PEBP1 Antibody
- Known as:
- PEBP1 Antibody
- Catalog number:
- abx000768
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- PEBP1 Antibody
Related genes to: PEBP1 Antibody
- Gene:
- PEBP1 NIH gene
- Name:
- phosphatidylethanolamine binding protein 1
- Previous symbol:
- PBP
- Synonyms:
- RKIP, HCNP, PEBP
- Chromosome:
- 12q24.23
- Locus Type:
- gene with protein product
- Date approved:
- 1988-04-15
- Date modifiied:
- 2016-10-05
Related products to: PEBP1 Antibody
Related articles to: PEBP1 Antibody
- Ischemic stroke poses a substantial clinical and socioeconomic burden due to limited therapeutic efficacy and poor neurological outcomes. To uncover novel gene targets for intervention, we conducted an integrative analysis combining single-cell RNA sequencing with Mendelian randomization using large-scale genomic datasets from the European Bioinformatics Institute (34,593 cases and 624,214 controls), with validation in an independent European Bioinformatics Institute dataset (86,668 cases and 1,503,898 controls) and the UK Biobank (26,052 cases and 487,214 controls). Colocalization analysis identified four core genes-PEBP1, BMP4, APOA1 and CD86-strongly associated with ischemic stroke risk, with a posterior probability of a shared causal variant greater than 0.8. Among them, PEBP1 was markedly upregulated post-ischemia, particularly in endothelial cells, as confirmed by quantitative PCR and immunofluorescence in a middle cerebral artery occlusion model. Both pharmacological inhibition of PEBP1 with FerroLOXIN-1 and AAV-BI30-mediated shRNA knockdown reduced cerebral infarct volume, enhanced neuronal survival, and improved neurological functional recovery. In vitro, FerroLOXIN-1 enhanced cell proliferation and viability under oxygen-glucose deprivation conditions, with potential off-target effects of the interventions validated. Mechanistically, these effects were mediated through activation of the Akt/p38 MAPK signaling cascade. These findings highlight PEBP1 as a central mediator of ischemia-induced neuronal injury and a potential therapeutic target. The convergence of transcriptomic, genetic and experimental validation supports the translational relevance of PEBP1 inhibition in post-stroke neuroregeneration. - Source: PubMed
Publication date: 2026/04/30
Niu Yu-QianCai Ze-YuZhi Hao-YangZhu Yu-ChunXi Xin-YuanYang ZhenFeng Dong-Fu - MicroRNA (miRNA) profiling of visceral adipose tissue in Type-2 diabetes mellitus (T2DM) remains limited. We compared the expression of obesity-associated miRNAs in visceral fat from individuals with T2DM versus metabolically healthy obesity (MHO) and examined Raf kinase inhibitory protein (RKIP) as a candidate miR-543 target. - Source: PubMed
Al-Temaimi RabeahAhmad RasheedKapila KusumAl-Mulla Fahd - A principal challenge in modern biology and biomedical research is the comprehensive elucidation of the molecular and cellular mechanisms that underpin human disease, with the ultimate aim of identifying novel and effective therapeutic targets. Embryogenesis represents a paradigm of tightly regulated biological complexity, orchestrated by elaborate networks of signaling pathways and transcriptional programs. This highly dynamic process, which initially unfolds within a seemingly disordered and heterogeneous microenvironment, is progressively structured through the establishment of intricate molecular equilibriums mediated by a diverse array of regulatory factors. Perturbations of these homeostatic balances at later stages frequently precipitate the emergence of various pathological conditions. Raf kinase inhibitor protein (RKIP) and Yin Yang 1 (YY1) are pleiotropic regulatory molecules implicated in a broad range of fundamental cellular processes, including proliferation, differentiation, migration, invasion, and epithelial-mesenchymal transition. Although these factors have conventionally been examined as discrete entities, emerging evidence indicates that RKIP and, YY1 may engage in significant molecular cross-talk that not only influences embryonic development but also contributes to the pathogenesis of diverse diseases, including cancer, autoimmune disorders, and immunological dysfunctions. Focusing on the pivotal developmental process of embryogenesis, this review explores the individual regulatory functions of RKIP and YY1, while emphasizing their potential points of convergence within signaling networks during both physiological development and pathological states. - Source: PubMed
Publication date: 2026/02/27
Acikgoz EdaTaskıran AysegulOktem Gulperi - Invasive aspergillosis (IA) is a severe fungal infection with complex pathogenesis, and the role of ferroptosis, an iron-dependent regulated cell death, in IA remains largely unexplored. This study investigates the association between ferroptosis and IA using a bioinformatics approach. We analyzed the GSE78000 dataset to assess ferroptosis activity and identify differentially expressed genes (DEGs). Ferroptosis-related genes (FRGs) were curated from literature, and protein-protein interaction (PPI) networks and functional enrichment analyses (GO and KEGG) were performed. Three machine learning algorithms (SVM, LASSO, and Random Forest) identified five core FRGs (KIF20A, PEBP1, HMOX1, MTF1, QSOX1), which exhibited excellent diagnostic potential (AUCs: 0.884-0.981). IA patients were categorized into two ferroptosis-related subtypes (C1 and C2), characterized by distinct molecular profiles and pathway enrichments, such as ribosome biogenesis and DNA replication. Immune cell infiltration analysis, using ssGSEA, revealed significant alterations in IA, with increased innate immune cells (macrophages, neutrophils) positively correlating with core FRG expression, while adaptive immune cells (B cells, T cells) were decreased. Our findings indicate that ferroptosis is critically involved in IA pathogenesis, with identified core FRGs serving as promising diagnostic biomarkers. The revealed heterogeneity among IA patients and the interaction between ferroptosis and the immune microenvironment provide new insights into the disease's molecular mechanisms and potential therapeutic targets for further investigation. - Source: PubMed
Publication date: 2026/02/23
Tang LuYang LuyingQian Weiwei - Paraptosis plays a critical role in mediating anti-tumor effects by inducing cell death in cancer cells. However, its specific involvement in lung adenocarcinoma (LUAD) remains inadequately understood. This study aims to systematically investigate the prognostic significance and underlying mechanisms of paraptosis-related genes (PRGs) in LUAD. Differentially expressed genes were identified between LUAD and control samples from the training set and cross-referenced with PRGs to generate candidate genes (CGs). Prognostic genes were selected from CGs using regression analysis, leading to the development of a LUAD risk model, which was validated in an independent validation set. Clinical characteristics were analyzed to identify independent prognostic factors for constructing a nomogram. Functional and immune infiltration analyses were performed on high-/low-risk cohorts from the training set. Drug predictions related to prognostic genes were made and subsequently validated through molecular docking. Polymerase chain reaction was performed to validate the expression of prognostic genes. Four prognostic genes (CDKN3, PEBP1, TNFRSF19, and PHB) were identified from 27 CGs through regression analysis. The prognostic risk model demonstrated robust predictive capacity for LUAD prognosis and exhibited generalizability. Significant associations were observed between risk scores and clinical features, including age, TNM.stage, T-stage, and N-stage (P < .05). These risk scores served as independent prognostic factors for the nomogram model, offering strong predictive power for LUAD. Vorinostat and raloxifene exhibited notable binding affinity for PEBP1. Elevated CDKN3 expression was observed in LUAD, while PEBP1 and TNFRSF19 expressions were reduced. This study highlights the prognostic value of PRGs, specifically CDKN3, PEBP1, TNFRSF19, and PHB. CDKN3 and PHB emerged as risk factors for LUAD prognosis, whereas PEBP1 and TNFRSF19 did not. In-depth analysis of the tumor microenvironment revealed the distribution and correlations of immune cell types influenced by PRGs and risk score. Furthermore, an independent prognostic model for LUAD was developed, enhancing our understanding of high-/low-risk cohorts' functional pathways. Drug prediction results provided valuable insights into potential therapeutic strategies for LUAD, warranting further investigation. - Source: PubMed
Zhang TaoTang ShugengGuo QuanweiKuang JunYan JunMo YijunTan JianfengWu MengxiLi DongfangZhang Jianhua