PEBP1 Antibody
- Known as:
- PEBP1 Antibody
- Catalog number:
- 32078
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- 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
- Glaucoma is the leading cause of irreversible blindness worldwide, primarily driven by the progressive loss of retinal ganglion cells (RGCs) under pathological high intraocular pressure (ph-IOP). Despite the established role of ferroptosis in RGC degeneration, specific molecular targets that can be used for clinical intervention still need to be optimized, and the slow onset of conventional gene therapy vectors is incompatible with the acute clinical course of glaucoma. Here, we integrate single-cell RNA sequencing and spatial transcriptomics to profile the dynamic transcriptomic landscape of the rat retina across acute, subacute, and chronic stages of ph-IOP injury. Through ferroptosis-focused screening of an early-activated RGC gene cluster, we identify the lipid metabolism regulator phosphatidylethanolamine-binding protein 1 (PEBP1) as a candidate mediator of RGC ferroptosis. We demonstrate that Pebp1 is specifically upregulated in injured RGCs with a trajectory mirroring ferroptosis pathway activation, and that AAV-mediated Pebp1 knockdown suppresses ferroptosis through the GPX4/ACSL4 signaling axis, thereby preserving RGC survival, retinal structure, and visual function. To overcome the critical time-window bottleneck-the several weeks delay required for AAV-mediated silencing versus the rapid, irreversible RGC loss in acute glaucoma-we engineer Exosomes-siPebp1, a mesenchymal stem cell-derived exosome system loaded with siPebp1, which enables immediate single-dose intervention post-injury. This system exhibits efficient RGC uptake, prolonged intraocular retention, and robust target gene silencing, and, in a head-to-head comparison, significantly outperforms unloaded exosomes, liposomal formulations, and AAV vectors in RGC protection, without detectable acute systemic or local toxicity. Collectively, this study implicates Pebp1 in ph-IOP-associated RGC ferroptosis and supports exosome-mediated siRNA delivery as a rapid, cell-free intervention strategy for acute glaucomatous injury. - Source: PubMed
Huang YijiaGong DiGuo JunhongHuang WeiHu TingyuTang ShengbinLi LiFeng BingkaiDang KuanrongDeng SiminLiu YongTan ChunyanYao FeiWang Jiantao - Ferroptosis is a distinct form of regulated cell death characterized by iron-dependent lipid peroxidation, which plays crucial roles in tumor biology and therapeutic response. However, the prognostic significance of ferroptosis-related genes (FRGs) in lung adenocarcinoma (LUAD) remains incompletely understood. This study aimed to construct and validate a ferroptosis-related prognostic model for LUAD by integrating single-cell and bulk transcriptomic data. - Source: PubMed
Publication date: 2026/06/25
Wang JianWei YixiZhang JiaChai WenshuLi Yubin - The serine/threonine kinase glycogen synthase kinase-3 (GSK-3) was initially identified and studied in the regulation of glycogen synthesis. In some cases, suppression of GSK-3 activity by phosphorylation by Akt and other kinases has been associated with cancer progression. In these cases, GSK-3 has tumor suppressor functions. In other cases, GSK-3 has been associated with tumor progression by stabilizing components of the beta-catenin complex. In these situations, GSK-3 has oncogenic properties. The Raf kinase inhibitor protein (RKIP) has been reported to be under expressed in many cancers and plays a role in the regulation of tumor cells' survival, proliferation, invasion, and metastasis, hence, a tumor suppressor. RKIP also regulates tumor cell resistance to cytotoxic drugs/cells. Likewise, the tumor suppressor, phosphatase and tensin homolog (PTEN), which inhibits the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) pathway, is either mutated, under expressed, or deleted in many cancers and shares with RKIP its anti-tumor properties and its regulation in resistance. Several pathways are regulated by RKIP, GSK-3, PTEN, and the transcriptional and post-transcriptional regulations of RKIP, GSK-3, and PTEN are significantly altered in cancers. In addition, RKIP, GSK-3 and PTEN play a key role in the regulation of tumor cells response to chemotherapy and immunotherapy. In this review, we will focus on the roles that GSK-3, PTEN, and RKIP play in various human cancers. We will also discuss how this pivotal kinase interacts with multiple signaling pathways such as: PI3K/PTEN/Akt/mechanistic target of rapamycin complex 1 (mTORC1), nuclear Factor kappa-B (NF-κB)/Snail family transcriptional repressor 1 (Snail)/Yin Yang 1 (YY1) loop, and rat sarcoma virus oncogene (Ras)/rapidly accelerated fibrosarcoma (Raf)/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK). - Source: PubMed
Publication date: 2026/06/25
Mosalam Esraa MAbdallah Mahmoud SGardouh Ahmed RHamza EmanBahaa Mostafa MNazih MahmoudAl-Dhelaan Reham AKamal Noha - Epithelial barrier dysfunction plays a key role in asthma pathogenesis. Palmatine has been shown to reinforce epithelial integrity in colitis and ameliorate urticaria-like skin inflammation, suggesting potential barrier-protective effects. - Source: PubMed
Publication date: 2026/06/30
Zhao LeiWu JifeiZhang YichenZhao YongchangLin YanmeiZhang MinBao Wuping - Raf Kinase Inhibitory Protein (RKIP), also known as PEBP1, is a multifunctional modulator of intracellular signaling with pivotal roles in cellular homeostasis, cancer suppression, cardiac physiology, and neurobiology. Initially characterized by its inhibition of the Raf-1/MEK/ERK cascade, RKIP has since emerged as a dynamic regulator of numerous pathways, including NF-κB, GRK2, GSK3β, and Aurora B kinase. RKIP activity is modulated through phosphorylation-dependent conformational shifts that dictate its binding partners and regulatory outcomes. In oncology, RKIP acts as a metastasis suppressor by promoting let-7 microRNA expression and inhibiting pro-metastatic genes such as HMGA2, BACH1, MMPs, and CXCR4. In the nervous system, RKIP influences synaptic signaling, pain perception, and neuroprotection, while in cardiomyocytes, it enhances β-adrenergic signaling and protects mitochondria under stress. Dysregulation of RKIP is implicated in cancer progression, heart failure, and neurodegenerative diseases. Ongoing research into pharmacological modulation of RKIP holds promise for novel therapeutic interventions across diverse pathologies. - Source: PubMed
Publication date: 2026/06/20
Albeloushi ShaimaMohammad AnwarHasan AmalAl-Mulla Fahd