PTPRF Antibody
- Known as:
- PTPRF Antibody
- Catalog number:
- XW-7816
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- PTPRF Antibody
Ask about this productRelated genes to: PTPRF Antibody
- Gene:
- PTPRF NIH gene
- Name:
- protein tyrosine phosphatase receptor type F
- Previous symbol:
- LAR
- Synonyms:
- -
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-02-14
Related products to: PTPRF Antibody
Related articles to: PTPRF Antibody
- Canine oral cancers are difficult to manage due to complex biology and a lack of non-invasive biomarkers. Proteomic approaches, particularly gel-based liquid chromatography-tandem mass spectrometry (GeLC-MS/MS), have been used on tissue and saliva, but serum remains obscure despite its clinical accessibility and ability to reflect systemic disease. - Source: PubMed
Ploypetch SekkarinRoytrakul SittirukJaresitthikunchai JanthimaPhaonakrop NarumonSuriyaphol Gunnaporn - The surging demand for environmentally benign alternatives to petroleum-based resins has sparked interest in bio-derived phenolic systems for biocomposites and additive manufacturing. This study reports the development of an extruded tannin-PRF (phenol-resorcinol-formaldehyde) resin-wood composites using ponderosa pine bark tannins (PT) and commercial maritime pine bark tannins (CT) as renewable phenolic substitutes. The hybridization of tannins with PRF aimed to enhance renewable content while retaining the mechanical and thermal performance essential for extrusion-based manufacturing. All resin-wood blends exhibited shear-thinning behavior with consistent complex viscosity, confirming their processability for extrusion. Thermogravimetric (TGA) and dynamic mechanical (DMA) analyses revealed that tannin incorporation delayed degradation onset and increased glass transition temperature (T) due to enhanced aromatic condensation and crosslink formation. Among the formulations, the PT-PRF wood composite achieved the most balanced thermal performance, combining moderate T of 211 °C, delayed decomposition, and higher char yield. Mechanical testing demonstrated that tannin-PRF hybrid composites achieved flexural strength (40-47 MPa) and modulus (4.0-4.3 GPa) comparable to neat PRF, whereas neat tannin composites exhibited lower values due to reduced crosslink density. Water absorption studies showed that hybrid systems maintained low equilibrium uptake ranging from 19 to 24% and Fickian diffusion behavior, indicating improved dimensional stability and interfacial cohesion. Overall, these findings establish tannin-PRF hybrid resins as promising, high-performance, and partially bio-based alternatives for cleaner extrusion manufacturing of structural wood composites, advancing the transition toward renewable materials and circular bioeconomy applications. - Source: PubMed
Publication date: 2026/04/20
Ahmed ShafaetMcDonald Armando G - : Gastric-type adenocarcinoma (GAS) of the uterine cervix is a rare malignancy with poor clinical outcomes. However, the carcinogenic processes involved remain unclear. : Normal cervical glands, lobular endocervical glandular hyperplasia (LEGH), and GAS from the same patients were collected using laser microdissection for whole-exome sequencing. Single nucleotide variants (SNVs) and copy number alterations (CNAs) were analyzed. Phylogenetic trees were constructed based on the SNV and CNA profiles. : Analysis of seven matched samples demonstrated higher frequency of somatic mutations in the exonic regions in GAS than in LEGH. CNAs were prevalent in GAS but rare in LEGH. The phylogenetic analyses revealed various branching patterns. However, in three cases, the data suggested a sequential transition from LEGH to GAS, potentially associated with mutations in receptor-type protein tyrosine phosphatases such as and . and mutations were present in LEGH, with an increased variant allele frequency observed in GAS. In contrast, and showed frequent loss-of-function-type alterations in GAS, including copy-number loss, but were not detected in LEGH. : These findings provide insights into the genomic landscapes of LEGH and GAS and suggest potential molecular markers for this transition, which may inform future diagnostic and therapeutic research. - Source: PubMed
Publication date: 2026/02/17
Kuruma AiriMasuda TatsuoSato KazuakiKido KansukeMotooka DaisukeKomura NaokoYokoi TakeshiYoshihara KosukeKinose YasutoHashimoto KaeSawada KenjiroMorii EiichiKimura TadashiKodama Michiko - Asprosin, a fasting-induced glucogenic hormone, plays a crucial role in maintaining glucose homeostasis; however, its receptor remains elusive. This study identifies protein tyrosine phosphatase receptor F (Ptprf) as the receptor mediating Asprosin's metabolic functions. Using zebrafish models, we demonstrate the evolutionary conservation of Asprosin's role in glucose metabolism. Through binding assays, we determined Ptprf as Asprosin's interacting receptor in zebrafish liver. Zebrafish possess two Ptprf paralogs (Ptprfa/b), both hepatically expressed and binding Asprosin with high affinity. The genetic ablation of ptprfa/b reduced basal glucose levels and eliminated Asprosin-induced hyperglycemia. Conversely, the overexpression of soluble Ptprf ligand-binding domains neutralized Asprosin's glucogenic effects. These findings were validated in mammals: Asprosin binds PTPRF in mice and humans, and Ptprf knockout mice showed a blunted response to Asprosin. Our results establish Ptprf as an evolutionarily conserved Asprosin receptor across vertebrates, providing mechanistic insights for developing therapies targeting this pathway for diabetes and obesity. - Source: PubMed
Publication date: 2026/02/10
Liu ZhiquanWang PengyuHu YixuanZhang NanXu LitingKang TaoZhao ShengyouZhao DepingChan ChibunLi Jianzhen - A major goal of biomedical research is to assign functions to the myriad alternative RNA and protein isoforms. This challenge is particularly relevant to the mammalian nervous system, which produces complex repertoires of alternative splicing events. Here, we describe CHyMErA-seq, a platform that couples systematic deletion of exons to a single cell transcriptomics read-out, and apply this method to investigate a critical program of brain-specific microexons. Perturbation of microexons during neurogenesis reveals convergent roles in the temporal regulation of gene expression programs that direct signaling pathways and morphogenesis. We further observe microexons, including those in the Bin1, Clasp1, Gfra1, Med23, Ptprf and Ralgapb genes, that are required for the correct timing of autism-linked gene expression. Collectively, we describe a flexible system for isoform-resolution perturbation at a single cell level, together with insights into the roles of microexons in the developmental timing of neurogenesis transcriptomic signatures linked to brain disorders. - Source: PubMed
Publication date: 2026/02/03
Dupas Steven JParada Guillermo ELi Jack DaiyangBrown Kevin RMoffat JasonBlencowe Benjamin J