional area; DCM: diabetic cardiomyopathy; EIF4EBP1: eukaryotic translation initiation factor 4E binding protein 1; ELISA: enzyme-linked immunosorbent assay; HE: hematoxylin and eosin; HFD: high-fat diet; HG: high glucose; IR: insulin resistance; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MD: molecular dynamics; MTOR: mechanistic target of rapamycin kinase; NRCM: neonatal rat cardiomyocyte; PDGFRA: platelet derived growth factor receptor alpha; PECAM1/CD31: platelet and endothelial cell adhesion molecule 1; PTK2/FAK: protein tyrosine kinase 2; PTPRC/CD45: protein tyrosine phosphatase receptor type C; RPS6KB1: ribosomal protein S6 kinase B1; S100A4/FSP1: S100 calcium binding protein A4; SQSTM1/p62: sequestosome 1; STZ: streptozotocin; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling; WGA: wheat germ agglutinin. - Source: PubMed
Publication date: 2026/05/07
Hu Bo-AngZhang LeiSong MingKong Yan-RuJiao Ya-QiongJia XuZhu PingLi Yu-LinTi YunZhang WeiWang Zhi-HaoZhong Ming