PEDF
- Known as:
- PEDF
- Catalog number:
- RD172114100-HEK
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- PEDF
Related genes to: PEDF
- Gene:
- SERPINF1 NIH gene
- Name:
- serpin family F member 1
- Previous symbol:
- PEDF
- Synonyms:
- EPC-1, PIG35
- Chromosome:
- 17p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-18
- Date modifiied:
- 2018-03-02
Related products to: PEDF
Angiogenesis: PEDF, 20-418aa, Human, His tag, E.coliAngiogenesis: PEDF, 20-418aa, Human, His tag, E.coliAnserine Pigment Epithelium Derived Factor Elisa Kit (PEDF)Anserine anti - Pigment Epithelium Derived Factor Elisa Kit (PEDF)Anti PEDF Monoclonal Antibody ( Clone No.14K )Anti PEDF Monoclonal Antibody ( Clone No.14K )Anti PEDF Monoclonal Antibody ( Clone No.14K )Anti PEDF Monoclonal Antibody ( Clone No.14K )Anti PEDF Monoclonal Antibody ( Clone No.14K )Anti-human PEDF, Source: Monoclonal Murine , MABAnti-human PEDF, Source: Monoclonal Murine , MABAnti-human PEDF, Source: Monoclonal Murine , MABAnti-Human, Rabbit Polyclonal Antibody ; PEDFAnti-Human, Sheep Polyclonal Antibody ; PEDFanti-PEDF Related articles to: PEDF
- Medication-related osteonecrosis of the jaw (MRONJ) is a complex condition associated with the use of antiresorptive drugs, such as bisphosphonates and denosumab. The condition is characterized by the presence of exposed bone in the maxillofacial region that fails to heal. MRONJ remains highly intractable, as its pathogenic mechanisms are not yet fully understood. It is therefore essential to elucidate the molecular mechanisms underlying the disease. MiRNA expression analysis and proteomic studies were performed on a selected cohort of patients with MRONJ on jawbone tissue, using qRT-PCR and 2D electrophoresis followed by mass spectrometry. MiRNAs and proteomics data validation was carried out by Western blot analysis of differentially expressed proteins highlighted by a proteome study and predicted targets of differentially expressed miRNAs. Nineteen miRNAs were overexpressed and two downregulated in jawbone tissue from all MRONJ patients. Notably, five of these dysregulated miRNAs are involved in the regulation of angiogenesis and desmosome functions, suggesting a potential link to the molecular alterations observed at the protein level. Proteomic analysis revealed decreased concentrations of the pigment epithelium-derived factor, and of desmoglein-1, a desmosomal cadherin. Validation analysis confirmed the dysregulation of pathways involved in bone remodeling and necroptosis. The pathophysiology of MRONJ arises from a complex interplay of factors, including impaired bone remodeling, affected angiogenesis, and altered cell adhesion and differentiation mechanisms, ultimately leading to necroptosis. Through proteomic analysis and validation of miRNA expression, our study proposes specific molecular alteration in MRONJ-compromised bone tissue, involving desmosomal component imbalance and angiogenesis inhibition. - Source: PubMed
Publication date: 2026/06/05
Allegra AlessandroDe Salvo RossanaMarcianò AntoniaPolito FrancescaStagno FabioCarleo AlfonsoCostanzo MicheleCaterino MariannaRagusa MarcoLicitri LauraDrago Selene Francesca AnnaGasparo IreneAlberti GiuseppeKhouyyi MariemeSiniscalchi Enrico NastroOteri GiacomoBini LucaMacaione VincenzoBianchi LauraAguennouz M'hammed - Otosclerosis is a common cause of conductive hearing loss thought to result from dysregulated bone remodeling in the embryonic tissues of the globuli interossei. Both familial and sporadic cases have been reported. To date, 10 published loci and four genes ( (), (), , ) have been identified in autosomal dominant families. Using a combined genetic and genomics approach in five affected siblings, we identified a nonsense mutation in Karyopherin subunit α7 (, c.49C>T, p.R17X), the newest of the importin-α family of nuclear transporters. KPNA7 is a key maternal factor involved in the classical transport of NLS-containing cargo proteins, active during early embryonic cleavage events and zygotic genome activation. So far, 377 cargo proteins associated with KPNA7 have been identified. Recessive variants cause skeletal abnormalities, epilepsy, intellectual disabilities and preimplantation embryo arrest (PREMBA). A closer look at the genes reveals their involvement in endochondral ossification signaling pathways. We explore how KPNA7 haploinsufficiency in the embryonic tissues of the otic capsule may cause dysregulated bone remodeling. This study expands the phenotypic spectrum of KPNA7 and provides new insights into the pathobiology of otosclerosis. - Source: PubMed
Publication date: 2026/05/30
Benteau TammyAbdelfatah NellyGriffin AnnePenney CindyHu PingzhaoStanton Susan GZhai GuangjuMaheu MaximeFrench Curtis RYoung Terry-Lynn - Primary open-angle glaucoma (POAG) is a leading cause of irreversible blindness driven by elevated intraocular pressure from compromised aqueous outflow. While genome-wide association studies have identified numerous risk loci, specific candidate proteins and their cellular mechanisms remain elusive. We employed a multi-omics framework integrating UK Biobank plasma proteomics (N = 53,022) and large-scale POAG GWAS summary statistics. We performed a Proteome-Wide Association Study, Mendelian Randomization, and Bayesian colocalization to infer causality. Identified candidates were mapped to human and mouse ocular scRNA-seq atlases to characterize cell-type specificity, followed by druggability assessments. We prioritized five putative causal proteins, with SEL1L and TFPI demonstrating the strongest evidence. Cross-species scRNA-seq revealed that SEL1L and SERPINF1 are robustly expressed in the trabecular meshwork (TM), particularly the juxtacanalicular tissue, implicating them in outflow resistance. Conversely, TFPI and SLC9A3R2 localize to Schlemm's canal endothelium, suggesting a role in modulating barrier function. Pathway analyses highlighted endoplasmic reticulum protein processing and coagulation cascades. This study maps putative causal POAG proteins to conventional outflow pathway cells, highlighting SEL1L as a novel target for TM homeostasis and TFPI for drug repurposing, thereby providing data-driven hypotheses to facilitate precision glaucoma therapeutics. - Source: PubMed
Publication date: 2026/05/22
Kan HaoWen LeiLiu YuanZhang KaMao AiqinGeng LiYu FanFeng Lei - This review illustrates how environmental stressors disrupt glutamate homeostasis via specific mechanisms: lead-induced thiol modification, manganese mediated yin yang 1 (YY1)-histone deacetylases (HDAC) repression, PM2.5-triggered microglia-astrocyte crosstalk, and advanced glycation end products (AGEs)-receptor for advanced glycation end products (RAGE)-nuclear factor kappa-B (NF-κB) signaling from high-sugar diets. Together with genetic susceptibility and pigment epithelium-derived factor (PEDF), these factors impair astrocytic glutamate uptake, promoting synaptic glutamate accumulation. Subsequent N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptor overactivation triggers calcium overload, mitochondrial dysfunction, oxidative stress, and neuroinflammation-termed "degenerative excitotoxicity". Excitotoxicity manifests in Alzheimer's disease (amyloid-beta-excitatory amino acid transporter 2 (EAAT2) interplay), Parkinson's disease (subthalamic nucleus-driven excitatory storm), and amyotrophic lateral sclerosis (astrocytic failure versus neuronal cell-autonomous mechanisms). Future interventions need multi-target strategies, emerging technologies, and lifestyle modifications. This convergent framework offers a unified understanding linking environmental exposure to neurodegeneration and charts a roadmap toward mechanism-based prevention and treatment. - Source: PubMed
Publication date: 2026/06/11
He YuluYi TingtingMin MeixinXu KeLin HuanXu RongDeng DanXiao Xiaoping - Obesity is a major global public health challenge that contributes to numerous comorbidities and increased mortality. A better understanding of the biological mechanisms and disease risks associated with obesity requires robust monitoring of key circulating biomarkers, including adipokines, apolipoproteins, and inflammatory proteins. Targeted mass spectrometry (MS) offers a promising platform for developing specific, standardized, and multiplexed assays for biomarker quantification. In this study, we developed a multiplex targeted MS assay for the quantification of 42 obesity-associated biomarker candidates in human plasma. The assay was optimized for surrogate peptide selection, digestion incubation time, and LC gradient, and evaluated for linearity, lower limit of quantification (LLOQ), imprecision, and stability. A semi-automated sample preparation workflow using 96-well plates was also established to support high-throughput implementation. The assay was applied to a clinical cohort undergoing weight loss interventions to evaluate differences in protein abundance across obesity-related groups and to monitor biomarker changes over time. Statistical analyses were performed to identify proteins with significantly different abundances between study groups and before versus after intervention. The assay demonstrated acceptable linearity, LLOQ, imprecision, and stability. Inter-laboratory validation using samples from 70 healthy individuals showed strong correlation with the finalized standard operating procedure (SOP). Application of the assay to an obesity cohort revealed significant differences in the levels of 6 proteins across obese, overweight, and healthy control groups, as well as 16 proteins that were differentially abundant in obese individuals compared with non-obese individuals (overweight and healthy controls combined). In subjects undergoing weight loss interventions, four proteins-CRP, PRG4, SERPINF1, and SHBG-showed significant concentration changes in individuals who achieved > 5% weight loss. These results demonstrate the robustness and high-throughput capability of this multiplex targeted MS assay for measuring obesity-associated plasma biomarkers. The assay shows potential clinical utility for improving the diagnosis, stratification, and risk assessment of obesity-related conditions, as well as for monitoring responses to weight loss interventions. - Source: PubMed
Publication date: 2026/05/20
Lin Tai-TuDakup PanshakSchepmoes Athena AFillmore Thomas LSwensen Adam CKelly Shane SZhang TongPu JieJacobs Jon MDeLany James PGoodpaster Bret HShi TujinQu JunQian Wei-Jun